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Enthesitis, arthritis, tenosynovitis linked to dupilumab use for atopic dermatitis
Around 5% of patients treated with dupilumab (Dupixent) for moderate-to-severe atopic dermatitis experience musculoskeletal (MSK) symptoms, according to the results of a descriptive study.
The main MSK symptom seen in the observational cohort was enthesitis, but some patients also experienced arthritis and tenosynovitis a median of 17 weeks after starting dupilumab treatment. Together these symptoms represent a new MSK syndrome, say researchers from the United Kingdom.
“The pattern of MSK symptoms and signs is characteristic of psoriatic arthritis/peripheral spondyloarthritis,” Bruce Kirkham, MD, and collaborators report in Arthritis & Rheumatology.
“We started a few years ago and have been following the patients for quite a long time,” Dr. Kirkham, a consultant rheumatologist at Guy’s and St. Thomas’ NHS Foundation Trust, London, told this news organization.
“We’re still seeing patients with the same type of syndrome presenting occasionally. It’s not a very common adverse event, but we think it continues,” he observed.
“Most of them don’t have very severe problems, and a lot of them can be treated with quite simple drugs or, alternatively, reducing the frequency of the injection,” Dr. Kirkham added.
Characterizing the MSK symptoms
Of 470 patients with atopic dermatitis who started treatment with dupilumab at Guy’s and St. Thomas’ NHS Foundation Trust between October 2018 and February 2021, 36 (7.65%) developed rheumatic symptoms and were referred to the rheumatology department. These individuals had their family history assessed and thorough MSK evaluations, which included antibody and inflammatory markers, ultrasound of the peripheral small joints, and MRI of the large joints and spine.
A total of 26 (5.5%) patients – 14 of whom were male – had inflammatory enthesitis, arthritis, and/or tenosynovitis. Of the others, seven had osteoarthritis and three had degenerative spine disease.
Enthesitis was the most common finding in those with rheumatic symptoms, occurring on its own in 11 patients, with arthritis in three patients, and tenosynovitis in two patients.
These symptoms appeared 2-48 weeks after starting dupilumab treatment and were categorized as mild in 16 (61%) cases, moderate in six cases, and severe in four cases.
No specific predictors of the MSK symptoms seen were noted. Patient age, sex, duration of their atopic dermatitis, or how their skin condition had been previously treated did not help identify those who might develop rheumatic problems.
Conservative management approach
All patients had “outstanding” responses to treatment, Dr. Kirkham noted: The mean Eczema Area and Severity Index score before dupilumab treatment was 21, falling to 4.2 with treatment, indicating a mean 80% improvement.
Co-author Joseph Nathan, MBChB, of London North West Healthcare NHS Trust, who collaborated on the research while working within Dr. Kirkham’s group, said separately: “The concern that patients have is that when they start a medication and develop a side effect is that the medication is going to be stopped.”
Clinicians treating the patients took a conservative approach, prescribing NSAIDs such as cyclooxygenase-2 inhibitors or altering the frequency with which dupilumab was given.
With this approach, MSK symptoms resolved in 15 patients who remained on treatment and in seven who had to stop dupilumab. There were four patients, however, who had unresolved symptoms even once dupilumab treatment had been stopped.
Altering the local cytokine balance
Dupilumab is a monoclonal antibody that binds to the alpha subunit of the interleukin-4 receptor. This results in blocking the function of not only IL-4 but also IL-13.
Dr. Kirkham and colleagues think this might not only alter the balance of cytokines in the skin but also in the joints and entheses with IL-17, IL-23, or even tumor necrosis factor playing a possible role. Another thought is that many circulating T-cells in the skin move to the joints and entheses to trigger symptoms.
IL-13 inhibition does seem to be important, as another British research team, from the Centre for Epidemiology Versus Arthritis at the University of Manchester (England), has found.
At the recent annual meeting of the British Society for Rheumatology, Sizheng Steven Zhao, MBChB, PhD, and colleagues reported that among people who carried a genetic variant predisposing them to having low IL-13 function, there was a higher risk for inflammatory diseases such as psoriatic arthritis and other spondyloarthropathy-related diseases.
Indeed, when the single nucleotide polymorphism rs20541 was present, the odds for having psoriatic arthritis and psoriasis were higher than when it was not.
The findings are consistent with the idea that IL-4 and IL-13 may be acting as a restraint towards MSK diseases in some patients, Dr. Zhao and co-authors suggest.
“The genetic data supports what [Dr. Kirkham and team] have said from a mechanistic point of view,” Dr. Zhao said in an interview. “What you’re observing has a genetic basis.”
Dermatology perspective
Approved by the U.S. Food and Drug Administration in 2017, dupilumab has since been hailed as a “breakthrough” in atopic dermatitis treatment. Given as a subcutaneous injection every 2 weeks, it provides a much-needed option for people who have moderate-to-severe disease and have tried other available treatments, including corticosteroids.
Dupilumab has since also been approved for asthma, chronic sinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis and is used off-label for other skin conditions such as contact dermatitis, chronic spontaneous urticaria, and alopecia areata.
“Dupilumab, like a lot of medications for atopic dermatitis, is a relatively new drug, and we are still learning about its safety,” Joel M. Gelfand, MD, MSCE, of the University of Pennsylvania Perelman School of Medicine, Philadelphia, told this news organization.
“Inflammatory arthritis has been reported in patients treated with dupilumab, and this new study provides some useful estimates,” added Dr. Gelfand, who is a professor of dermatology and epidemiology and directs the Psoriasis and Phototherapy Treatment Center, Philadelphia.
“There was no control group,” Dr. Gelfand said, so “a causal relationship cannot be well established based on these data alone. The mechanism is not known but may result from a shifting of the immune system.”
Dr. Zhao observed: “We don’t know what the natural history of these adverse events is. We don’t know if stopping the drug early will prevent long-term adverse events. So, we don’t know if people will ultimately develop permanent psoriatic arthritis if we don’t intervene quick enough when we observe an adverse event.”
Being aware of the possibility of rheumatic side effects occurring with dupilumab and similar agents is key, Dr. Gelfand and Dr. Kirkham both said independently.
“I have personally seen this entity in my practice,” Dr. Gelfand said. “It is important to clinicians prescribing dupilumab to alert patients about this potential side effect and ask about joint symptoms in follow-up.”
Dr. Kirkham said: “Prescribers need to be aware of it, because up until now it’s been just very vaguely discussed as sort of aches and pains, arthralgias, and it’s a much more specific of a kind of syndrome of enthesitis, arthritis, tenosynovitis – a little like psoriatic arthritis.”
Not everyone has come across these side effects, however, as Steven Daveluy, MD, associate professor and dermatology program director at Wayne State University, Detroit, said in an interview.
“This article and the other case series both noted the musculoskeletal symptoms occurred in about 5% of patients, which surprised me since I haven’t seen it in my practice and have enough patients being treated with dupilumab that I would expect to see a case at that rate,” Dr. Daveluy said.
“The majority of cases are mild and respond to treatment with anti-inflammatories like naproxen, which is available over the counter. It’s likely that patients with a mild case could simply treat their pain with naproxen that’s already in their medicine cabinet until it resolves, never bringing it to the doctor’s attention,” he suggested.
“Dupilumab is still a safe and effective medication that can change the lives of patients suffering from atopic dermatitis,” he said.
“Awareness of this potential side effect can help dermatologists recognize it early and work together with patients to determine the best course of action.”
All research mentioned in this article was independently supported. Dr. Kirkham, Mr. Nathan, Dr. Zhao, and Dr. Daveluy report no relevant financial relationships. Dr. Gelfand has served as a consultant for numerous pharmaceutical companies and receives research grants from Amgen, Boehringer Ingelheim, and Pfizer. He is a co-patent holder of resiquimod for treatment of cutaneous T-cell lymphoma.
A version of this article first appeared on Medscape.com.
Around 5% of patients treated with dupilumab (Dupixent) for moderate-to-severe atopic dermatitis experience musculoskeletal (MSK) symptoms, according to the results of a descriptive study.
The main MSK symptom seen in the observational cohort was enthesitis, but some patients also experienced arthritis and tenosynovitis a median of 17 weeks after starting dupilumab treatment. Together these symptoms represent a new MSK syndrome, say researchers from the United Kingdom.
“The pattern of MSK symptoms and signs is characteristic of psoriatic arthritis/peripheral spondyloarthritis,” Bruce Kirkham, MD, and collaborators report in Arthritis & Rheumatology.
“We started a few years ago and have been following the patients for quite a long time,” Dr. Kirkham, a consultant rheumatologist at Guy’s and St. Thomas’ NHS Foundation Trust, London, told this news organization.
“We’re still seeing patients with the same type of syndrome presenting occasionally. It’s not a very common adverse event, but we think it continues,” he observed.
“Most of them don’t have very severe problems, and a lot of them can be treated with quite simple drugs or, alternatively, reducing the frequency of the injection,” Dr. Kirkham added.
Characterizing the MSK symptoms
Of 470 patients with atopic dermatitis who started treatment with dupilumab at Guy’s and St. Thomas’ NHS Foundation Trust between October 2018 and February 2021, 36 (7.65%) developed rheumatic symptoms and were referred to the rheumatology department. These individuals had their family history assessed and thorough MSK evaluations, which included antibody and inflammatory markers, ultrasound of the peripheral small joints, and MRI of the large joints and spine.
A total of 26 (5.5%) patients – 14 of whom were male – had inflammatory enthesitis, arthritis, and/or tenosynovitis. Of the others, seven had osteoarthritis and three had degenerative spine disease.
Enthesitis was the most common finding in those with rheumatic symptoms, occurring on its own in 11 patients, with arthritis in three patients, and tenosynovitis in two patients.
These symptoms appeared 2-48 weeks after starting dupilumab treatment and were categorized as mild in 16 (61%) cases, moderate in six cases, and severe in four cases.
No specific predictors of the MSK symptoms seen were noted. Patient age, sex, duration of their atopic dermatitis, or how their skin condition had been previously treated did not help identify those who might develop rheumatic problems.
Conservative management approach
All patients had “outstanding” responses to treatment, Dr. Kirkham noted: The mean Eczema Area and Severity Index score before dupilumab treatment was 21, falling to 4.2 with treatment, indicating a mean 80% improvement.
Co-author Joseph Nathan, MBChB, of London North West Healthcare NHS Trust, who collaborated on the research while working within Dr. Kirkham’s group, said separately: “The concern that patients have is that when they start a medication and develop a side effect is that the medication is going to be stopped.”
Clinicians treating the patients took a conservative approach, prescribing NSAIDs such as cyclooxygenase-2 inhibitors or altering the frequency with which dupilumab was given.
With this approach, MSK symptoms resolved in 15 patients who remained on treatment and in seven who had to stop dupilumab. There were four patients, however, who had unresolved symptoms even once dupilumab treatment had been stopped.
Altering the local cytokine balance
Dupilumab is a monoclonal antibody that binds to the alpha subunit of the interleukin-4 receptor. This results in blocking the function of not only IL-4 but also IL-13.
Dr. Kirkham and colleagues think this might not only alter the balance of cytokines in the skin but also in the joints and entheses with IL-17, IL-23, or even tumor necrosis factor playing a possible role. Another thought is that many circulating T-cells in the skin move to the joints and entheses to trigger symptoms.
IL-13 inhibition does seem to be important, as another British research team, from the Centre for Epidemiology Versus Arthritis at the University of Manchester (England), has found.
At the recent annual meeting of the British Society for Rheumatology, Sizheng Steven Zhao, MBChB, PhD, and colleagues reported that among people who carried a genetic variant predisposing them to having low IL-13 function, there was a higher risk for inflammatory diseases such as psoriatic arthritis and other spondyloarthropathy-related diseases.
Indeed, when the single nucleotide polymorphism rs20541 was present, the odds for having psoriatic arthritis and psoriasis were higher than when it was not.
The findings are consistent with the idea that IL-4 and IL-13 may be acting as a restraint towards MSK diseases in some patients, Dr. Zhao and co-authors suggest.
“The genetic data supports what [Dr. Kirkham and team] have said from a mechanistic point of view,” Dr. Zhao said in an interview. “What you’re observing has a genetic basis.”
Dermatology perspective
Approved by the U.S. Food and Drug Administration in 2017, dupilumab has since been hailed as a “breakthrough” in atopic dermatitis treatment. Given as a subcutaneous injection every 2 weeks, it provides a much-needed option for people who have moderate-to-severe disease and have tried other available treatments, including corticosteroids.
Dupilumab has since also been approved for asthma, chronic sinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis and is used off-label for other skin conditions such as contact dermatitis, chronic spontaneous urticaria, and alopecia areata.
“Dupilumab, like a lot of medications for atopic dermatitis, is a relatively new drug, and we are still learning about its safety,” Joel M. Gelfand, MD, MSCE, of the University of Pennsylvania Perelman School of Medicine, Philadelphia, told this news organization.
“Inflammatory arthritis has been reported in patients treated with dupilumab, and this new study provides some useful estimates,” added Dr. Gelfand, who is a professor of dermatology and epidemiology and directs the Psoriasis and Phototherapy Treatment Center, Philadelphia.
“There was no control group,” Dr. Gelfand said, so “a causal relationship cannot be well established based on these data alone. The mechanism is not known but may result from a shifting of the immune system.”
Dr. Zhao observed: “We don’t know what the natural history of these adverse events is. We don’t know if stopping the drug early will prevent long-term adverse events. So, we don’t know if people will ultimately develop permanent psoriatic arthritis if we don’t intervene quick enough when we observe an adverse event.”
Being aware of the possibility of rheumatic side effects occurring with dupilumab and similar agents is key, Dr. Gelfand and Dr. Kirkham both said independently.
“I have personally seen this entity in my practice,” Dr. Gelfand said. “It is important to clinicians prescribing dupilumab to alert patients about this potential side effect and ask about joint symptoms in follow-up.”
Dr. Kirkham said: “Prescribers need to be aware of it, because up until now it’s been just very vaguely discussed as sort of aches and pains, arthralgias, and it’s a much more specific of a kind of syndrome of enthesitis, arthritis, tenosynovitis – a little like psoriatic arthritis.”
Not everyone has come across these side effects, however, as Steven Daveluy, MD, associate professor and dermatology program director at Wayne State University, Detroit, said in an interview.
“This article and the other case series both noted the musculoskeletal symptoms occurred in about 5% of patients, which surprised me since I haven’t seen it in my practice and have enough patients being treated with dupilumab that I would expect to see a case at that rate,” Dr. Daveluy said.
“The majority of cases are mild and respond to treatment with anti-inflammatories like naproxen, which is available over the counter. It’s likely that patients with a mild case could simply treat their pain with naproxen that’s already in their medicine cabinet until it resolves, never bringing it to the doctor’s attention,” he suggested.
“Dupilumab is still a safe and effective medication that can change the lives of patients suffering from atopic dermatitis,” he said.
“Awareness of this potential side effect can help dermatologists recognize it early and work together with patients to determine the best course of action.”
All research mentioned in this article was independently supported. Dr. Kirkham, Mr. Nathan, Dr. Zhao, and Dr. Daveluy report no relevant financial relationships. Dr. Gelfand has served as a consultant for numerous pharmaceutical companies and receives research grants from Amgen, Boehringer Ingelheim, and Pfizer. He is a co-patent holder of resiquimod for treatment of cutaneous T-cell lymphoma.
A version of this article first appeared on Medscape.com.
Around 5% of patients treated with dupilumab (Dupixent) for moderate-to-severe atopic dermatitis experience musculoskeletal (MSK) symptoms, according to the results of a descriptive study.
The main MSK symptom seen in the observational cohort was enthesitis, but some patients also experienced arthritis and tenosynovitis a median of 17 weeks after starting dupilumab treatment. Together these symptoms represent a new MSK syndrome, say researchers from the United Kingdom.
“The pattern of MSK symptoms and signs is characteristic of psoriatic arthritis/peripheral spondyloarthritis,” Bruce Kirkham, MD, and collaborators report in Arthritis & Rheumatology.
“We started a few years ago and have been following the patients for quite a long time,” Dr. Kirkham, a consultant rheumatologist at Guy’s and St. Thomas’ NHS Foundation Trust, London, told this news organization.
“We’re still seeing patients with the same type of syndrome presenting occasionally. It’s not a very common adverse event, but we think it continues,” he observed.
“Most of them don’t have very severe problems, and a lot of them can be treated with quite simple drugs or, alternatively, reducing the frequency of the injection,” Dr. Kirkham added.
Characterizing the MSK symptoms
Of 470 patients with atopic dermatitis who started treatment with dupilumab at Guy’s and St. Thomas’ NHS Foundation Trust between October 2018 and February 2021, 36 (7.65%) developed rheumatic symptoms and were referred to the rheumatology department. These individuals had their family history assessed and thorough MSK evaluations, which included antibody and inflammatory markers, ultrasound of the peripheral small joints, and MRI of the large joints and spine.
A total of 26 (5.5%) patients – 14 of whom were male – had inflammatory enthesitis, arthritis, and/or tenosynovitis. Of the others, seven had osteoarthritis and three had degenerative spine disease.
Enthesitis was the most common finding in those with rheumatic symptoms, occurring on its own in 11 patients, with arthritis in three patients, and tenosynovitis in two patients.
These symptoms appeared 2-48 weeks after starting dupilumab treatment and were categorized as mild in 16 (61%) cases, moderate in six cases, and severe in four cases.
No specific predictors of the MSK symptoms seen were noted. Patient age, sex, duration of their atopic dermatitis, or how their skin condition had been previously treated did not help identify those who might develop rheumatic problems.
Conservative management approach
All patients had “outstanding” responses to treatment, Dr. Kirkham noted: The mean Eczema Area and Severity Index score before dupilumab treatment was 21, falling to 4.2 with treatment, indicating a mean 80% improvement.
Co-author Joseph Nathan, MBChB, of London North West Healthcare NHS Trust, who collaborated on the research while working within Dr. Kirkham’s group, said separately: “The concern that patients have is that when they start a medication and develop a side effect is that the medication is going to be stopped.”
Clinicians treating the patients took a conservative approach, prescribing NSAIDs such as cyclooxygenase-2 inhibitors or altering the frequency with which dupilumab was given.
With this approach, MSK symptoms resolved in 15 patients who remained on treatment and in seven who had to stop dupilumab. There were four patients, however, who had unresolved symptoms even once dupilumab treatment had been stopped.
Altering the local cytokine balance
Dupilumab is a monoclonal antibody that binds to the alpha subunit of the interleukin-4 receptor. This results in blocking the function of not only IL-4 but also IL-13.
Dr. Kirkham and colleagues think this might not only alter the balance of cytokines in the skin but also in the joints and entheses with IL-17, IL-23, or even tumor necrosis factor playing a possible role. Another thought is that many circulating T-cells in the skin move to the joints and entheses to trigger symptoms.
IL-13 inhibition does seem to be important, as another British research team, from the Centre for Epidemiology Versus Arthritis at the University of Manchester (England), has found.
At the recent annual meeting of the British Society for Rheumatology, Sizheng Steven Zhao, MBChB, PhD, and colleagues reported that among people who carried a genetic variant predisposing them to having low IL-13 function, there was a higher risk for inflammatory diseases such as psoriatic arthritis and other spondyloarthropathy-related diseases.
Indeed, when the single nucleotide polymorphism rs20541 was present, the odds for having psoriatic arthritis and psoriasis were higher than when it was not.
The findings are consistent with the idea that IL-4 and IL-13 may be acting as a restraint towards MSK diseases in some patients, Dr. Zhao and co-authors suggest.
“The genetic data supports what [Dr. Kirkham and team] have said from a mechanistic point of view,” Dr. Zhao said in an interview. “What you’re observing has a genetic basis.”
Dermatology perspective
Approved by the U.S. Food and Drug Administration in 2017, dupilumab has since been hailed as a “breakthrough” in atopic dermatitis treatment. Given as a subcutaneous injection every 2 weeks, it provides a much-needed option for people who have moderate-to-severe disease and have tried other available treatments, including corticosteroids.
Dupilumab has since also been approved for asthma, chronic sinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis and is used off-label for other skin conditions such as contact dermatitis, chronic spontaneous urticaria, and alopecia areata.
“Dupilumab, like a lot of medications for atopic dermatitis, is a relatively new drug, and we are still learning about its safety,” Joel M. Gelfand, MD, MSCE, of the University of Pennsylvania Perelman School of Medicine, Philadelphia, told this news organization.
“Inflammatory arthritis has been reported in patients treated with dupilumab, and this new study provides some useful estimates,” added Dr. Gelfand, who is a professor of dermatology and epidemiology and directs the Psoriasis and Phototherapy Treatment Center, Philadelphia.
“There was no control group,” Dr. Gelfand said, so “a causal relationship cannot be well established based on these data alone. The mechanism is not known but may result from a shifting of the immune system.”
Dr. Zhao observed: “We don’t know what the natural history of these adverse events is. We don’t know if stopping the drug early will prevent long-term adverse events. So, we don’t know if people will ultimately develop permanent psoriatic arthritis if we don’t intervene quick enough when we observe an adverse event.”
Being aware of the possibility of rheumatic side effects occurring with dupilumab and similar agents is key, Dr. Gelfand and Dr. Kirkham both said independently.
“I have personally seen this entity in my practice,” Dr. Gelfand said. “It is important to clinicians prescribing dupilumab to alert patients about this potential side effect and ask about joint symptoms in follow-up.”
Dr. Kirkham said: “Prescribers need to be aware of it, because up until now it’s been just very vaguely discussed as sort of aches and pains, arthralgias, and it’s a much more specific of a kind of syndrome of enthesitis, arthritis, tenosynovitis – a little like psoriatic arthritis.”
Not everyone has come across these side effects, however, as Steven Daveluy, MD, associate professor and dermatology program director at Wayne State University, Detroit, said in an interview.
“This article and the other case series both noted the musculoskeletal symptoms occurred in about 5% of patients, which surprised me since I haven’t seen it in my practice and have enough patients being treated with dupilumab that I would expect to see a case at that rate,” Dr. Daveluy said.
“The majority of cases are mild and respond to treatment with anti-inflammatories like naproxen, which is available over the counter. It’s likely that patients with a mild case could simply treat their pain with naproxen that’s already in their medicine cabinet until it resolves, never bringing it to the doctor’s attention,” he suggested.
“Dupilumab is still a safe and effective medication that can change the lives of patients suffering from atopic dermatitis,” he said.
“Awareness of this potential side effect can help dermatologists recognize it early and work together with patients to determine the best course of action.”
All research mentioned in this article was independently supported. Dr. Kirkham, Mr. Nathan, Dr. Zhao, and Dr. Daveluy report no relevant financial relationships. Dr. Gelfand has served as a consultant for numerous pharmaceutical companies and receives research grants from Amgen, Boehringer Ingelheim, and Pfizer. He is a co-patent holder of resiquimod for treatment of cutaneous T-cell lymphoma.
A version of this article first appeared on Medscape.com.
FROM ARTHRITIS & RHEUMATOLOGY
Sublingual immunotherapy stops onset and worsening of asthma
PARIS – The EfficAPSI study showed with real-world data that sublingual immunotherapy (SLIT) reduces the risks for asthma onset and the worsening of asthma symptoms for patients with allergic rhinitis. The research was presented at the 18th French-language allergy conference.
These results confirm that allergen immunotherapy, or “desensitization,” is indeed an etiologic treatment of this allergic condition.
SLIT encompasses personalized solutions created for an individual specifically for allergies to dust mites, grass, birch, cats, and so on. These preparations are commonly used by allergy specialists when establishing an AIT treatment plan.
In 2017, the French Health Authority published a report indicating that there was insufficient clinical proof regarding the efficacy of SLIT. It subsequently removed injectable forms of these allergen extracts from the list of drugs reimbursed by the state and reduced state reimbursement of sublingual SLIT preparations from 30% to 15%, a step it confirmed in March 2018 and that led to outrage from allergy specialists. The chair of the French allergy society at the time, Jocelyne Just, MD, PhD, argued that conducting double-blind, placebo-controlled studies for all types (grass pollen, birch pollen, dust mites, asthma, allergic rhinitis, subcutaneous injections, sublingual treatments, tablets, liquid preparations) would take decades. Furthermore, meta-analyses on the subject, despite being heterogeneous and unable to answer all questions, are indeed pointing to the effectiveness of SLIT. To supplement existing data and to answer the queries raised by the HAS, several studies have been launched, including EfficAPSI.
The pharmacoepidemiologic EfficAPSI study is the largest retrospective, real-world, longitudinal cohort study ever carried out regarding liquid SLIT using data stored in the French National Health Data System (SNDS). The primary objective of the study was to evaluate the real-world impact of liquid SLIT on the onset and worsening of asthma for patients with allergic rhinitis and to evaluate the impact of sublingual treatments on public health.
A cohort analysis of patients treated with SLIT and control patients treated for allergic rhinitis with or without treatment for asthma was carried out. The patients treated with SLIT for at least 2 consecutive years were anonymously selected from the SNDS using the Stallergenes Greer prescription database.
In all, 99,538 patients who received SLIT were compared with 333,082 control patients (those who had received treatment for allergic rhinitis without taking SLIT). Participants were stratified according to their treatment history for asthma and were paired using a propensity score to minimize comparison bias.
The main definition of the onset of asthma included the first prescription of an asthma medication, hospital admission for asthma, or a diagnosis of chronic asthma. The secondary definition omitted the prescription of any treatment, and the third (sensitive and specific) took into consideration an initial prescription of omalizumab or a prescription of three inhaled corticosteroids (ICSs) associated with or without a long-acting beta-2 agonist (LABA) for a period of 1 year, admission to the hospital, or chronic asthma.
Asthma risk reduced
Among patients with allergic rhinitis without preexisting asthma, liquid SLIT was associated with a significantly lower risk of asthma onset in comparison with the control group (primary hazard ratio: 0.77; secondary HR: 0.66; and tertiary HR: 0.62).
The risk reductions were significant and were consistent regardless of the allergens analyzed (tertiary HR, dust mites: 0.57; grass: 0.52) for all age groups. These new results that were based on the tertiary definition corroborate the results from the primary and secondary definitions.
said study co-author Philippe Devillier, MD, PhD, research director at the respiratory tract diseases center of Foch Hospital, Paris. “These results are consistent with previous studies in the same French health care database, as well as in a German database with SLIT preparations in tablet form. This not only confirms the soundness of the methodology but also the benefit of liquid SLIT as an etiological treatment of respiratory allergies.”
Risk for worsening
Furthermore, in the same study, liquid SLIT treatment was associated with a 27% reduced risk for worsening asthma and a 36% reduced risk for severe asthma. Among patients with allergic rhinitis and preexisting asthma, liquid SLIT was associated with a significantly lower risk for worsening of asthma, compared with the control group (primary HR: 0.73; secondary HR: 0.61; and tertiary HR: 0.64). The primary definition was an initial prescription of an ICS-LABA combination in a patient treated with ICS alone, severe exacerbation of asthma symptoms, hospital admission, or a diagnosis of chronic asthma.
“The risk reductions were significant and consistent for the allergens analyzed,” said study co-author Pascal Demoly, MD, PhD, head of pulmonology at Montpellier University Hospital, France (tertiary HR, dust mites: 0.66; grass: 0.59; birch: 0.34; and cats: 0.77). “This was across all age groups,” he added.
“The results of the EfficAPSI real-world study on health data from the SNDS are consistent with outcomes from clinical trials, suggestive of a reduced risk of asthma onset in patients with allergic rhinitis receiving liquid SLIT, as well as a reduced risk of worsening of preexisting asthma,” said Devillier. “SLIT, in this case in the form of a liquid, thus appears to be an effective etiological treatment, since the use of symptomatic drugs, in particular preventer inhalers, but also reliever inhalers, is lower in patients treated with SLIT over at least two consecutive years, compared with paired control subjects. And it’s the same for the risk of treating asthma in nonasthmatic patients at the start of the study. EfficAPSI is the largest study using data from a comprehensive state drug reimbursement database, allowing us to assess the impact of liquid SLIT on public health. These results, also obtained with other allergen preparations, particularly in tablet form in French and German studies using data from health care databases, demonstrate the consistency of the data regarding the efficacy of SLIT.”
This article was translated from the Medscape French Edition. A version appeared on Medscape.com.
PARIS – The EfficAPSI study showed with real-world data that sublingual immunotherapy (SLIT) reduces the risks for asthma onset and the worsening of asthma symptoms for patients with allergic rhinitis. The research was presented at the 18th French-language allergy conference.
These results confirm that allergen immunotherapy, or “desensitization,” is indeed an etiologic treatment of this allergic condition.
SLIT encompasses personalized solutions created for an individual specifically for allergies to dust mites, grass, birch, cats, and so on. These preparations are commonly used by allergy specialists when establishing an AIT treatment plan.
In 2017, the French Health Authority published a report indicating that there was insufficient clinical proof regarding the efficacy of SLIT. It subsequently removed injectable forms of these allergen extracts from the list of drugs reimbursed by the state and reduced state reimbursement of sublingual SLIT preparations from 30% to 15%, a step it confirmed in March 2018 and that led to outrage from allergy specialists. The chair of the French allergy society at the time, Jocelyne Just, MD, PhD, argued that conducting double-blind, placebo-controlled studies for all types (grass pollen, birch pollen, dust mites, asthma, allergic rhinitis, subcutaneous injections, sublingual treatments, tablets, liquid preparations) would take decades. Furthermore, meta-analyses on the subject, despite being heterogeneous and unable to answer all questions, are indeed pointing to the effectiveness of SLIT. To supplement existing data and to answer the queries raised by the HAS, several studies have been launched, including EfficAPSI.
The pharmacoepidemiologic EfficAPSI study is the largest retrospective, real-world, longitudinal cohort study ever carried out regarding liquid SLIT using data stored in the French National Health Data System (SNDS). The primary objective of the study was to evaluate the real-world impact of liquid SLIT on the onset and worsening of asthma for patients with allergic rhinitis and to evaluate the impact of sublingual treatments on public health.
A cohort analysis of patients treated with SLIT and control patients treated for allergic rhinitis with or without treatment for asthma was carried out. The patients treated with SLIT for at least 2 consecutive years were anonymously selected from the SNDS using the Stallergenes Greer prescription database.
In all, 99,538 patients who received SLIT were compared with 333,082 control patients (those who had received treatment for allergic rhinitis without taking SLIT). Participants were stratified according to their treatment history for asthma and were paired using a propensity score to minimize comparison bias.
The main definition of the onset of asthma included the first prescription of an asthma medication, hospital admission for asthma, or a diagnosis of chronic asthma. The secondary definition omitted the prescription of any treatment, and the third (sensitive and specific) took into consideration an initial prescription of omalizumab or a prescription of three inhaled corticosteroids (ICSs) associated with or without a long-acting beta-2 agonist (LABA) for a period of 1 year, admission to the hospital, or chronic asthma.
Asthma risk reduced
Among patients with allergic rhinitis without preexisting asthma, liquid SLIT was associated with a significantly lower risk of asthma onset in comparison with the control group (primary hazard ratio: 0.77; secondary HR: 0.66; and tertiary HR: 0.62).
The risk reductions were significant and were consistent regardless of the allergens analyzed (tertiary HR, dust mites: 0.57; grass: 0.52) for all age groups. These new results that were based on the tertiary definition corroborate the results from the primary and secondary definitions.
said study co-author Philippe Devillier, MD, PhD, research director at the respiratory tract diseases center of Foch Hospital, Paris. “These results are consistent with previous studies in the same French health care database, as well as in a German database with SLIT preparations in tablet form. This not only confirms the soundness of the methodology but also the benefit of liquid SLIT as an etiological treatment of respiratory allergies.”
Risk for worsening
Furthermore, in the same study, liquid SLIT treatment was associated with a 27% reduced risk for worsening asthma and a 36% reduced risk for severe asthma. Among patients with allergic rhinitis and preexisting asthma, liquid SLIT was associated with a significantly lower risk for worsening of asthma, compared with the control group (primary HR: 0.73; secondary HR: 0.61; and tertiary HR: 0.64). The primary definition was an initial prescription of an ICS-LABA combination in a patient treated with ICS alone, severe exacerbation of asthma symptoms, hospital admission, or a diagnosis of chronic asthma.
“The risk reductions were significant and consistent for the allergens analyzed,” said study co-author Pascal Demoly, MD, PhD, head of pulmonology at Montpellier University Hospital, France (tertiary HR, dust mites: 0.66; grass: 0.59; birch: 0.34; and cats: 0.77). “This was across all age groups,” he added.
“The results of the EfficAPSI real-world study on health data from the SNDS are consistent with outcomes from clinical trials, suggestive of a reduced risk of asthma onset in patients with allergic rhinitis receiving liquid SLIT, as well as a reduced risk of worsening of preexisting asthma,” said Devillier. “SLIT, in this case in the form of a liquid, thus appears to be an effective etiological treatment, since the use of symptomatic drugs, in particular preventer inhalers, but also reliever inhalers, is lower in patients treated with SLIT over at least two consecutive years, compared with paired control subjects. And it’s the same for the risk of treating asthma in nonasthmatic patients at the start of the study. EfficAPSI is the largest study using data from a comprehensive state drug reimbursement database, allowing us to assess the impact of liquid SLIT on public health. These results, also obtained with other allergen preparations, particularly in tablet form in French and German studies using data from health care databases, demonstrate the consistency of the data regarding the efficacy of SLIT.”
This article was translated from the Medscape French Edition. A version appeared on Medscape.com.
PARIS – The EfficAPSI study showed with real-world data that sublingual immunotherapy (SLIT) reduces the risks for asthma onset and the worsening of asthma symptoms for patients with allergic rhinitis. The research was presented at the 18th French-language allergy conference.
These results confirm that allergen immunotherapy, or “desensitization,” is indeed an etiologic treatment of this allergic condition.
SLIT encompasses personalized solutions created for an individual specifically for allergies to dust mites, grass, birch, cats, and so on. These preparations are commonly used by allergy specialists when establishing an AIT treatment plan.
In 2017, the French Health Authority published a report indicating that there was insufficient clinical proof regarding the efficacy of SLIT. It subsequently removed injectable forms of these allergen extracts from the list of drugs reimbursed by the state and reduced state reimbursement of sublingual SLIT preparations from 30% to 15%, a step it confirmed in March 2018 and that led to outrage from allergy specialists. The chair of the French allergy society at the time, Jocelyne Just, MD, PhD, argued that conducting double-blind, placebo-controlled studies for all types (grass pollen, birch pollen, dust mites, asthma, allergic rhinitis, subcutaneous injections, sublingual treatments, tablets, liquid preparations) would take decades. Furthermore, meta-analyses on the subject, despite being heterogeneous and unable to answer all questions, are indeed pointing to the effectiveness of SLIT. To supplement existing data and to answer the queries raised by the HAS, several studies have been launched, including EfficAPSI.
The pharmacoepidemiologic EfficAPSI study is the largest retrospective, real-world, longitudinal cohort study ever carried out regarding liquid SLIT using data stored in the French National Health Data System (SNDS). The primary objective of the study was to evaluate the real-world impact of liquid SLIT on the onset and worsening of asthma for patients with allergic rhinitis and to evaluate the impact of sublingual treatments on public health.
A cohort analysis of patients treated with SLIT and control patients treated for allergic rhinitis with or without treatment for asthma was carried out. The patients treated with SLIT for at least 2 consecutive years were anonymously selected from the SNDS using the Stallergenes Greer prescription database.
In all, 99,538 patients who received SLIT were compared with 333,082 control patients (those who had received treatment for allergic rhinitis without taking SLIT). Participants were stratified according to their treatment history for asthma and were paired using a propensity score to minimize comparison bias.
The main definition of the onset of asthma included the first prescription of an asthma medication, hospital admission for asthma, or a diagnosis of chronic asthma. The secondary definition omitted the prescription of any treatment, and the third (sensitive and specific) took into consideration an initial prescription of omalizumab or a prescription of three inhaled corticosteroids (ICSs) associated with or without a long-acting beta-2 agonist (LABA) for a period of 1 year, admission to the hospital, or chronic asthma.
Asthma risk reduced
Among patients with allergic rhinitis without preexisting asthma, liquid SLIT was associated with a significantly lower risk of asthma onset in comparison with the control group (primary hazard ratio: 0.77; secondary HR: 0.66; and tertiary HR: 0.62).
The risk reductions were significant and were consistent regardless of the allergens analyzed (tertiary HR, dust mites: 0.57; grass: 0.52) for all age groups. These new results that were based on the tertiary definition corroborate the results from the primary and secondary definitions.
said study co-author Philippe Devillier, MD, PhD, research director at the respiratory tract diseases center of Foch Hospital, Paris. “These results are consistent with previous studies in the same French health care database, as well as in a German database with SLIT preparations in tablet form. This not only confirms the soundness of the methodology but also the benefit of liquid SLIT as an etiological treatment of respiratory allergies.”
Risk for worsening
Furthermore, in the same study, liquid SLIT treatment was associated with a 27% reduced risk for worsening asthma and a 36% reduced risk for severe asthma. Among patients with allergic rhinitis and preexisting asthma, liquid SLIT was associated with a significantly lower risk for worsening of asthma, compared with the control group (primary HR: 0.73; secondary HR: 0.61; and tertiary HR: 0.64). The primary definition was an initial prescription of an ICS-LABA combination in a patient treated with ICS alone, severe exacerbation of asthma symptoms, hospital admission, or a diagnosis of chronic asthma.
“The risk reductions were significant and consistent for the allergens analyzed,” said study co-author Pascal Demoly, MD, PhD, head of pulmonology at Montpellier University Hospital, France (tertiary HR, dust mites: 0.66; grass: 0.59; birch: 0.34; and cats: 0.77). “This was across all age groups,” he added.
“The results of the EfficAPSI real-world study on health data from the SNDS are consistent with outcomes from clinical trials, suggestive of a reduced risk of asthma onset in patients with allergic rhinitis receiving liquid SLIT, as well as a reduced risk of worsening of preexisting asthma,” said Devillier. “SLIT, in this case in the form of a liquid, thus appears to be an effective etiological treatment, since the use of symptomatic drugs, in particular preventer inhalers, but also reliever inhalers, is lower in patients treated with SLIT over at least two consecutive years, compared with paired control subjects. And it’s the same for the risk of treating asthma in nonasthmatic patients at the start of the study. EfficAPSI is the largest study using data from a comprehensive state drug reimbursement database, allowing us to assess the impact of liquid SLIT on public health. These results, also obtained with other allergen preparations, particularly in tablet form in French and German studies using data from health care databases, demonstrate the consistency of the data regarding the efficacy of SLIT.”
This article was translated from the Medscape French Edition. A version appeared on Medscape.com.
General, abdominal obesity linked to chronic respiratory illness
A recent Swedish study found that both abdominal and general obesity were independently associated with respiratory illnesses, including asthma and self-reported chronic obstructive pulmonary disease.
Relationships between respiratory conditions with characterized obesity types in adults were assessed using self-report surveys from participants originally enrolled in the European Community Respiratory Health Survey (ECRHS) investigating asthma, allergy, and risk factors. The Respiratory Health in Northern Europe (RHINE) III provides a second follow-up substudy of ECRHS focused on two forms of obesity associated with respiratory illnesses.
Obesity is a characteristic risk factor linked to respiratory ailments such as asthma and COPD. High body mass index (BMI) and waist circumference (WC) provide quantitative measurements for defining conditions of comprehensive general and abdominal obesity, respectively.
Although both types of obesity have been associated with asthma incidence, studies on their independent impact on this disease have been limited. Previous reports on abdominal obesity associated with asthma have been inconsistent when considering sexes in the analysis. Additionally, COPD and related outcomes differed between abdominal and general obesity, indicating a need to discover whether self-reported WC abdominal obesity and BMI-based general obesity are independently associated with respiratory symptoms, early- and late-onset asthma, COPD, chronic bronchitis, rhinitis, and sex, Marta A. Kisiel, MD, PhD, of the department of environmental and occupational medicine, Uppsala University, Sweden, and colleagues write.
In a prospective study published in the journal Respiratory Medicine, the researchers report on a cross-sectional investigation of responses to a questionnaire similar to one utilized 10 years earlier in the RHINE II study. Questions required simple yes/no responses that covered asthma, respiratory symptoms, allergic rhinitis, chronic bronchitis, and COPD. Additional requested information included age of asthma onset, potential confounding variables of age, smoking, physical activity, and highest education level, weight and height for BMI calculation, and WC measurement with instructions and a provided tape measure.
The population of the RHINE III study conducted from 2010 to 2012 was composed of 12,290 participants (53% response frequency) obtained from a total of seven research centers located in five northern European countries. Obesity categorization classified 1,837 (6.7%) participants as generally obese based on a high BMI ≥ 30 kg/m2 and 4,261 (34.7%) as abdominally obese by WC measurements of ≥ 102 cm for men and ≥ 88 cm for women. Of the 4,261 total participants, 1,669 met both general and abdominal obesity criteria. Mean age was in the low 50s range and the obese population consisted of more women than men.
Simple linear regression revealed that BMI and WC were highly correlated, and both were associated with tested respiratory conditions when adjusted for confounding variables. Differences with respect to WC and BMI were independently associated with most of the examined respiratory conditions when WC was adjusted for BMI and vice versa. Neither early-onset asthma nor allergic rhinitis were associated with WC, BMI, or abdominal or general obesity.
An independent association of abdominal obesity (with or without general obesity) was found to occur with respiratory symptoms, asthma, late-onset asthma, and chronic bronchitis.
After adjusting for abdominal obesity, general obesity showed an independent and significant association with respiratory symptoms, asthma, adult-onset asthma, and COPD. An analysis stratified by sex indicated a significant association of abdominal and general obesity with asthma in women presented as an odds ratio of 1.56 (95% confidence interval, 1.30-1.87) and 1.95 (95% CI, 1.56-2.43), respectively, compared with men, with an OR of 1.22 (95% CI, 0.97-3.17) and 1.28 (95% CI, 0.97-1.68), respectively. The association of abdominal and general obesity with COPD was also stronger in women, compared with men.
The researchers conclude that “both general and abdominal obesity [were], independent of each other, associated with respiratory symptoms in adults.” There is also a distinct difference between women and men for the association of self-reported asthma and COPD with abdominal and general obesity.
The large randomly selected sample size of participants from research centers located in five northern European countries was considered a major strength of this study as it permitted simultaneous adjustment for multiple potential confounders. Several limitations were acknowledged, including absence of data on obstructive respiratory disease severity, WC measurements not being performed by trained staff, and self-reported height and weight measurements.
The authors have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
A recent Swedish study found that both abdominal and general obesity were independently associated with respiratory illnesses, including asthma and self-reported chronic obstructive pulmonary disease.
Relationships between respiratory conditions with characterized obesity types in adults were assessed using self-report surveys from participants originally enrolled in the European Community Respiratory Health Survey (ECRHS) investigating asthma, allergy, and risk factors. The Respiratory Health in Northern Europe (RHINE) III provides a second follow-up substudy of ECRHS focused on two forms of obesity associated with respiratory illnesses.
Obesity is a characteristic risk factor linked to respiratory ailments such as asthma and COPD. High body mass index (BMI) and waist circumference (WC) provide quantitative measurements for defining conditions of comprehensive general and abdominal obesity, respectively.
Although both types of obesity have been associated with asthma incidence, studies on their independent impact on this disease have been limited. Previous reports on abdominal obesity associated with asthma have been inconsistent when considering sexes in the analysis. Additionally, COPD and related outcomes differed between abdominal and general obesity, indicating a need to discover whether self-reported WC abdominal obesity and BMI-based general obesity are independently associated with respiratory symptoms, early- and late-onset asthma, COPD, chronic bronchitis, rhinitis, and sex, Marta A. Kisiel, MD, PhD, of the department of environmental and occupational medicine, Uppsala University, Sweden, and colleagues write.
In a prospective study published in the journal Respiratory Medicine, the researchers report on a cross-sectional investigation of responses to a questionnaire similar to one utilized 10 years earlier in the RHINE II study. Questions required simple yes/no responses that covered asthma, respiratory symptoms, allergic rhinitis, chronic bronchitis, and COPD. Additional requested information included age of asthma onset, potential confounding variables of age, smoking, physical activity, and highest education level, weight and height for BMI calculation, and WC measurement with instructions and a provided tape measure.
The population of the RHINE III study conducted from 2010 to 2012 was composed of 12,290 participants (53% response frequency) obtained from a total of seven research centers located in five northern European countries. Obesity categorization classified 1,837 (6.7%) participants as generally obese based on a high BMI ≥ 30 kg/m2 and 4,261 (34.7%) as abdominally obese by WC measurements of ≥ 102 cm for men and ≥ 88 cm for women. Of the 4,261 total participants, 1,669 met both general and abdominal obesity criteria. Mean age was in the low 50s range and the obese population consisted of more women than men.
Simple linear regression revealed that BMI and WC were highly correlated, and both were associated with tested respiratory conditions when adjusted for confounding variables. Differences with respect to WC and BMI were independently associated with most of the examined respiratory conditions when WC was adjusted for BMI and vice versa. Neither early-onset asthma nor allergic rhinitis were associated with WC, BMI, or abdominal or general obesity.
An independent association of abdominal obesity (with or without general obesity) was found to occur with respiratory symptoms, asthma, late-onset asthma, and chronic bronchitis.
After adjusting for abdominal obesity, general obesity showed an independent and significant association with respiratory symptoms, asthma, adult-onset asthma, and COPD. An analysis stratified by sex indicated a significant association of abdominal and general obesity with asthma in women presented as an odds ratio of 1.56 (95% confidence interval, 1.30-1.87) and 1.95 (95% CI, 1.56-2.43), respectively, compared with men, with an OR of 1.22 (95% CI, 0.97-3.17) and 1.28 (95% CI, 0.97-1.68), respectively. The association of abdominal and general obesity with COPD was also stronger in women, compared with men.
The researchers conclude that “both general and abdominal obesity [were], independent of each other, associated with respiratory symptoms in adults.” There is also a distinct difference between women and men for the association of self-reported asthma and COPD with abdominal and general obesity.
The large randomly selected sample size of participants from research centers located in five northern European countries was considered a major strength of this study as it permitted simultaneous adjustment for multiple potential confounders. Several limitations were acknowledged, including absence of data on obstructive respiratory disease severity, WC measurements not being performed by trained staff, and self-reported height and weight measurements.
The authors have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
A recent Swedish study found that both abdominal and general obesity were independently associated with respiratory illnesses, including asthma and self-reported chronic obstructive pulmonary disease.
Relationships between respiratory conditions with characterized obesity types in adults were assessed using self-report surveys from participants originally enrolled in the European Community Respiratory Health Survey (ECRHS) investigating asthma, allergy, and risk factors. The Respiratory Health in Northern Europe (RHINE) III provides a second follow-up substudy of ECRHS focused on two forms of obesity associated with respiratory illnesses.
Obesity is a characteristic risk factor linked to respiratory ailments such as asthma and COPD. High body mass index (BMI) and waist circumference (WC) provide quantitative measurements for defining conditions of comprehensive general and abdominal obesity, respectively.
Although both types of obesity have been associated with asthma incidence, studies on their independent impact on this disease have been limited. Previous reports on abdominal obesity associated with asthma have been inconsistent when considering sexes in the analysis. Additionally, COPD and related outcomes differed between abdominal and general obesity, indicating a need to discover whether self-reported WC abdominal obesity and BMI-based general obesity are independently associated with respiratory symptoms, early- and late-onset asthma, COPD, chronic bronchitis, rhinitis, and sex, Marta A. Kisiel, MD, PhD, of the department of environmental and occupational medicine, Uppsala University, Sweden, and colleagues write.
In a prospective study published in the journal Respiratory Medicine, the researchers report on a cross-sectional investigation of responses to a questionnaire similar to one utilized 10 years earlier in the RHINE II study. Questions required simple yes/no responses that covered asthma, respiratory symptoms, allergic rhinitis, chronic bronchitis, and COPD. Additional requested information included age of asthma onset, potential confounding variables of age, smoking, physical activity, and highest education level, weight and height for BMI calculation, and WC measurement with instructions and a provided tape measure.
The population of the RHINE III study conducted from 2010 to 2012 was composed of 12,290 participants (53% response frequency) obtained from a total of seven research centers located in five northern European countries. Obesity categorization classified 1,837 (6.7%) participants as generally obese based on a high BMI ≥ 30 kg/m2 and 4,261 (34.7%) as abdominally obese by WC measurements of ≥ 102 cm for men and ≥ 88 cm for women. Of the 4,261 total participants, 1,669 met both general and abdominal obesity criteria. Mean age was in the low 50s range and the obese population consisted of more women than men.
Simple linear regression revealed that BMI and WC were highly correlated, and both were associated with tested respiratory conditions when adjusted for confounding variables. Differences with respect to WC and BMI were independently associated with most of the examined respiratory conditions when WC was adjusted for BMI and vice versa. Neither early-onset asthma nor allergic rhinitis were associated with WC, BMI, or abdominal or general obesity.
An independent association of abdominal obesity (with or without general obesity) was found to occur with respiratory symptoms, asthma, late-onset asthma, and chronic bronchitis.
After adjusting for abdominal obesity, general obesity showed an independent and significant association with respiratory symptoms, asthma, adult-onset asthma, and COPD. An analysis stratified by sex indicated a significant association of abdominal and general obesity with asthma in women presented as an odds ratio of 1.56 (95% confidence interval, 1.30-1.87) and 1.95 (95% CI, 1.56-2.43), respectively, compared with men, with an OR of 1.22 (95% CI, 0.97-3.17) and 1.28 (95% CI, 0.97-1.68), respectively. The association of abdominal and general obesity with COPD was also stronger in women, compared with men.
The researchers conclude that “both general and abdominal obesity [were], independent of each other, associated with respiratory symptoms in adults.” There is also a distinct difference between women and men for the association of self-reported asthma and COPD with abdominal and general obesity.
The large randomly selected sample size of participants from research centers located in five northern European countries was considered a major strength of this study as it permitted simultaneous adjustment for multiple potential confounders. Several limitations were acknowledged, including absence of data on obstructive respiratory disease severity, WC measurements not being performed by trained staff, and self-reported height and weight measurements.
The authors have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The breathtaking effects of climate change
To see the harmful effects of climate change firsthand, you need look no farther than the nearest pulmonary clinic.
The causes and effects are unmistakable: pollen storms leading to allergy sufferers flooding into allergists’ offices; rising air pollution levels increasing risk for obstructive airway diseases, cardiopulmonary complications, and non–small cell lung cancer; melting snowpacks and atmospheric rivers inundating neighborhoods and leaving moldy debris and incipient fungal infections in their wake.
“The reason why we think climate change is going to change the type of disease patterns and the severity of illness that we see in patients with respiratory diseases is that it changes a lot of the environment as well as the exposures,” said Bathmapriya Balakrishnan, BMedSci, BMBS, from the section of Pulmonary, Critical Care, and Sleep Medicine in the department of medicine at West Virginia University, Morgantown.
“What we’re going to see is not just new diseases but also exacerbation of chronic diseases, things like asthma [and] COPD. And there’s also concern that patients who are otherwise healthy, because they now have more exposures that are due to climate change, can then develop these diseases,” she said in an interview.
Ms. Balakrishnan is the lead author of a comprehensive, evidence-based review focused on the effects of climate change and air pollution across the spectrum of pulmonary disorders. The review is published online ahead of print in the journal Chest.
“ To inform health care providers of evidence-based methods and improve patient counselling, further research regarding measures that limit exposure is needed. Empowering patients with resources to monitor air quality and minimize exposure is a key preventative measure for decreasing morbidity and mortality while improving quality of life,” Ms. Balakrishnan and colleagues write.
Similarly, in a statement on the effects of climate change on respiratory health, the American Public Health Association succinctly summarized the problem: “Warmer temperatures lead to an increase in pollutants and allergens. Poor air quality leads to reduced lung function, increased risk of asthma complications, heart attacks, heart failure, and death. Air pollution and allergens are the main exposures affecting lung and heart health in this changing climate.”
Early spring
Stanley Fineman, MD, MBA, a past president of the American College of Allergy, Asthma, & Immunology and an allergist in private practice in Atlanta, has seen firsthand how global warming and an earlier start to spring allergy season is affecting his patients.
“The season, at least in our area metro Atlanta, started earlier and has been lasting longer. The pollen counts are very high,” he told this news organization.
“In February we started seeing pollen counts over 1,000 [grams per cubic meter], which is unheard of, and in March about half the days we counted levels that were over 1,000, which is also unheard of. In April it was over 1,000 almost half the days.”
Dr. Fineman and colleagues both in Atlanta and across the country have reported sharp increases in the proportion of new adult patients and in existing patients who have experienced exacerbation of previously mild disease.
“Probably what’s happened is that they may have had some allergic sensitivity that resulted in milder manifestations, but this year they’re getting major manifestations,” Dr. Fineman said.
In a 2014 article in the journal European Respiratory Review, Gennaro D’Amato, MD, from High Speciality Hospital Antonio Cardarelli, Naples, Italy, and colleagues outlined the main effects of climate on pollen levels: “1) an increase in plant growth and faster plant growth; 2) an increase in the amount of pollen produced by each plant; 3) an increase in the amount of allergenic proteins contained in pollen; 4) an increase in the start time of plant growth and, therefore, the start of pollen production; 5) an earlier and longer pollen season; 6) change in the geospatial distribution of pollen, that is plant ranges and long-distance atmospheric transport moving polewards,” they write.
Bad air
In addition to pollen, the ambient air in many places is increasingly becoming saturated with bioallergenic proteins such as bacteria, viruses, animal dander, insects, molds, and plant species, Ms. Balakrishnan and colleagues noted, adding that “atmospheric levels of carbon dioxide have also been found to increase pollen productivity. These changes result in greater over-the-counter medication use, emergency department visits, and outpatient visits for respiratory illnesses.”
The rash of violent storms that has washed over much of the United States in recent months is also likely to increase the incidence of so-called “thunderstorm asthma,” caused when large quantities of respirable particulate matter are released before or during a thunderstorm.
Air pollution from the burning of carbon-based fuels and from wildfires sparked by hotter and drier conditions increase airborne particulate matter that can seriously exacerbate asthma, COPD, and other obstructive airway conditions.
In addition, as previously reported by Medscape, exposure to particulate matter has been implicated as a possible cause of non–small cell lung cancer in persons who have never smoked.
Critical care challenges
Among the myriad other effects of climate change postulated in evidence enumerated by Ms. Balakrishnan and colleagues are chest infections and pleural diseases, such as aspergillosis infections that occur after catastrophic flooding; increased incidence of Mycobacterium avium complex infections and hypersensitivity pneumonitis; increased demands on critical care specialists from natural disasters; pollution-induced cardiac arrest; and heat prostration and heat stroke from increasingly prevalent heat waves.
The reviewers also examined evidence suggesting links between climate change and pulmonary hypertension, interstitial lung disease, sleep disorders, and occupational pulmonary disorders.
Power to the patients
“Pulmonologists should counsel patients on ways to minimize outdoor and indoor pollution, using tight-fitting respirators and home air-purifying systems without encroaching on patients’ beliefs and choices,” the authors advise.
“Empowering patients with resources to monitor air quality daily, in inclement weather, and during disasters would help minimize exposure and thus improve overall health. The pulmonologist can play an important role in emphasizing the impact of climate change on pulmonary disorders during patient care encounters,” they write.
Ms. Balakrishan adds that another important mitigation measure that can be taken today is education.
“In medical school we don’t really learn about the impact of climate change – at least in my generation of physicians, climate change or global warming weren’t part of the medical curriculum – but now I think that there’s a lot of advocacy work being done by medical students who actually want more education on climate change and its effects on pulmonary diseases,” she said.
The study by Ms. Balakrishnan and colleagues was unfunded. Ms. Balakrishnan reports no relevant financial relationships. Co-author Mary-Beth Scholand, MD, has received personal fees from serving on advisory boards and speakers bureaus for Genentech, Boehringer Ingelheim, Veracyte, and United Therapeutics. Co-author Sean Callahan, MD, has received personal fees for serving on advisory boards for Gilead and Boehringer Ingelheim. Dr. Fineman reports no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
To see the harmful effects of climate change firsthand, you need look no farther than the nearest pulmonary clinic.
The causes and effects are unmistakable: pollen storms leading to allergy sufferers flooding into allergists’ offices; rising air pollution levels increasing risk for obstructive airway diseases, cardiopulmonary complications, and non–small cell lung cancer; melting snowpacks and atmospheric rivers inundating neighborhoods and leaving moldy debris and incipient fungal infections in their wake.
“The reason why we think climate change is going to change the type of disease patterns and the severity of illness that we see in patients with respiratory diseases is that it changes a lot of the environment as well as the exposures,” said Bathmapriya Balakrishnan, BMedSci, BMBS, from the section of Pulmonary, Critical Care, and Sleep Medicine in the department of medicine at West Virginia University, Morgantown.
“What we’re going to see is not just new diseases but also exacerbation of chronic diseases, things like asthma [and] COPD. And there’s also concern that patients who are otherwise healthy, because they now have more exposures that are due to climate change, can then develop these diseases,” she said in an interview.
Ms. Balakrishnan is the lead author of a comprehensive, evidence-based review focused on the effects of climate change and air pollution across the spectrum of pulmonary disorders. The review is published online ahead of print in the journal Chest.
“ To inform health care providers of evidence-based methods and improve patient counselling, further research regarding measures that limit exposure is needed. Empowering patients with resources to monitor air quality and minimize exposure is a key preventative measure for decreasing morbidity and mortality while improving quality of life,” Ms. Balakrishnan and colleagues write.
Similarly, in a statement on the effects of climate change on respiratory health, the American Public Health Association succinctly summarized the problem: “Warmer temperatures lead to an increase in pollutants and allergens. Poor air quality leads to reduced lung function, increased risk of asthma complications, heart attacks, heart failure, and death. Air pollution and allergens are the main exposures affecting lung and heart health in this changing climate.”
Early spring
Stanley Fineman, MD, MBA, a past president of the American College of Allergy, Asthma, & Immunology and an allergist in private practice in Atlanta, has seen firsthand how global warming and an earlier start to spring allergy season is affecting his patients.
“The season, at least in our area metro Atlanta, started earlier and has been lasting longer. The pollen counts are very high,” he told this news organization.
“In February we started seeing pollen counts over 1,000 [grams per cubic meter], which is unheard of, and in March about half the days we counted levels that were over 1,000, which is also unheard of. In April it was over 1,000 almost half the days.”
Dr. Fineman and colleagues both in Atlanta and across the country have reported sharp increases in the proportion of new adult patients and in existing patients who have experienced exacerbation of previously mild disease.
“Probably what’s happened is that they may have had some allergic sensitivity that resulted in milder manifestations, but this year they’re getting major manifestations,” Dr. Fineman said.
In a 2014 article in the journal European Respiratory Review, Gennaro D’Amato, MD, from High Speciality Hospital Antonio Cardarelli, Naples, Italy, and colleagues outlined the main effects of climate on pollen levels: “1) an increase in plant growth and faster plant growth; 2) an increase in the amount of pollen produced by each plant; 3) an increase in the amount of allergenic proteins contained in pollen; 4) an increase in the start time of plant growth and, therefore, the start of pollen production; 5) an earlier and longer pollen season; 6) change in the geospatial distribution of pollen, that is plant ranges and long-distance atmospheric transport moving polewards,” they write.
Bad air
In addition to pollen, the ambient air in many places is increasingly becoming saturated with bioallergenic proteins such as bacteria, viruses, animal dander, insects, molds, and plant species, Ms. Balakrishnan and colleagues noted, adding that “atmospheric levels of carbon dioxide have also been found to increase pollen productivity. These changes result in greater over-the-counter medication use, emergency department visits, and outpatient visits for respiratory illnesses.”
The rash of violent storms that has washed over much of the United States in recent months is also likely to increase the incidence of so-called “thunderstorm asthma,” caused when large quantities of respirable particulate matter are released before or during a thunderstorm.
Air pollution from the burning of carbon-based fuels and from wildfires sparked by hotter and drier conditions increase airborne particulate matter that can seriously exacerbate asthma, COPD, and other obstructive airway conditions.
In addition, as previously reported by Medscape, exposure to particulate matter has been implicated as a possible cause of non–small cell lung cancer in persons who have never smoked.
Critical care challenges
Among the myriad other effects of climate change postulated in evidence enumerated by Ms. Balakrishnan and colleagues are chest infections and pleural diseases, such as aspergillosis infections that occur after catastrophic flooding; increased incidence of Mycobacterium avium complex infections and hypersensitivity pneumonitis; increased demands on critical care specialists from natural disasters; pollution-induced cardiac arrest; and heat prostration and heat stroke from increasingly prevalent heat waves.
The reviewers also examined evidence suggesting links between climate change and pulmonary hypertension, interstitial lung disease, sleep disorders, and occupational pulmonary disorders.
Power to the patients
“Pulmonologists should counsel patients on ways to minimize outdoor and indoor pollution, using tight-fitting respirators and home air-purifying systems without encroaching on patients’ beliefs and choices,” the authors advise.
“Empowering patients with resources to monitor air quality daily, in inclement weather, and during disasters would help minimize exposure and thus improve overall health. The pulmonologist can play an important role in emphasizing the impact of climate change on pulmonary disorders during patient care encounters,” they write.
Ms. Balakrishan adds that another important mitigation measure that can be taken today is education.
“In medical school we don’t really learn about the impact of climate change – at least in my generation of physicians, climate change or global warming weren’t part of the medical curriculum – but now I think that there’s a lot of advocacy work being done by medical students who actually want more education on climate change and its effects on pulmonary diseases,” she said.
The study by Ms. Balakrishnan and colleagues was unfunded. Ms. Balakrishnan reports no relevant financial relationships. Co-author Mary-Beth Scholand, MD, has received personal fees from serving on advisory boards and speakers bureaus for Genentech, Boehringer Ingelheim, Veracyte, and United Therapeutics. Co-author Sean Callahan, MD, has received personal fees for serving on advisory boards for Gilead and Boehringer Ingelheim. Dr. Fineman reports no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
To see the harmful effects of climate change firsthand, you need look no farther than the nearest pulmonary clinic.
The causes and effects are unmistakable: pollen storms leading to allergy sufferers flooding into allergists’ offices; rising air pollution levels increasing risk for obstructive airway diseases, cardiopulmonary complications, and non–small cell lung cancer; melting snowpacks and atmospheric rivers inundating neighborhoods and leaving moldy debris and incipient fungal infections in their wake.
“The reason why we think climate change is going to change the type of disease patterns and the severity of illness that we see in patients with respiratory diseases is that it changes a lot of the environment as well as the exposures,” said Bathmapriya Balakrishnan, BMedSci, BMBS, from the section of Pulmonary, Critical Care, and Sleep Medicine in the department of medicine at West Virginia University, Morgantown.
“What we’re going to see is not just new diseases but also exacerbation of chronic diseases, things like asthma [and] COPD. And there’s also concern that patients who are otherwise healthy, because they now have more exposures that are due to climate change, can then develop these diseases,” she said in an interview.
Ms. Balakrishnan is the lead author of a comprehensive, evidence-based review focused on the effects of climate change and air pollution across the spectrum of pulmonary disorders. The review is published online ahead of print in the journal Chest.
“ To inform health care providers of evidence-based methods and improve patient counselling, further research regarding measures that limit exposure is needed. Empowering patients with resources to monitor air quality and minimize exposure is a key preventative measure for decreasing morbidity and mortality while improving quality of life,” Ms. Balakrishnan and colleagues write.
Similarly, in a statement on the effects of climate change on respiratory health, the American Public Health Association succinctly summarized the problem: “Warmer temperatures lead to an increase in pollutants and allergens. Poor air quality leads to reduced lung function, increased risk of asthma complications, heart attacks, heart failure, and death. Air pollution and allergens are the main exposures affecting lung and heart health in this changing climate.”
Early spring
Stanley Fineman, MD, MBA, a past president of the American College of Allergy, Asthma, & Immunology and an allergist in private practice in Atlanta, has seen firsthand how global warming and an earlier start to spring allergy season is affecting his patients.
“The season, at least in our area metro Atlanta, started earlier and has been lasting longer. The pollen counts are very high,” he told this news organization.
“In February we started seeing pollen counts over 1,000 [grams per cubic meter], which is unheard of, and in March about half the days we counted levels that were over 1,000, which is also unheard of. In April it was over 1,000 almost half the days.”
Dr. Fineman and colleagues both in Atlanta and across the country have reported sharp increases in the proportion of new adult patients and in existing patients who have experienced exacerbation of previously mild disease.
“Probably what’s happened is that they may have had some allergic sensitivity that resulted in milder manifestations, but this year they’re getting major manifestations,” Dr. Fineman said.
In a 2014 article in the journal European Respiratory Review, Gennaro D’Amato, MD, from High Speciality Hospital Antonio Cardarelli, Naples, Italy, and colleagues outlined the main effects of climate on pollen levels: “1) an increase in plant growth and faster plant growth; 2) an increase in the amount of pollen produced by each plant; 3) an increase in the amount of allergenic proteins contained in pollen; 4) an increase in the start time of plant growth and, therefore, the start of pollen production; 5) an earlier and longer pollen season; 6) change in the geospatial distribution of pollen, that is plant ranges and long-distance atmospheric transport moving polewards,” they write.
Bad air
In addition to pollen, the ambient air in many places is increasingly becoming saturated with bioallergenic proteins such as bacteria, viruses, animal dander, insects, molds, and plant species, Ms. Balakrishnan and colleagues noted, adding that “atmospheric levels of carbon dioxide have also been found to increase pollen productivity. These changes result in greater over-the-counter medication use, emergency department visits, and outpatient visits for respiratory illnesses.”
The rash of violent storms that has washed over much of the United States in recent months is also likely to increase the incidence of so-called “thunderstorm asthma,” caused when large quantities of respirable particulate matter are released before or during a thunderstorm.
Air pollution from the burning of carbon-based fuels and from wildfires sparked by hotter and drier conditions increase airborne particulate matter that can seriously exacerbate asthma, COPD, and other obstructive airway conditions.
In addition, as previously reported by Medscape, exposure to particulate matter has been implicated as a possible cause of non–small cell lung cancer in persons who have never smoked.
Critical care challenges
Among the myriad other effects of climate change postulated in evidence enumerated by Ms. Balakrishnan and colleagues are chest infections and pleural diseases, such as aspergillosis infections that occur after catastrophic flooding; increased incidence of Mycobacterium avium complex infections and hypersensitivity pneumonitis; increased demands on critical care specialists from natural disasters; pollution-induced cardiac arrest; and heat prostration and heat stroke from increasingly prevalent heat waves.
The reviewers also examined evidence suggesting links between climate change and pulmonary hypertension, interstitial lung disease, sleep disorders, and occupational pulmonary disorders.
Power to the patients
“Pulmonologists should counsel patients on ways to minimize outdoor and indoor pollution, using tight-fitting respirators and home air-purifying systems without encroaching on patients’ beliefs and choices,” the authors advise.
“Empowering patients with resources to monitor air quality daily, in inclement weather, and during disasters would help minimize exposure and thus improve overall health. The pulmonologist can play an important role in emphasizing the impact of climate change on pulmonary disorders during patient care encounters,” they write.
Ms. Balakrishan adds that another important mitigation measure that can be taken today is education.
“In medical school we don’t really learn about the impact of climate change – at least in my generation of physicians, climate change or global warming weren’t part of the medical curriculum – but now I think that there’s a lot of advocacy work being done by medical students who actually want more education on climate change and its effects on pulmonary diseases,” she said.
The study by Ms. Balakrishnan and colleagues was unfunded. Ms. Balakrishnan reports no relevant financial relationships. Co-author Mary-Beth Scholand, MD, has received personal fees from serving on advisory boards and speakers bureaus for Genentech, Boehringer Ingelheim, Veracyte, and United Therapeutics. Co-author Sean Callahan, MD, has received personal fees for serving on advisory boards for Gilead and Boehringer Ingelheim. Dr. Fineman reports no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Asthma tied to increased risk for multiple cancers
People with asthma have an elevated risk for a variety of cancers other than lung cancer, including melanoma as well as blood, kidney, and ovarian cancers, new research suggests.
But, the authors found, treatment with an inhaled steroid may lower that risk, perhaps by keeping inflammation in check.
“Using real-world data, our study is the first to provide evidence of a positive association between asthma and cancer risk in United States patients,” Yi Guo, PhD, with the University of Florida, Gainesville, said in a news release.
The study was published online in Cancer Medicine.
The relationship between chronic inflammation and cancer remains a key area of exploration in cancer etiology. Data show that the risk for developing cancer is higher in patients with chronic inflammatory diseases, and patients with asthma have complex and chronic inflammation. However, prior studies exploring a possible link between asthma and cancer have yielded mixed results.
To investigate further, Dr. Guo and colleagues analyzed electronic health records and claims data in the OneFlorida+ clinical research network for roughly 90,000 adults with asthma and a matched cohort of about 270,000 adults without asthma.
Multivariable analysis revealed that adults with asthma were more likely to develop cancer, compared with peers without asthma (hazard ratio, 1.36), the investigators found.
Adults with asthma had an elevated cancer risk for five of the 13 cancers assessed, including melanoma (HR, 1.98), ovarian cancer (HR, 1.88), lung cancer (HR, 1.56), kidney cancer (HR, 1.48), and blood cancer (HR, 1.26).
Compared with adults without asthma, those with asthma who did not treat it with an inhaled steroid had a more pronounced overall cancer risk, compared with those who were on an inhaled steroid (HR, 1.60 vs. 1.11).
For specific cancer types, the risk was elevated for nine of 13 cancers in patients with asthma not taking an inhaled steroid: prostate (HR, 1.50), lung (HR, 1.74), colorectal (HR, 1.51), blood (HR, 1.44), melanoma (HR, 2.05), corpus uteri (HR, 1.76), kidney (HR, 1.52), ovarian (HR, 2.31), and cervical (HR, 1.46).
In contrast, in patients with asthma who did use an inhaled steroid, an elevated cancer risk was observed for only two cancers, lung cancer (HR, 1.39) and melanoma (HR, 1.92), suggesting a potential protective effect of inhaled steroid use on cancer, the researchers said.
Although prior studies have shown a protective effect of inhaled steroid use on some cancers, potentially by reducing inflammation, the “speculative nature of chronic inflammation (asthma as a common example) as a driver for pan-cancer development requires more investigation,” Dr. Guo and colleagues cautioned.
And because of the observational nature of the current study, Dr. Guo’s team stressed that these findings do not prove a causal relationship between asthma and cancer.
“More in-depth studies using real-word data are needed to further explore the causal mechanisms of asthma on cancer risk,” the researchers concluded.
Funding for the study was provided in part by grants to the researchers from the National Institutes of Health, National Cancer Institute, National Institute on Aging, and the Centers for Disease Control and Prevention. This project was supported by the Cancer Informatics Shared Resource in the University of Florida Health Cancer Center. The authors have disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
People with asthma have an elevated risk for a variety of cancers other than lung cancer, including melanoma as well as blood, kidney, and ovarian cancers, new research suggests.
But, the authors found, treatment with an inhaled steroid may lower that risk, perhaps by keeping inflammation in check.
“Using real-world data, our study is the first to provide evidence of a positive association between asthma and cancer risk in United States patients,” Yi Guo, PhD, with the University of Florida, Gainesville, said in a news release.
The study was published online in Cancer Medicine.
The relationship between chronic inflammation and cancer remains a key area of exploration in cancer etiology. Data show that the risk for developing cancer is higher in patients with chronic inflammatory diseases, and patients with asthma have complex and chronic inflammation. However, prior studies exploring a possible link between asthma and cancer have yielded mixed results.
To investigate further, Dr. Guo and colleagues analyzed electronic health records and claims data in the OneFlorida+ clinical research network for roughly 90,000 adults with asthma and a matched cohort of about 270,000 adults without asthma.
Multivariable analysis revealed that adults with asthma were more likely to develop cancer, compared with peers without asthma (hazard ratio, 1.36), the investigators found.
Adults with asthma had an elevated cancer risk for five of the 13 cancers assessed, including melanoma (HR, 1.98), ovarian cancer (HR, 1.88), lung cancer (HR, 1.56), kidney cancer (HR, 1.48), and blood cancer (HR, 1.26).
Compared with adults without asthma, those with asthma who did not treat it with an inhaled steroid had a more pronounced overall cancer risk, compared with those who were on an inhaled steroid (HR, 1.60 vs. 1.11).
For specific cancer types, the risk was elevated for nine of 13 cancers in patients with asthma not taking an inhaled steroid: prostate (HR, 1.50), lung (HR, 1.74), colorectal (HR, 1.51), blood (HR, 1.44), melanoma (HR, 2.05), corpus uteri (HR, 1.76), kidney (HR, 1.52), ovarian (HR, 2.31), and cervical (HR, 1.46).
In contrast, in patients with asthma who did use an inhaled steroid, an elevated cancer risk was observed for only two cancers, lung cancer (HR, 1.39) and melanoma (HR, 1.92), suggesting a potential protective effect of inhaled steroid use on cancer, the researchers said.
Although prior studies have shown a protective effect of inhaled steroid use on some cancers, potentially by reducing inflammation, the “speculative nature of chronic inflammation (asthma as a common example) as a driver for pan-cancer development requires more investigation,” Dr. Guo and colleagues cautioned.
And because of the observational nature of the current study, Dr. Guo’s team stressed that these findings do not prove a causal relationship between asthma and cancer.
“More in-depth studies using real-word data are needed to further explore the causal mechanisms of asthma on cancer risk,” the researchers concluded.
Funding for the study was provided in part by grants to the researchers from the National Institutes of Health, National Cancer Institute, National Institute on Aging, and the Centers for Disease Control and Prevention. This project was supported by the Cancer Informatics Shared Resource in the University of Florida Health Cancer Center. The authors have disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
People with asthma have an elevated risk for a variety of cancers other than lung cancer, including melanoma as well as blood, kidney, and ovarian cancers, new research suggests.
But, the authors found, treatment with an inhaled steroid may lower that risk, perhaps by keeping inflammation in check.
“Using real-world data, our study is the first to provide evidence of a positive association between asthma and cancer risk in United States patients,” Yi Guo, PhD, with the University of Florida, Gainesville, said in a news release.
The study was published online in Cancer Medicine.
The relationship between chronic inflammation and cancer remains a key area of exploration in cancer etiology. Data show that the risk for developing cancer is higher in patients with chronic inflammatory diseases, and patients with asthma have complex and chronic inflammation. However, prior studies exploring a possible link between asthma and cancer have yielded mixed results.
To investigate further, Dr. Guo and colleagues analyzed electronic health records and claims data in the OneFlorida+ clinical research network for roughly 90,000 adults with asthma and a matched cohort of about 270,000 adults without asthma.
Multivariable analysis revealed that adults with asthma were more likely to develop cancer, compared with peers without asthma (hazard ratio, 1.36), the investigators found.
Adults with asthma had an elevated cancer risk for five of the 13 cancers assessed, including melanoma (HR, 1.98), ovarian cancer (HR, 1.88), lung cancer (HR, 1.56), kidney cancer (HR, 1.48), and blood cancer (HR, 1.26).
Compared with adults without asthma, those with asthma who did not treat it with an inhaled steroid had a more pronounced overall cancer risk, compared with those who were on an inhaled steroid (HR, 1.60 vs. 1.11).
For specific cancer types, the risk was elevated for nine of 13 cancers in patients with asthma not taking an inhaled steroid: prostate (HR, 1.50), lung (HR, 1.74), colorectal (HR, 1.51), blood (HR, 1.44), melanoma (HR, 2.05), corpus uteri (HR, 1.76), kidney (HR, 1.52), ovarian (HR, 2.31), and cervical (HR, 1.46).
In contrast, in patients with asthma who did use an inhaled steroid, an elevated cancer risk was observed for only two cancers, lung cancer (HR, 1.39) and melanoma (HR, 1.92), suggesting a potential protective effect of inhaled steroid use on cancer, the researchers said.
Although prior studies have shown a protective effect of inhaled steroid use on some cancers, potentially by reducing inflammation, the “speculative nature of chronic inflammation (asthma as a common example) as a driver for pan-cancer development requires more investigation,” Dr. Guo and colleagues cautioned.
And because of the observational nature of the current study, Dr. Guo’s team stressed that these findings do not prove a causal relationship between asthma and cancer.
“More in-depth studies using real-word data are needed to further explore the causal mechanisms of asthma on cancer risk,” the researchers concluded.
Funding for the study was provided in part by grants to the researchers from the National Institutes of Health, National Cancer Institute, National Institute on Aging, and the Centers for Disease Control and Prevention. This project was supported by the Cancer Informatics Shared Resource in the University of Florida Health Cancer Center. The authors have disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
What will vaping lead to? Emerging research shows damage, and addiction
Jake Warn calls vaping “a toxic artificial love.”
Jake, of Winslow, Maine, was 16 years old when he began vaping. Unlike cigarettes, vaping can be odorless, and its smoke leaves no trace, which allowed him and his friends to use the devices in school bathrooms without fear of being caught.
He would use an entire cartridge containing the vape liquid, the equivalent of smoking one pack of tobacco cigarettes, within 1 school day. By the fall semester of his first year in college, Jake said his use had increased even more.
“It got pricey, so that’s when I really started to notice” the extent of his dependency, he said recently.
Vaping rates among teenagers in Maine doubled from 15.3% to 28.7% between 2017 and 2019, while Jake was in high school. In 2021, 11% of high schoolers across the nation said they regularly smoked e-cigarettes, and an estimated 28% have ever tried the devices, according to the Centers for Disease Control and Prevention.
The Food and Drug Administration classifies e-cigarettes as a tobacco product because many contain nicotine, which comes from tobacco. Like Jake, the habit is likely to carry into adulthood for many who start in their teenage years, experts say.
Electronic nicotine delivery systems (ENDS) such as vapes have been touted by their manufacturers and by some in the medical field as a healthier alternative to cigarettes and as a method to help smokers give up the habit.
But, that’s not how Jake – who had never used combustible cigarettes – picked up vaping, or how he sold the idea to his mother.
“It’s all organic and natural flavoring, it’s just flavored water,” Mary Lou Warn recalled her son saying to her. She researched the health effects of vaping but didn’t find much online. “I knew they were dangerous because you don’t put anything in your lungs that isn’t fresh air.”
A determined athlete in high school, Jake found that his asthma worsened as he transitioned to college, especially when he ran a track meet or during a soccer game.
Mrs. Warn noticed changes off the field, too.
“He was coughing constantly, he wasn’t sleeping well, he wasn’t eating well,” she said. “I knew the addiction was taking over.”
Vaping irritated Jake’s throat, and he would get nosebleeds that he couldn’t stop, she added.
Since Mrs. Warn first looked into the effects of e-cigarettes on respiratory health back in 2017, many studies have been conducted of the short-term health outcomes for first-time smokers who never used combustible tobacco products. Studies suggest that vaping may worsen bronchitis and asthma, raise blood pressure, interfere with brain development in young users, suppress the immune system, and increase the risk of developing a chronic lung disease (Am J Prev Med. 2020 Feb;58[2]:182-90). Studies of mice and cell cultures have found that the vapor or extracts from vapes damage the chemical structure of DNA.
Still, the limited number of long-term human studies has made it hard to know what the health outcomes of e-cigarette users will be in the future. Conclusive studies linking commercial cigarette use to deaths from heart disease and cancer didn’t emerge until the mid-1950s, decades after manufacturers began mass production and marketing in the early 20th century.
Years could pass before researchers gain a clearer understanding of the health implications of long-term e-cigarette use, according to Nigar Nargis, PhD, senior scientific director of tobacco control research at the American Cancer Society.
“There hasn’t been any such study to establish the direct link from ENDS to cancer, but it is understood that it [vaping] may promote the development of cancer and lung damage and inflammation,” Dr. Nargis said.
For decades, advocates built awareness of the harms of tobacco use, which led to a sharp decline in tobacco-related illnesses such as lung cancer. But Hilary Schneider, Maine’s director of government relations for the ACS Cancer Action Network, said she fears the uptick in the use of vapes – especially among those who never smoked or those who use both combustible cigarettes and e-cigarettes – may reverse declines in the rates of smoking-relating diseases.
Multiple studies suggest that inhaling chemicals found in e-cigarettes – including nicotine-carrying aerosols – can damage arteries and inflame and injure the lungs.
Vapes “basically have created a pediatric tobacco-use epidemic,” Ms. Schneider said. “What we’re seeing is unprecedented tobacco use rates, higher rates than we’ve seen in decades.”
One reason many young people start vaping is the attraction to flavors, which range from classic menthol to fruits and sweets. A handful of states have enacted bans or restrictions on the sale of flavored vapes.
“It’s new, and it’s just been marketed in a way that we’re really fighting the false narrative put out there by makers of these products that are trying to make them appealing to kids,” said Rachel Boykan, MD, clinical professor of pediatrics and attending physician at Stony Brook (N.Y.) Children’s Hospital.
The flavor Red Bull, in particular, hooked Jake. And though he wasn’t aware of it at the time, nicotine packed into the pods may have kept him from quitting: The average nicotine concentration in e-cigarettes more than doubled from 2013 to 2018, according to a study by the Truth Initiative and the CDC.
The immediate risks of nicotine on the developing brain are well documented. Studies suggest that nicotine – which is found in ENDS products – may affect adolescents’ ability to learn, remember, and maintain attention.
But many adolescents and young adults who use e-cigarettes say that vaping helps alleviate anxiety and keep them attentive, which adds to the complexity of their dependency, according to Dr. Boykan.
Nicotine “actually interrupts neural circuits, that it can be associated with more anxiety, depression, attention to learning, and susceptibility to other addictive substances,” she said. “That is enough to make it very scary.”
Jake also said a social environment in which so many of his friends vaped also made it difficult for him to quit.
“You’re hanging out with your friends at night, and all of them are using it, and you’re trying not to,” he said.
Jake eventually took a semester off from college for an unrelated surgery. He moved home, away from his vaping classmates. He eventually transferred to a different college and lived at home, where no one vaped and where he wasn’t allowed to smoke in the house, he said.
“He came home and we took him to a doctor, and they didn’t know quite how to handle kids and addiction to e-cigarettes,” Mrs. Warn said.
Not fully understanding the long-term health implications of e-cigarette use has precluded many clinicians from offering clear messaging on the risk of vaping to current and potential users.
“It’s taken pediatricians time to ask the right questions and recognize nicotine addiction” from vaping, said Dr. Boykan, who serves as chair of the Section on Nicotine and Tobacco Prevention and Treatment of the American Academy of Pediatrics. “It’s just hit us so fast.”
But once pediatricians do identify a nicotine dependency, it can be difficult to treat, Dr. Boykan said. Many pediatricians now recognize that e-cigarette addiction may occur in children as early as middle school.
“We don’t have a lot of evidence-based treatments for kids to recommend,” Dr. Boykan said.
Will vaping be a ‘phase?’
Aware of his vaping dependency and the possible risks to his long-term health, Jake, now 23, said he’s lessened his use, compared with his college days, but still struggles to kick the habit for good.
“I’d like to not be able to use all the time, not to feel the urge,” Jake said. “But I think over time it’ll just kind of phase out.”
But his mother said quitting may not be that simple.
“This will be a lifelong journey,” she said. “When I think of who he is, addiction is something he will always have. It’s a part of him now.”
Dr. Boykan, Ms. Schneider, and Dr. Nardis reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
Jake Warn calls vaping “a toxic artificial love.”
Jake, of Winslow, Maine, was 16 years old when he began vaping. Unlike cigarettes, vaping can be odorless, and its smoke leaves no trace, which allowed him and his friends to use the devices in school bathrooms without fear of being caught.
He would use an entire cartridge containing the vape liquid, the equivalent of smoking one pack of tobacco cigarettes, within 1 school day. By the fall semester of his first year in college, Jake said his use had increased even more.
“It got pricey, so that’s when I really started to notice” the extent of his dependency, he said recently.
Vaping rates among teenagers in Maine doubled from 15.3% to 28.7% between 2017 and 2019, while Jake was in high school. In 2021, 11% of high schoolers across the nation said they regularly smoked e-cigarettes, and an estimated 28% have ever tried the devices, according to the Centers for Disease Control and Prevention.
The Food and Drug Administration classifies e-cigarettes as a tobacco product because many contain nicotine, which comes from tobacco. Like Jake, the habit is likely to carry into adulthood for many who start in their teenage years, experts say.
Electronic nicotine delivery systems (ENDS) such as vapes have been touted by their manufacturers and by some in the medical field as a healthier alternative to cigarettes and as a method to help smokers give up the habit.
But, that’s not how Jake – who had never used combustible cigarettes – picked up vaping, or how he sold the idea to his mother.
“It’s all organic and natural flavoring, it’s just flavored water,” Mary Lou Warn recalled her son saying to her. She researched the health effects of vaping but didn’t find much online. “I knew they were dangerous because you don’t put anything in your lungs that isn’t fresh air.”
A determined athlete in high school, Jake found that his asthma worsened as he transitioned to college, especially when he ran a track meet or during a soccer game.
Mrs. Warn noticed changes off the field, too.
“He was coughing constantly, he wasn’t sleeping well, he wasn’t eating well,” she said. “I knew the addiction was taking over.”
Vaping irritated Jake’s throat, and he would get nosebleeds that he couldn’t stop, she added.
Since Mrs. Warn first looked into the effects of e-cigarettes on respiratory health back in 2017, many studies have been conducted of the short-term health outcomes for first-time smokers who never used combustible tobacco products. Studies suggest that vaping may worsen bronchitis and asthma, raise blood pressure, interfere with brain development in young users, suppress the immune system, and increase the risk of developing a chronic lung disease (Am J Prev Med. 2020 Feb;58[2]:182-90). Studies of mice and cell cultures have found that the vapor or extracts from vapes damage the chemical structure of DNA.
Still, the limited number of long-term human studies has made it hard to know what the health outcomes of e-cigarette users will be in the future. Conclusive studies linking commercial cigarette use to deaths from heart disease and cancer didn’t emerge until the mid-1950s, decades after manufacturers began mass production and marketing in the early 20th century.
Years could pass before researchers gain a clearer understanding of the health implications of long-term e-cigarette use, according to Nigar Nargis, PhD, senior scientific director of tobacco control research at the American Cancer Society.
“There hasn’t been any such study to establish the direct link from ENDS to cancer, but it is understood that it [vaping] may promote the development of cancer and lung damage and inflammation,” Dr. Nargis said.
For decades, advocates built awareness of the harms of tobacco use, which led to a sharp decline in tobacco-related illnesses such as lung cancer. But Hilary Schneider, Maine’s director of government relations for the ACS Cancer Action Network, said she fears the uptick in the use of vapes – especially among those who never smoked or those who use both combustible cigarettes and e-cigarettes – may reverse declines in the rates of smoking-relating diseases.
Multiple studies suggest that inhaling chemicals found in e-cigarettes – including nicotine-carrying aerosols – can damage arteries and inflame and injure the lungs.
Vapes “basically have created a pediatric tobacco-use epidemic,” Ms. Schneider said. “What we’re seeing is unprecedented tobacco use rates, higher rates than we’ve seen in decades.”
One reason many young people start vaping is the attraction to flavors, which range from classic menthol to fruits and sweets. A handful of states have enacted bans or restrictions on the sale of flavored vapes.
“It’s new, and it’s just been marketed in a way that we’re really fighting the false narrative put out there by makers of these products that are trying to make them appealing to kids,” said Rachel Boykan, MD, clinical professor of pediatrics and attending physician at Stony Brook (N.Y.) Children’s Hospital.
The flavor Red Bull, in particular, hooked Jake. And though he wasn’t aware of it at the time, nicotine packed into the pods may have kept him from quitting: The average nicotine concentration in e-cigarettes more than doubled from 2013 to 2018, according to a study by the Truth Initiative and the CDC.
The immediate risks of nicotine on the developing brain are well documented. Studies suggest that nicotine – which is found in ENDS products – may affect adolescents’ ability to learn, remember, and maintain attention.
But many adolescents and young adults who use e-cigarettes say that vaping helps alleviate anxiety and keep them attentive, which adds to the complexity of their dependency, according to Dr. Boykan.
Nicotine “actually interrupts neural circuits, that it can be associated with more anxiety, depression, attention to learning, and susceptibility to other addictive substances,” she said. “That is enough to make it very scary.”
Jake also said a social environment in which so many of his friends vaped also made it difficult for him to quit.
“You’re hanging out with your friends at night, and all of them are using it, and you’re trying not to,” he said.
Jake eventually took a semester off from college for an unrelated surgery. He moved home, away from his vaping classmates. He eventually transferred to a different college and lived at home, where no one vaped and where he wasn’t allowed to smoke in the house, he said.
“He came home and we took him to a doctor, and they didn’t know quite how to handle kids and addiction to e-cigarettes,” Mrs. Warn said.
Not fully understanding the long-term health implications of e-cigarette use has precluded many clinicians from offering clear messaging on the risk of vaping to current and potential users.
“It’s taken pediatricians time to ask the right questions and recognize nicotine addiction” from vaping, said Dr. Boykan, who serves as chair of the Section on Nicotine and Tobacco Prevention and Treatment of the American Academy of Pediatrics. “It’s just hit us so fast.”
But once pediatricians do identify a nicotine dependency, it can be difficult to treat, Dr. Boykan said. Many pediatricians now recognize that e-cigarette addiction may occur in children as early as middle school.
“We don’t have a lot of evidence-based treatments for kids to recommend,” Dr. Boykan said.
Will vaping be a ‘phase?’
Aware of his vaping dependency and the possible risks to his long-term health, Jake, now 23, said he’s lessened his use, compared with his college days, but still struggles to kick the habit for good.
“I’d like to not be able to use all the time, not to feel the urge,” Jake said. “But I think over time it’ll just kind of phase out.”
But his mother said quitting may not be that simple.
“This will be a lifelong journey,” she said. “When I think of who he is, addiction is something he will always have. It’s a part of him now.”
Dr. Boykan, Ms. Schneider, and Dr. Nardis reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
Jake Warn calls vaping “a toxic artificial love.”
Jake, of Winslow, Maine, was 16 years old when he began vaping. Unlike cigarettes, vaping can be odorless, and its smoke leaves no trace, which allowed him and his friends to use the devices in school bathrooms without fear of being caught.
He would use an entire cartridge containing the vape liquid, the equivalent of smoking one pack of tobacco cigarettes, within 1 school day. By the fall semester of his first year in college, Jake said his use had increased even more.
“It got pricey, so that’s when I really started to notice” the extent of his dependency, he said recently.
Vaping rates among teenagers in Maine doubled from 15.3% to 28.7% between 2017 and 2019, while Jake was in high school. In 2021, 11% of high schoolers across the nation said they regularly smoked e-cigarettes, and an estimated 28% have ever tried the devices, according to the Centers for Disease Control and Prevention.
The Food and Drug Administration classifies e-cigarettes as a tobacco product because many contain nicotine, which comes from tobacco. Like Jake, the habit is likely to carry into adulthood for many who start in their teenage years, experts say.
Electronic nicotine delivery systems (ENDS) such as vapes have been touted by their manufacturers and by some in the medical field as a healthier alternative to cigarettes and as a method to help smokers give up the habit.
But, that’s not how Jake – who had never used combustible cigarettes – picked up vaping, or how he sold the idea to his mother.
“It’s all organic and natural flavoring, it’s just flavored water,” Mary Lou Warn recalled her son saying to her. She researched the health effects of vaping but didn’t find much online. “I knew they were dangerous because you don’t put anything in your lungs that isn’t fresh air.”
A determined athlete in high school, Jake found that his asthma worsened as he transitioned to college, especially when he ran a track meet or during a soccer game.
Mrs. Warn noticed changes off the field, too.
“He was coughing constantly, he wasn’t sleeping well, he wasn’t eating well,” she said. “I knew the addiction was taking over.”
Vaping irritated Jake’s throat, and he would get nosebleeds that he couldn’t stop, she added.
Since Mrs. Warn first looked into the effects of e-cigarettes on respiratory health back in 2017, many studies have been conducted of the short-term health outcomes for first-time smokers who never used combustible tobacco products. Studies suggest that vaping may worsen bronchitis and asthma, raise blood pressure, interfere with brain development in young users, suppress the immune system, and increase the risk of developing a chronic lung disease (Am J Prev Med. 2020 Feb;58[2]:182-90). Studies of mice and cell cultures have found that the vapor or extracts from vapes damage the chemical structure of DNA.
Still, the limited number of long-term human studies has made it hard to know what the health outcomes of e-cigarette users will be in the future. Conclusive studies linking commercial cigarette use to deaths from heart disease and cancer didn’t emerge until the mid-1950s, decades after manufacturers began mass production and marketing in the early 20th century.
Years could pass before researchers gain a clearer understanding of the health implications of long-term e-cigarette use, according to Nigar Nargis, PhD, senior scientific director of tobacco control research at the American Cancer Society.
“There hasn’t been any such study to establish the direct link from ENDS to cancer, but it is understood that it [vaping] may promote the development of cancer and lung damage and inflammation,” Dr. Nargis said.
For decades, advocates built awareness of the harms of tobacco use, which led to a sharp decline in tobacco-related illnesses such as lung cancer. But Hilary Schneider, Maine’s director of government relations for the ACS Cancer Action Network, said she fears the uptick in the use of vapes – especially among those who never smoked or those who use both combustible cigarettes and e-cigarettes – may reverse declines in the rates of smoking-relating diseases.
Multiple studies suggest that inhaling chemicals found in e-cigarettes – including nicotine-carrying aerosols – can damage arteries and inflame and injure the lungs.
Vapes “basically have created a pediatric tobacco-use epidemic,” Ms. Schneider said. “What we’re seeing is unprecedented tobacco use rates, higher rates than we’ve seen in decades.”
One reason many young people start vaping is the attraction to flavors, which range from classic menthol to fruits and sweets. A handful of states have enacted bans or restrictions on the sale of flavored vapes.
“It’s new, and it’s just been marketed in a way that we’re really fighting the false narrative put out there by makers of these products that are trying to make them appealing to kids,” said Rachel Boykan, MD, clinical professor of pediatrics and attending physician at Stony Brook (N.Y.) Children’s Hospital.
The flavor Red Bull, in particular, hooked Jake. And though he wasn’t aware of it at the time, nicotine packed into the pods may have kept him from quitting: The average nicotine concentration in e-cigarettes more than doubled from 2013 to 2018, according to a study by the Truth Initiative and the CDC.
The immediate risks of nicotine on the developing brain are well documented. Studies suggest that nicotine – which is found in ENDS products – may affect adolescents’ ability to learn, remember, and maintain attention.
But many adolescents and young adults who use e-cigarettes say that vaping helps alleviate anxiety and keep them attentive, which adds to the complexity of their dependency, according to Dr. Boykan.
Nicotine “actually interrupts neural circuits, that it can be associated with more anxiety, depression, attention to learning, and susceptibility to other addictive substances,” she said. “That is enough to make it very scary.”
Jake also said a social environment in which so many of his friends vaped also made it difficult for him to quit.
“You’re hanging out with your friends at night, and all of them are using it, and you’re trying not to,” he said.
Jake eventually took a semester off from college for an unrelated surgery. He moved home, away from his vaping classmates. He eventually transferred to a different college and lived at home, where no one vaped and where he wasn’t allowed to smoke in the house, he said.
“He came home and we took him to a doctor, and they didn’t know quite how to handle kids and addiction to e-cigarettes,” Mrs. Warn said.
Not fully understanding the long-term health implications of e-cigarette use has precluded many clinicians from offering clear messaging on the risk of vaping to current and potential users.
“It’s taken pediatricians time to ask the right questions and recognize nicotine addiction” from vaping, said Dr. Boykan, who serves as chair of the Section on Nicotine and Tobacco Prevention and Treatment of the American Academy of Pediatrics. “It’s just hit us so fast.”
But once pediatricians do identify a nicotine dependency, it can be difficult to treat, Dr. Boykan said. Many pediatricians now recognize that e-cigarette addiction may occur in children as early as middle school.
“We don’t have a lot of evidence-based treatments for kids to recommend,” Dr. Boykan said.
Will vaping be a ‘phase?’
Aware of his vaping dependency and the possible risks to his long-term health, Jake, now 23, said he’s lessened his use, compared with his college days, but still struggles to kick the habit for good.
“I’d like to not be able to use all the time, not to feel the urge,” Jake said. “But I think over time it’ll just kind of phase out.”
But his mother said quitting may not be that simple.
“This will be a lifelong journey,” she said. “When I think of who he is, addiction is something he will always have. It’s a part of him now.”
Dr. Boykan, Ms. Schneider, and Dr. Nardis reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
Can asthma incidence be reduced by attention to sleep disorders?
Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.
The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.
Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.
The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.
Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.
Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.
In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.
Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.
“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.
Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.
Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.
The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
Complex and multifactorial
“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.
“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.
“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.
The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.
The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.
Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.
The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.
Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.
Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.
In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.
Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.
“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.
Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.
Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.
The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
Complex and multifactorial
“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.
“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.
“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.
The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.
The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.
Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.
The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.
Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.
Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.
In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.
Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.
“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.
Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.
Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.
The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
Complex and multifactorial
“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.
“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.
“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.
The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM BMJ OPEN RESPIRATORY RESEARCH
Mucus plugging phenotype associated with adverse features
In a real-life clinic setting study aimed at determining phenotypic associations of mucus plugging
Rory Chan, MBChB, of the University of Dundee (Scotland) and colleagues found conversely that the presence of these features was associated with an increased likelihood of mucus plugging.
Important pathophysiological characteristics of persistent asthma include mucus plugging, goblet cell hyperplasia, smooth muscle hypertrophy, and eosinophilic infiltration. Mucus plugging contributes significantly to airway obstruction and death in acute asthma, the investigators stated, noting further that the understanding of mucus plugging’s role in chronic asthma is increasing.
Their retrospective cohort study included 126 patients with respiratory physician-diagnosed moderate to severe asthma who had attended their clinic (January 2016–March 2022) and were receiving daily doses of inhaled corticosteroid (ICS) (≥ 800 mcg) and a second-line controller. All had prior high-resolution CT (HRCT) scans with mucus plugs identified by an experienced thoracic radiologist. Prior to the start of biologic therapy, a mucus plug score (MPS) signifying the number of affected lung segments (0-20) was calculated subsequently and considered along with pulmonary function testing, T2 inflammatory markers, asthma control data, and measures of peripheral blood eosinophils (PBE), as well as total IgG and IgE antibodies to Apergillus fumigatus.
The analysis showed that reduced forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio (OR, 3.01; 95% confidence interval, 1.14-7.97), two or more exacerbations per year (OR, 5.00; 95% CI, 1.55-16.11), raised PBE (OR, 3.23; 95% CI, 1.16-8.96), raised total IgE (OR, 3.20; 95% CI, 1.09-9.37), and Aspergillus fumigatus IgE titers (OR, 9.37; 95% CI, 1.82-48.20) all conferred significantly higher likelihood of the presence of mucus plugging. Highest prevalence of mucus plugs was in the right and left lower lung lobes (about 26% vs. about 10% and 14% in the middle and upper lobes).
Adjusted ORs in patients with impaired FEV1/FVC, showed the likelihood of mucus plugging to be 67% higher. In those with frequent exacerbations, they were 80% higher, and in those with raised PBE and IgE, 69% higher. Patients without mucus plugging had preserved FEV1 and FEV1/FVC.
Asthma patients with mucus plugging in the study exhibited higher levels of routinely measured T2 biomarkers, including blood eosinophils, FeNO, and total IgE, with median values all exceeding traditionally accepted cut points. Although patients with mucus plugging were receiving significantly higher ICS doses, and despite the suppressive effect of ICS on FeNO, they still had higher FeNO levels. “We therefore postulate that asthma patients with the MP phenotype might potentially experience greater treatment response to biologics targeting the underlying inflammatory endotype,” the investigators stated, adding that “the presence of mucus plugging should be recognized as a treatable trait for patients with severe asthma in terms of targeting therapy with biologics.”
They wrote that, “in a real-life clinic setting, the presence of mucus plugging detected on HRCT was associated with more severe exacerbations, more severe airflow obstruction, and greater T2 inflammation. This, in turn, suggests that imaging should be part of the routine workup of patients with poorly controlled severe asthma.”
In an accompanying editorial, Jorge Cedano, MD, Jiwoong Choi, PhD, and Mario Castro, MD, MPH, of the University of Kansas, Kansas City, cited that the prevalence and contribution of mucus plugging in the pathophysiology and morbidity of uncontrolled asthma is much greater than has been appreciated. They focused particularly on the suggestion that, even after adjusting for confounders, molds such as Apergillus may play a causal role, along with blood eosinophils, fractional exhaled nitric oxide, and total IgE, in T2 inflammation.
While current biologic therapies targeting the T2 phenotype have not yet been shown to reverse the progressive loss of lung function or lung remodeling process, the editorialists referenced a recent post hoc analysis of the CASCADE study showing mucus plugging reduction with the biologic tezepelumab versus placebo correlated with lung function improvement. “At least 20% of patients with moderate to severe asthma will experience progressive decline in lung function, more exacerbations, and worse asthma control despite the use of controller therapies. If physicians could identify the MP phenotype using computed tomography, then potentially earlier treatment with biologic therapy may improve asthma control and prevent future decline in lung function,” they said.
The study limitations listed included its retrospective observational nature and the fact that the study had only one senior thoracic radiologist interpreting the lung scans.
The study authors cited numerous conflicts of interest with pharmaceutical companies and medical societies. Dr. Castro reported affiliation or involvement in multiple organizations or entities with a financial or nonfinancial interest in the subject matter or materials discussed in the article.
In a real-life clinic setting study aimed at determining phenotypic associations of mucus plugging
Rory Chan, MBChB, of the University of Dundee (Scotland) and colleagues found conversely that the presence of these features was associated with an increased likelihood of mucus plugging.
Important pathophysiological characteristics of persistent asthma include mucus plugging, goblet cell hyperplasia, smooth muscle hypertrophy, and eosinophilic infiltration. Mucus plugging contributes significantly to airway obstruction and death in acute asthma, the investigators stated, noting further that the understanding of mucus plugging’s role in chronic asthma is increasing.
Their retrospective cohort study included 126 patients with respiratory physician-diagnosed moderate to severe asthma who had attended their clinic (January 2016–March 2022) and were receiving daily doses of inhaled corticosteroid (ICS) (≥ 800 mcg) and a second-line controller. All had prior high-resolution CT (HRCT) scans with mucus plugs identified by an experienced thoracic radiologist. Prior to the start of biologic therapy, a mucus plug score (MPS) signifying the number of affected lung segments (0-20) was calculated subsequently and considered along with pulmonary function testing, T2 inflammatory markers, asthma control data, and measures of peripheral blood eosinophils (PBE), as well as total IgG and IgE antibodies to Apergillus fumigatus.
The analysis showed that reduced forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio (OR, 3.01; 95% confidence interval, 1.14-7.97), two or more exacerbations per year (OR, 5.00; 95% CI, 1.55-16.11), raised PBE (OR, 3.23; 95% CI, 1.16-8.96), raised total IgE (OR, 3.20; 95% CI, 1.09-9.37), and Aspergillus fumigatus IgE titers (OR, 9.37; 95% CI, 1.82-48.20) all conferred significantly higher likelihood of the presence of mucus plugging. Highest prevalence of mucus plugs was in the right and left lower lung lobes (about 26% vs. about 10% and 14% in the middle and upper lobes).
Adjusted ORs in patients with impaired FEV1/FVC, showed the likelihood of mucus plugging to be 67% higher. In those with frequent exacerbations, they were 80% higher, and in those with raised PBE and IgE, 69% higher. Patients without mucus plugging had preserved FEV1 and FEV1/FVC.
Asthma patients with mucus plugging in the study exhibited higher levels of routinely measured T2 biomarkers, including blood eosinophils, FeNO, and total IgE, with median values all exceeding traditionally accepted cut points. Although patients with mucus plugging were receiving significantly higher ICS doses, and despite the suppressive effect of ICS on FeNO, they still had higher FeNO levels. “We therefore postulate that asthma patients with the MP phenotype might potentially experience greater treatment response to biologics targeting the underlying inflammatory endotype,” the investigators stated, adding that “the presence of mucus plugging should be recognized as a treatable trait for patients with severe asthma in terms of targeting therapy with biologics.”
They wrote that, “in a real-life clinic setting, the presence of mucus plugging detected on HRCT was associated with more severe exacerbations, more severe airflow obstruction, and greater T2 inflammation. This, in turn, suggests that imaging should be part of the routine workup of patients with poorly controlled severe asthma.”
In an accompanying editorial, Jorge Cedano, MD, Jiwoong Choi, PhD, and Mario Castro, MD, MPH, of the University of Kansas, Kansas City, cited that the prevalence and contribution of mucus plugging in the pathophysiology and morbidity of uncontrolled asthma is much greater than has been appreciated. They focused particularly on the suggestion that, even after adjusting for confounders, molds such as Apergillus may play a causal role, along with blood eosinophils, fractional exhaled nitric oxide, and total IgE, in T2 inflammation.
While current biologic therapies targeting the T2 phenotype have not yet been shown to reverse the progressive loss of lung function or lung remodeling process, the editorialists referenced a recent post hoc analysis of the CASCADE study showing mucus plugging reduction with the biologic tezepelumab versus placebo correlated with lung function improvement. “At least 20% of patients with moderate to severe asthma will experience progressive decline in lung function, more exacerbations, and worse asthma control despite the use of controller therapies. If physicians could identify the MP phenotype using computed tomography, then potentially earlier treatment with biologic therapy may improve asthma control and prevent future decline in lung function,” they said.
The study limitations listed included its retrospective observational nature and the fact that the study had only one senior thoracic radiologist interpreting the lung scans.
The study authors cited numerous conflicts of interest with pharmaceutical companies and medical societies. Dr. Castro reported affiliation or involvement in multiple organizations or entities with a financial or nonfinancial interest in the subject matter or materials discussed in the article.
In a real-life clinic setting study aimed at determining phenotypic associations of mucus plugging
Rory Chan, MBChB, of the University of Dundee (Scotland) and colleagues found conversely that the presence of these features was associated with an increased likelihood of mucus plugging.
Important pathophysiological characteristics of persistent asthma include mucus plugging, goblet cell hyperplasia, smooth muscle hypertrophy, and eosinophilic infiltration. Mucus plugging contributes significantly to airway obstruction and death in acute asthma, the investigators stated, noting further that the understanding of mucus plugging’s role in chronic asthma is increasing.
Their retrospective cohort study included 126 patients with respiratory physician-diagnosed moderate to severe asthma who had attended their clinic (January 2016–March 2022) and were receiving daily doses of inhaled corticosteroid (ICS) (≥ 800 mcg) and a second-line controller. All had prior high-resolution CT (HRCT) scans with mucus plugs identified by an experienced thoracic radiologist. Prior to the start of biologic therapy, a mucus plug score (MPS) signifying the number of affected lung segments (0-20) was calculated subsequently and considered along with pulmonary function testing, T2 inflammatory markers, asthma control data, and measures of peripheral blood eosinophils (PBE), as well as total IgG and IgE antibodies to Apergillus fumigatus.
The analysis showed that reduced forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio (OR, 3.01; 95% confidence interval, 1.14-7.97), two or more exacerbations per year (OR, 5.00; 95% CI, 1.55-16.11), raised PBE (OR, 3.23; 95% CI, 1.16-8.96), raised total IgE (OR, 3.20; 95% CI, 1.09-9.37), and Aspergillus fumigatus IgE titers (OR, 9.37; 95% CI, 1.82-48.20) all conferred significantly higher likelihood of the presence of mucus plugging. Highest prevalence of mucus plugs was in the right and left lower lung lobes (about 26% vs. about 10% and 14% in the middle and upper lobes).
Adjusted ORs in patients with impaired FEV1/FVC, showed the likelihood of mucus plugging to be 67% higher. In those with frequent exacerbations, they were 80% higher, and in those with raised PBE and IgE, 69% higher. Patients without mucus plugging had preserved FEV1 and FEV1/FVC.
Asthma patients with mucus plugging in the study exhibited higher levels of routinely measured T2 biomarkers, including blood eosinophils, FeNO, and total IgE, with median values all exceeding traditionally accepted cut points. Although patients with mucus plugging were receiving significantly higher ICS doses, and despite the suppressive effect of ICS on FeNO, they still had higher FeNO levels. “We therefore postulate that asthma patients with the MP phenotype might potentially experience greater treatment response to biologics targeting the underlying inflammatory endotype,” the investigators stated, adding that “the presence of mucus plugging should be recognized as a treatable trait for patients with severe asthma in terms of targeting therapy with biologics.”
They wrote that, “in a real-life clinic setting, the presence of mucus plugging detected on HRCT was associated with more severe exacerbations, more severe airflow obstruction, and greater T2 inflammation. This, in turn, suggests that imaging should be part of the routine workup of patients with poorly controlled severe asthma.”
In an accompanying editorial, Jorge Cedano, MD, Jiwoong Choi, PhD, and Mario Castro, MD, MPH, of the University of Kansas, Kansas City, cited that the prevalence and contribution of mucus plugging in the pathophysiology and morbidity of uncontrolled asthma is much greater than has been appreciated. They focused particularly on the suggestion that, even after adjusting for confounders, molds such as Apergillus may play a causal role, along with blood eosinophils, fractional exhaled nitric oxide, and total IgE, in T2 inflammation.
While current biologic therapies targeting the T2 phenotype have not yet been shown to reverse the progressive loss of lung function or lung remodeling process, the editorialists referenced a recent post hoc analysis of the CASCADE study showing mucus plugging reduction with the biologic tezepelumab versus placebo correlated with lung function improvement. “At least 20% of patients with moderate to severe asthma will experience progressive decline in lung function, more exacerbations, and worse asthma control despite the use of controller therapies. If physicians could identify the MP phenotype using computed tomography, then potentially earlier treatment with biologic therapy may improve asthma control and prevent future decline in lung function,” they said.
The study limitations listed included its retrospective observational nature and the fact that the study had only one senior thoracic radiologist interpreting the lung scans.
The study authors cited numerous conflicts of interest with pharmaceutical companies and medical societies. Dr. Castro reported affiliation or involvement in multiple organizations or entities with a financial or nonfinancial interest in the subject matter or materials discussed in the article.
FROM THE JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY: IN PRACTICE
Liquid albuterol shortage effects reduced by alternative drugs, similar shortages may be increasingly common
The shortage of 0.5% albuterol sulfate inhalation solution, first reported by the FDA last October, gained increasing attention earlier this month when Akorn Pharmaceuticals – one of just two companies making the product – shut down after years of financial and regulatory troubles.
The other manufacturer, Nephron Pharmaceuticals, is producing 0.5% albuterol “as fast as possible” to overcome the shortage, CEO Lou Kennedy said in a written comment.
Meanwhile, the more commonly used version of liquid albuterol, with a concentration of 0.083%, remains in “good supply from several manufacturers,” according to an FDA spokesperson.
Still, headlines concerning the shortage have caused “a bit of a panic” for patients with asthma and parents with asthmatic children, according to David R. Stukus, MD, professor of clinical pediatrics in the division of allergy and immunology at Nationwide Children’s, Columbus, Ohio.
Much of the media coverage has lacked context, causing unnecessary worry, he said, as the shortage only affects one type of albuterol generally reserved for inpatient and emergency use.
“The shortage has not impacted our albuterol inhalers thus far,” Dr. Stukus said in an interview. “So I certainly don’t want people with asthma to panic that they’re going to run out of their inhaler anytime soon.”
Even infants and toddlers can use inhalers
Although Dr. Stukus noted that certain patients do require nebulizers, such as those with conditions that physically limit their breathing, like muscular dystrophy, most patients can use inhalers just fine. He said it’s a “pretty common misconception, even among medical professionals,” that infants and toddlers need nebulizers instead.
“In our institution, for example, we rarely ever start babies on a nebulizer when we diagnose them with asthma,” Dr. Stukus said. “We often just start right away with an inhaler with a spacer and a face mask.”
The shortage of liquid albuterol may therefore have a silver lining, he suggested, as it prompts clinicians to reconsider their routine practice.
“When situations like this arise, it’s a great opportunity for all of us to just take a step back and reevaluate the way we do things,” Dr. Stukus said. “Sometimes we just get caught up with inertia and we continue to do things the same way even though new options are available, or evidence has changed to the contrary.”
Nathan Rabinovitch, MD, professor of pediatrics in the division of pediatric allergy and clinical immunology at National Jewish Health, Denver, said that his center had trouble obtaining liquid albuterol about 2 weeks ago, so they pivoted to the more expensive levalbuterol for about a week and a half, until their albuterol supply was restored.
While Dr. Rabinovitch agreed that most children don’t need a nebulizer, he said about 5%-10% of kids with severe asthma should have one on hand in case their inhaler fails to control an exacerbation.
Personal preferences may also considered, he added.
“If [a parent] says, ‘I like to use the nebulizer. The kid likes it,’ I’m fine if they just use a nebulizer.”
One possible downside of relying on a nebulizer, however, is portability, according to Kelly O’Shea, MD, assistant professor in the division of allergy and clinical immunology at the University of Michigan, Ann Arbor.
“If you’re out at the park or out at a soccer game with your kids, and they are having trouble breathing ... and they need their albuterol, you don’t have that ability if you are tied to a nebulizer,” Dr. O’Shea said in an interview. “As long as a parent feels comfortable – they feel like [their child] can get deep breaths in, I agree that you can use [an inhaler] in the infant and toddler population.”
She also agreed that a nebulizer may serve as a kind of second step if an inhaler isn’t controlling an exacerbation; however, she emphasized that a nebulizer should not be considered a replacement for professional care, and should not give a false sense of security.
“I caution parents to make sure that when they need it, they also take the next step and head over to the emergency room,” Dr. O’Shea said.
Generic drug shortages becoming more common
While the present scarcity of liquid albuterol appears relatively mild in terms of clinical impact, it brings up broader concerns about generic drug supply, and why shortages like this are becoming more common, according to Katie J. Suda, PharmD, MS, professor of medicine and pharmacy, and associate director, center for pharmaceutical policy and prescribing at the University of Pittsburgh.
“Drug shortages continue to increase in frequency, and the duration and severity of the shortages are also getting worse,” Dr. Suda said in an interview.
The reasons for these shortages can be elusive, according to 2022 report by the American Society of Health-System Pharmacists, which found that more than half of shortages came with no explanation from manufacturers.
The same report showed that only 5% of shortages were due to a “business decision,” but this factor is likely more central than publicly stated.
A recent FDA analysis on drug shortages, for instance, lists “lack of incentives to produce less profitable drugs,” as the first “root cause,” and Dr. Suda agrees.
“It’s important that we have generic medicines to decrease costs to our health systems, as well as for our patients,” Dr. Suda said. “But frequently, with those generic products, the price is driven so low that it increases the risk of a shortage.”
The drive to maintain profit margins may motivate companies to cut corners in production, Dr. Suda explained. She emphasized that this connection is speculative, because motivations are effectively unknowable, but the rationale is supported by past and present shortages.
Akorn Pharmaceuticals, for example, received a warning letter from the FDA in 2019 because of a variety of manufacturing issues, including defective bottles, questionable data, and metal shavings on aseptic filling equipment.
When a manufacturer like Akorn fails, the effects can be far-reaching, Dr. Suda said, noting their broad catalog of agents. Beyond liquid albuterol, Akorn was producing cardiac drugs, antibiotics, vitamins, local anesthetics, eye products, and others.
Drug shortages cause “a significant strain on our health care system,” Dr. Suda said, and substituting other medications increases risk of medical errors.
Fortunately, the increasing number of drug shortages is not going unnoticed, according to Dr. Suda. The FDA and multiple other organizations, including the ASHP, American Medical Association, and National Academies of Sciences, Engineering, and Medicine, are all taking steps to ensure that essential medicines are in steady supply, including moves to gather more data from manufacturers.
“I hope that a lot of the efforts that are moving forward ... will help us decrease the impact of shortages on our patients,” Dr. Suda said.
Lou Kennedy is the CEO of Nephron Pharmaceuticals, which commercially produces liquid albuterol. The other interviewees disclosed no relevant conflicts of interest.
The shortage of 0.5% albuterol sulfate inhalation solution, first reported by the FDA last October, gained increasing attention earlier this month when Akorn Pharmaceuticals – one of just two companies making the product – shut down after years of financial and regulatory troubles.
The other manufacturer, Nephron Pharmaceuticals, is producing 0.5% albuterol “as fast as possible” to overcome the shortage, CEO Lou Kennedy said in a written comment.
Meanwhile, the more commonly used version of liquid albuterol, with a concentration of 0.083%, remains in “good supply from several manufacturers,” according to an FDA spokesperson.
Still, headlines concerning the shortage have caused “a bit of a panic” for patients with asthma and parents with asthmatic children, according to David R. Stukus, MD, professor of clinical pediatrics in the division of allergy and immunology at Nationwide Children’s, Columbus, Ohio.
Much of the media coverage has lacked context, causing unnecessary worry, he said, as the shortage only affects one type of albuterol generally reserved for inpatient and emergency use.
“The shortage has not impacted our albuterol inhalers thus far,” Dr. Stukus said in an interview. “So I certainly don’t want people with asthma to panic that they’re going to run out of their inhaler anytime soon.”
Even infants and toddlers can use inhalers
Although Dr. Stukus noted that certain patients do require nebulizers, such as those with conditions that physically limit their breathing, like muscular dystrophy, most patients can use inhalers just fine. He said it’s a “pretty common misconception, even among medical professionals,” that infants and toddlers need nebulizers instead.
“In our institution, for example, we rarely ever start babies on a nebulizer when we diagnose them with asthma,” Dr. Stukus said. “We often just start right away with an inhaler with a spacer and a face mask.”
The shortage of liquid albuterol may therefore have a silver lining, he suggested, as it prompts clinicians to reconsider their routine practice.
“When situations like this arise, it’s a great opportunity for all of us to just take a step back and reevaluate the way we do things,” Dr. Stukus said. “Sometimes we just get caught up with inertia and we continue to do things the same way even though new options are available, or evidence has changed to the contrary.”
Nathan Rabinovitch, MD, professor of pediatrics in the division of pediatric allergy and clinical immunology at National Jewish Health, Denver, said that his center had trouble obtaining liquid albuterol about 2 weeks ago, so they pivoted to the more expensive levalbuterol for about a week and a half, until their albuterol supply was restored.
While Dr. Rabinovitch agreed that most children don’t need a nebulizer, he said about 5%-10% of kids with severe asthma should have one on hand in case their inhaler fails to control an exacerbation.
Personal preferences may also considered, he added.
“If [a parent] says, ‘I like to use the nebulizer. The kid likes it,’ I’m fine if they just use a nebulizer.”
One possible downside of relying on a nebulizer, however, is portability, according to Kelly O’Shea, MD, assistant professor in the division of allergy and clinical immunology at the University of Michigan, Ann Arbor.
“If you’re out at the park or out at a soccer game with your kids, and they are having trouble breathing ... and they need their albuterol, you don’t have that ability if you are tied to a nebulizer,” Dr. O’Shea said in an interview. “As long as a parent feels comfortable – they feel like [their child] can get deep breaths in, I agree that you can use [an inhaler] in the infant and toddler population.”
She also agreed that a nebulizer may serve as a kind of second step if an inhaler isn’t controlling an exacerbation; however, she emphasized that a nebulizer should not be considered a replacement for professional care, and should not give a false sense of security.
“I caution parents to make sure that when they need it, they also take the next step and head over to the emergency room,” Dr. O’Shea said.
Generic drug shortages becoming more common
While the present scarcity of liquid albuterol appears relatively mild in terms of clinical impact, it brings up broader concerns about generic drug supply, and why shortages like this are becoming more common, according to Katie J. Suda, PharmD, MS, professor of medicine and pharmacy, and associate director, center for pharmaceutical policy and prescribing at the University of Pittsburgh.
“Drug shortages continue to increase in frequency, and the duration and severity of the shortages are also getting worse,” Dr. Suda said in an interview.
The reasons for these shortages can be elusive, according to 2022 report by the American Society of Health-System Pharmacists, which found that more than half of shortages came with no explanation from manufacturers.
The same report showed that only 5% of shortages were due to a “business decision,” but this factor is likely more central than publicly stated.
A recent FDA analysis on drug shortages, for instance, lists “lack of incentives to produce less profitable drugs,” as the first “root cause,” and Dr. Suda agrees.
“It’s important that we have generic medicines to decrease costs to our health systems, as well as for our patients,” Dr. Suda said. “But frequently, with those generic products, the price is driven so low that it increases the risk of a shortage.”
The drive to maintain profit margins may motivate companies to cut corners in production, Dr. Suda explained. She emphasized that this connection is speculative, because motivations are effectively unknowable, but the rationale is supported by past and present shortages.
Akorn Pharmaceuticals, for example, received a warning letter from the FDA in 2019 because of a variety of manufacturing issues, including defective bottles, questionable data, and metal shavings on aseptic filling equipment.
When a manufacturer like Akorn fails, the effects can be far-reaching, Dr. Suda said, noting their broad catalog of agents. Beyond liquid albuterol, Akorn was producing cardiac drugs, antibiotics, vitamins, local anesthetics, eye products, and others.
Drug shortages cause “a significant strain on our health care system,” Dr. Suda said, and substituting other medications increases risk of medical errors.
Fortunately, the increasing number of drug shortages is not going unnoticed, according to Dr. Suda. The FDA and multiple other organizations, including the ASHP, American Medical Association, and National Academies of Sciences, Engineering, and Medicine, are all taking steps to ensure that essential medicines are in steady supply, including moves to gather more data from manufacturers.
“I hope that a lot of the efforts that are moving forward ... will help us decrease the impact of shortages on our patients,” Dr. Suda said.
Lou Kennedy is the CEO of Nephron Pharmaceuticals, which commercially produces liquid albuterol. The other interviewees disclosed no relevant conflicts of interest.
The shortage of 0.5% albuterol sulfate inhalation solution, first reported by the FDA last October, gained increasing attention earlier this month when Akorn Pharmaceuticals – one of just two companies making the product – shut down after years of financial and regulatory troubles.
The other manufacturer, Nephron Pharmaceuticals, is producing 0.5% albuterol “as fast as possible” to overcome the shortage, CEO Lou Kennedy said in a written comment.
Meanwhile, the more commonly used version of liquid albuterol, with a concentration of 0.083%, remains in “good supply from several manufacturers,” according to an FDA spokesperson.
Still, headlines concerning the shortage have caused “a bit of a panic” for patients with asthma and parents with asthmatic children, according to David R. Stukus, MD, professor of clinical pediatrics in the division of allergy and immunology at Nationwide Children’s, Columbus, Ohio.
Much of the media coverage has lacked context, causing unnecessary worry, he said, as the shortage only affects one type of albuterol generally reserved for inpatient and emergency use.
“The shortage has not impacted our albuterol inhalers thus far,” Dr. Stukus said in an interview. “So I certainly don’t want people with asthma to panic that they’re going to run out of their inhaler anytime soon.”
Even infants and toddlers can use inhalers
Although Dr. Stukus noted that certain patients do require nebulizers, such as those with conditions that physically limit their breathing, like muscular dystrophy, most patients can use inhalers just fine. He said it’s a “pretty common misconception, even among medical professionals,” that infants and toddlers need nebulizers instead.
“In our institution, for example, we rarely ever start babies on a nebulizer when we diagnose them with asthma,” Dr. Stukus said. “We often just start right away with an inhaler with a spacer and a face mask.”
The shortage of liquid albuterol may therefore have a silver lining, he suggested, as it prompts clinicians to reconsider their routine practice.
“When situations like this arise, it’s a great opportunity for all of us to just take a step back and reevaluate the way we do things,” Dr. Stukus said. “Sometimes we just get caught up with inertia and we continue to do things the same way even though new options are available, or evidence has changed to the contrary.”
Nathan Rabinovitch, MD, professor of pediatrics in the division of pediatric allergy and clinical immunology at National Jewish Health, Denver, said that his center had trouble obtaining liquid albuterol about 2 weeks ago, so they pivoted to the more expensive levalbuterol for about a week and a half, until their albuterol supply was restored.
While Dr. Rabinovitch agreed that most children don’t need a nebulizer, he said about 5%-10% of kids with severe asthma should have one on hand in case their inhaler fails to control an exacerbation.
Personal preferences may also considered, he added.
“If [a parent] says, ‘I like to use the nebulizer. The kid likes it,’ I’m fine if they just use a nebulizer.”
One possible downside of relying on a nebulizer, however, is portability, according to Kelly O’Shea, MD, assistant professor in the division of allergy and clinical immunology at the University of Michigan, Ann Arbor.
“If you’re out at the park or out at a soccer game with your kids, and they are having trouble breathing ... and they need their albuterol, you don’t have that ability if you are tied to a nebulizer,” Dr. O’Shea said in an interview. “As long as a parent feels comfortable – they feel like [their child] can get deep breaths in, I agree that you can use [an inhaler] in the infant and toddler population.”
She also agreed that a nebulizer may serve as a kind of second step if an inhaler isn’t controlling an exacerbation; however, she emphasized that a nebulizer should not be considered a replacement for professional care, and should not give a false sense of security.
“I caution parents to make sure that when they need it, they also take the next step and head over to the emergency room,” Dr. O’Shea said.
Generic drug shortages becoming more common
While the present scarcity of liquid albuterol appears relatively mild in terms of clinical impact, it brings up broader concerns about generic drug supply, and why shortages like this are becoming more common, according to Katie J. Suda, PharmD, MS, professor of medicine and pharmacy, and associate director, center for pharmaceutical policy and prescribing at the University of Pittsburgh.
“Drug shortages continue to increase in frequency, and the duration and severity of the shortages are also getting worse,” Dr. Suda said in an interview.
The reasons for these shortages can be elusive, according to 2022 report by the American Society of Health-System Pharmacists, which found that more than half of shortages came with no explanation from manufacturers.
The same report showed that only 5% of shortages were due to a “business decision,” but this factor is likely more central than publicly stated.
A recent FDA analysis on drug shortages, for instance, lists “lack of incentives to produce less profitable drugs,” as the first “root cause,” and Dr. Suda agrees.
“It’s important that we have generic medicines to decrease costs to our health systems, as well as for our patients,” Dr. Suda said. “But frequently, with those generic products, the price is driven so low that it increases the risk of a shortage.”
The drive to maintain profit margins may motivate companies to cut corners in production, Dr. Suda explained. She emphasized that this connection is speculative, because motivations are effectively unknowable, but the rationale is supported by past and present shortages.
Akorn Pharmaceuticals, for example, received a warning letter from the FDA in 2019 because of a variety of manufacturing issues, including defective bottles, questionable data, and metal shavings on aseptic filling equipment.
When a manufacturer like Akorn fails, the effects can be far-reaching, Dr. Suda said, noting their broad catalog of agents. Beyond liquid albuterol, Akorn was producing cardiac drugs, antibiotics, vitamins, local anesthetics, eye products, and others.
Drug shortages cause “a significant strain on our health care system,” Dr. Suda said, and substituting other medications increases risk of medical errors.
Fortunately, the increasing number of drug shortages is not going unnoticed, according to Dr. Suda. The FDA and multiple other organizations, including the ASHP, American Medical Association, and National Academies of Sciences, Engineering, and Medicine, are all taking steps to ensure that essential medicines are in steady supply, including moves to gather more data from manufacturers.
“I hope that a lot of the efforts that are moving forward ... will help us decrease the impact of shortages on our patients,” Dr. Suda said.
Lou Kennedy is the CEO of Nephron Pharmaceuticals, which commercially produces liquid albuterol. The other interviewees disclosed no relevant conflicts of interest.
Are early childhood viral infections linked with asthma?
MARSEILLE, France – It is well known that viral infections, especially respiratory syncytial virus (RSV) and rhinovirus (RV), exacerbate symptoms of asthma. But could they also play a part in triggering the onset of asthma?
The link between RSV and RV infections in early childhood and the development of asthma symptoms is well established, said Camille Taillé, MD, PhD, of the department of respiratory medicine and the rare diseases center of excellence at Bichat Hospital, Paris. But getting asthma is probably not just a matter of having a viral infection at a young age or of having a severe form of it. Gene polymorphisms, immune system disorders, and preexisting atopy are also associated with the risk of asthma. This was the focus of the 27th French-language respiratory medicine conference, held in Marseille, France.
RV and RSV
Persons with asthma are vulnerable to certain viral respiratory infections, in particular the flu and RV, which can exacerbate asthma symptoms. Inhaled corticosteroids have an overall protective effect against viral-induced exacerbations. For worsening asthma symptoms during an epidemic or pandemic, there is no contraindication to inhaled or oral corticosteroids.
Young children from the time of birth to 4 years of age are particularly susceptible to viral respiratory infections. According to data from France’s clinical surveillance network, Sentinelles, from the period covering winter 2021-2022, the rate of incidence per 100,000 inhabitants was systematically greater for the 0 to 4-year age range than for older age ranges.
Of the most common viruses that infect young children, RV, the virus that causes the common cold, is a nonenveloped RNA virus from the enterovirus family. There are 160 types, which are classified into three strains (A, B, and C). Of those strains, A and C confer the most severe infections. The virus is highly variable, which makes developing a vaccine challenging. The virus circulates year round, usually peaking in the fall and at the end of spring. RSV is an RNA virus that is classed as a respiratory virus. It comprises two serotypes: type A and B. Almost all children will have been infected with RSV by the time they are 2 years old. Epidemics occur each year during winter or in early spring in temperate climates. Vaccines are currently being developed and will soon be marketed. A monoclonal antibody (palivizumab), which targets fusion proteins of the virus, is available as prophylactic treatment for at-risk children.
RSV infection
During an RSV infection, the severe inflammation of the bronchial and alveolar wall causes acute respiratory distress. “But not all infants will develop severe forms of bronchiolitis,” said Dr. Taillé. “The risk factors for the severe form of the illness are well known: being under 6 months of age, prematurity, comorbidities (neurovascular, cardiovascular, respiratory, etc.), history of a stay in a neonatal intensive care unit at birth, living in low socioeconomic status towns, and exposure to smoking.”
Asthma development
The issue of whether or not viral diseases cause asthma has been the subject of intense debate. The studies are starting to stack up, however. They seem to show that RSV or RV infections are associated with the risk of subsequent asthma development. “For example, in a study published in 2022,” said Dr. Taillé, “in children admitted with an RSV infection, 60% of those who had been admitted to neonatal intensive care presented with symptoms of asthma between 3 and 6 years of age, compared with 18% of those who had had a milder case of RSV (admitted to nonintensive care settings). A serious RSV infection is a risk factor for later development of asthma.”
However, the link between RSV and later onset of asthma is also seen in milder cases of the infection. The American COAST study was designed to examine the effect of childhood respiratory infections on the risk of developing asthma. Researchers followed 259 newborns prospectively for 1, 3, and 6 years. To qualify, at least one parent was required to have respiratory allergies (defined as one or more positive aeroallergen skin tests) or a history of physician-diagnosed asthma. Regular samples taken during infectious episodes identified a virus in 90% of cases.
“We now know that RSV is not the only pathogen responsible for bronchiolitis. RV is often found, now that it can routinely be detected by PCR tests,” said Dr. Taillé. In the COAST study, the onset of wheezing during an RSV or RV infection in children aged 0-3 years was associated with an increased risk of asthma at 6 years of age. Globally, 28% of children infected by either virus were deemed to have asthma at 6 years of age. “There is clearly a link between having had a respiratory virus like RV or RSV and getting asthma symptoms at 6 years of age,” said Dr. Taillé. “What’s more, the effect of RV is not changed in this study by allergic sensitization.”
Many articles have been published on this topic. The results of cohort studies, from Japan to Finland and the United States, Italy, and Australia, are consistent with each other. Persons who have contracted RV or RSV are more likely to suffer from recurrent wheezing or asthma, especially if the infection is contracted in infancy or if it is severe. “Some studies even suggest that viral-induced asthma is more severe,” said Dr. Taillé. “For example, a Scottish study ... showed that children with a previous history of RSV infection had more hospital admissions and required more medication than asthmatics with no history of an RSV infection, suggesting the link between a previous history of RSV infection and the development of a more severe form of asthma.”
Reaching adulthood
Few longitudinal cohorts explore this issue in adulthood. A relatively old study reported an increased rate of asthma among adults who had required hospital admission for bronchiolitis in early childhood, as well as the effect on respiratory function. A 2023 study of the effects of respiratory illnesses in childhood reported similar findings. The authors evaluated lung structure and function via CT scans of 39 patients aged 26 years and concluded that participants who had been infected with RSV in childhood presented with increased air trapping, which is suggestive of airway abnormalities, possibly linked to a direct effect of viruses on lung development.
Mechanisms of action
“The real question is understanding if it’s the virus itself that causes asthma, or if the virus is simply uncovering underlying asthma in predisposed children,” said Dr. Taillé. From 30% to 40% of children who have had RSV will go on to develop wheezing or asthma in childhood. This observation suggests that there are factors favoring the development of asthma after infection with RSV. It has been shown that there is a genetic predisposition for RV. The roles of cigarette smoke, air pollution, environmental exposures to allergens, rapid urbanization, low vitamin D levels, low maternal omega-3 long-chain polyunsaturated fatty acid levels, maternal stress, and depression have also been highlighted.
It would seem that RSV and RV are a bit different. RV is thought to be associated with the development of asthma and wheezing, especially in people with a preexisting atopy or a reduced interferon immune response, while RSV, which occurs at a younger age and among the most vulnerable populations, seems to act independently of a person’s predisposition to allergies. RV stands out from other viral factors, owing to its tendency to create a Th2-biased inflammatory environment and its association with specific risk genes in people predisposed to asthma development (CDHR3).
Dr. Taillé has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
MARSEILLE, France – It is well known that viral infections, especially respiratory syncytial virus (RSV) and rhinovirus (RV), exacerbate symptoms of asthma. But could they also play a part in triggering the onset of asthma?
The link between RSV and RV infections in early childhood and the development of asthma symptoms is well established, said Camille Taillé, MD, PhD, of the department of respiratory medicine and the rare diseases center of excellence at Bichat Hospital, Paris. But getting asthma is probably not just a matter of having a viral infection at a young age or of having a severe form of it. Gene polymorphisms, immune system disorders, and preexisting atopy are also associated with the risk of asthma. This was the focus of the 27th French-language respiratory medicine conference, held in Marseille, France.
RV and RSV
Persons with asthma are vulnerable to certain viral respiratory infections, in particular the flu and RV, which can exacerbate asthma symptoms. Inhaled corticosteroids have an overall protective effect against viral-induced exacerbations. For worsening asthma symptoms during an epidemic or pandemic, there is no contraindication to inhaled or oral corticosteroids.
Young children from the time of birth to 4 years of age are particularly susceptible to viral respiratory infections. According to data from France’s clinical surveillance network, Sentinelles, from the period covering winter 2021-2022, the rate of incidence per 100,000 inhabitants was systematically greater for the 0 to 4-year age range than for older age ranges.
Of the most common viruses that infect young children, RV, the virus that causes the common cold, is a nonenveloped RNA virus from the enterovirus family. There are 160 types, which are classified into three strains (A, B, and C). Of those strains, A and C confer the most severe infections. The virus is highly variable, which makes developing a vaccine challenging. The virus circulates year round, usually peaking in the fall and at the end of spring. RSV is an RNA virus that is classed as a respiratory virus. It comprises two serotypes: type A and B. Almost all children will have been infected with RSV by the time they are 2 years old. Epidemics occur each year during winter or in early spring in temperate climates. Vaccines are currently being developed and will soon be marketed. A monoclonal antibody (palivizumab), which targets fusion proteins of the virus, is available as prophylactic treatment for at-risk children.
RSV infection
During an RSV infection, the severe inflammation of the bronchial and alveolar wall causes acute respiratory distress. “But not all infants will develop severe forms of bronchiolitis,” said Dr. Taillé. “The risk factors for the severe form of the illness are well known: being under 6 months of age, prematurity, comorbidities (neurovascular, cardiovascular, respiratory, etc.), history of a stay in a neonatal intensive care unit at birth, living in low socioeconomic status towns, and exposure to smoking.”
Asthma development
The issue of whether or not viral diseases cause asthma has been the subject of intense debate. The studies are starting to stack up, however. They seem to show that RSV or RV infections are associated with the risk of subsequent asthma development. “For example, in a study published in 2022,” said Dr. Taillé, “in children admitted with an RSV infection, 60% of those who had been admitted to neonatal intensive care presented with symptoms of asthma between 3 and 6 years of age, compared with 18% of those who had had a milder case of RSV (admitted to nonintensive care settings). A serious RSV infection is a risk factor for later development of asthma.”
However, the link between RSV and later onset of asthma is also seen in milder cases of the infection. The American COAST study was designed to examine the effect of childhood respiratory infections on the risk of developing asthma. Researchers followed 259 newborns prospectively for 1, 3, and 6 years. To qualify, at least one parent was required to have respiratory allergies (defined as one or more positive aeroallergen skin tests) or a history of physician-diagnosed asthma. Regular samples taken during infectious episodes identified a virus in 90% of cases.
“We now know that RSV is not the only pathogen responsible for bronchiolitis. RV is often found, now that it can routinely be detected by PCR tests,” said Dr. Taillé. In the COAST study, the onset of wheezing during an RSV or RV infection in children aged 0-3 years was associated with an increased risk of asthma at 6 years of age. Globally, 28% of children infected by either virus were deemed to have asthma at 6 years of age. “There is clearly a link between having had a respiratory virus like RV or RSV and getting asthma symptoms at 6 years of age,” said Dr. Taillé. “What’s more, the effect of RV is not changed in this study by allergic sensitization.”
Many articles have been published on this topic. The results of cohort studies, from Japan to Finland and the United States, Italy, and Australia, are consistent with each other. Persons who have contracted RV or RSV are more likely to suffer from recurrent wheezing or asthma, especially if the infection is contracted in infancy or if it is severe. “Some studies even suggest that viral-induced asthma is more severe,” said Dr. Taillé. “For example, a Scottish study ... showed that children with a previous history of RSV infection had more hospital admissions and required more medication than asthmatics with no history of an RSV infection, suggesting the link between a previous history of RSV infection and the development of a more severe form of asthma.”
Reaching adulthood
Few longitudinal cohorts explore this issue in adulthood. A relatively old study reported an increased rate of asthma among adults who had required hospital admission for bronchiolitis in early childhood, as well as the effect on respiratory function. A 2023 study of the effects of respiratory illnesses in childhood reported similar findings. The authors evaluated lung structure and function via CT scans of 39 patients aged 26 years and concluded that participants who had been infected with RSV in childhood presented with increased air trapping, which is suggestive of airway abnormalities, possibly linked to a direct effect of viruses on lung development.
Mechanisms of action
“The real question is understanding if it’s the virus itself that causes asthma, or if the virus is simply uncovering underlying asthma in predisposed children,” said Dr. Taillé. From 30% to 40% of children who have had RSV will go on to develop wheezing or asthma in childhood. This observation suggests that there are factors favoring the development of asthma after infection with RSV. It has been shown that there is a genetic predisposition for RV. The roles of cigarette smoke, air pollution, environmental exposures to allergens, rapid urbanization, low vitamin D levels, low maternal omega-3 long-chain polyunsaturated fatty acid levels, maternal stress, and depression have also been highlighted.
It would seem that RSV and RV are a bit different. RV is thought to be associated with the development of asthma and wheezing, especially in people with a preexisting atopy or a reduced interferon immune response, while RSV, which occurs at a younger age and among the most vulnerable populations, seems to act independently of a person’s predisposition to allergies. RV stands out from other viral factors, owing to its tendency to create a Th2-biased inflammatory environment and its association with specific risk genes in people predisposed to asthma development (CDHR3).
Dr. Taillé has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
MARSEILLE, France – It is well known that viral infections, especially respiratory syncytial virus (RSV) and rhinovirus (RV), exacerbate symptoms of asthma. But could they also play a part in triggering the onset of asthma?
The link between RSV and RV infections in early childhood and the development of asthma symptoms is well established, said Camille Taillé, MD, PhD, of the department of respiratory medicine and the rare diseases center of excellence at Bichat Hospital, Paris. But getting asthma is probably not just a matter of having a viral infection at a young age or of having a severe form of it. Gene polymorphisms, immune system disorders, and preexisting atopy are also associated with the risk of asthma. This was the focus of the 27th French-language respiratory medicine conference, held in Marseille, France.
RV and RSV
Persons with asthma are vulnerable to certain viral respiratory infections, in particular the flu and RV, which can exacerbate asthma symptoms. Inhaled corticosteroids have an overall protective effect against viral-induced exacerbations. For worsening asthma symptoms during an epidemic or pandemic, there is no contraindication to inhaled or oral corticosteroids.
Young children from the time of birth to 4 years of age are particularly susceptible to viral respiratory infections. According to data from France’s clinical surveillance network, Sentinelles, from the period covering winter 2021-2022, the rate of incidence per 100,000 inhabitants was systematically greater for the 0 to 4-year age range than for older age ranges.
Of the most common viruses that infect young children, RV, the virus that causes the common cold, is a nonenveloped RNA virus from the enterovirus family. There are 160 types, which are classified into three strains (A, B, and C). Of those strains, A and C confer the most severe infections. The virus is highly variable, which makes developing a vaccine challenging. The virus circulates year round, usually peaking in the fall and at the end of spring. RSV is an RNA virus that is classed as a respiratory virus. It comprises two serotypes: type A and B. Almost all children will have been infected with RSV by the time they are 2 years old. Epidemics occur each year during winter or in early spring in temperate climates. Vaccines are currently being developed and will soon be marketed. A monoclonal antibody (palivizumab), which targets fusion proteins of the virus, is available as prophylactic treatment for at-risk children.
RSV infection
During an RSV infection, the severe inflammation of the bronchial and alveolar wall causes acute respiratory distress. “But not all infants will develop severe forms of bronchiolitis,” said Dr. Taillé. “The risk factors for the severe form of the illness are well known: being under 6 months of age, prematurity, comorbidities (neurovascular, cardiovascular, respiratory, etc.), history of a stay in a neonatal intensive care unit at birth, living in low socioeconomic status towns, and exposure to smoking.”
Asthma development
The issue of whether or not viral diseases cause asthma has been the subject of intense debate. The studies are starting to stack up, however. They seem to show that RSV or RV infections are associated with the risk of subsequent asthma development. “For example, in a study published in 2022,” said Dr. Taillé, “in children admitted with an RSV infection, 60% of those who had been admitted to neonatal intensive care presented with symptoms of asthma between 3 and 6 years of age, compared with 18% of those who had had a milder case of RSV (admitted to nonintensive care settings). A serious RSV infection is a risk factor for later development of asthma.”
However, the link between RSV and later onset of asthma is also seen in milder cases of the infection. The American COAST study was designed to examine the effect of childhood respiratory infections on the risk of developing asthma. Researchers followed 259 newborns prospectively for 1, 3, and 6 years. To qualify, at least one parent was required to have respiratory allergies (defined as one or more positive aeroallergen skin tests) or a history of physician-diagnosed asthma. Regular samples taken during infectious episodes identified a virus in 90% of cases.
“We now know that RSV is not the only pathogen responsible for bronchiolitis. RV is often found, now that it can routinely be detected by PCR tests,” said Dr. Taillé. In the COAST study, the onset of wheezing during an RSV or RV infection in children aged 0-3 years was associated with an increased risk of asthma at 6 years of age. Globally, 28% of children infected by either virus were deemed to have asthma at 6 years of age. “There is clearly a link between having had a respiratory virus like RV or RSV and getting asthma symptoms at 6 years of age,” said Dr. Taillé. “What’s more, the effect of RV is not changed in this study by allergic sensitization.”
Many articles have been published on this topic. The results of cohort studies, from Japan to Finland and the United States, Italy, and Australia, are consistent with each other. Persons who have contracted RV or RSV are more likely to suffer from recurrent wheezing or asthma, especially if the infection is contracted in infancy or if it is severe. “Some studies even suggest that viral-induced asthma is more severe,” said Dr. Taillé. “For example, a Scottish study ... showed that children with a previous history of RSV infection had more hospital admissions and required more medication than asthmatics with no history of an RSV infection, suggesting the link between a previous history of RSV infection and the development of a more severe form of asthma.”
Reaching adulthood
Few longitudinal cohorts explore this issue in adulthood. A relatively old study reported an increased rate of asthma among adults who had required hospital admission for bronchiolitis in early childhood, as well as the effect on respiratory function. A 2023 study of the effects of respiratory illnesses in childhood reported similar findings. The authors evaluated lung structure and function via CT scans of 39 patients aged 26 years and concluded that participants who had been infected with RSV in childhood presented with increased air trapping, which is suggestive of airway abnormalities, possibly linked to a direct effect of viruses on lung development.
Mechanisms of action
“The real question is understanding if it’s the virus itself that causes asthma, or if the virus is simply uncovering underlying asthma in predisposed children,” said Dr. Taillé. From 30% to 40% of children who have had RSV will go on to develop wheezing or asthma in childhood. This observation suggests that there are factors favoring the development of asthma after infection with RSV. It has been shown that there is a genetic predisposition for RV. The roles of cigarette smoke, air pollution, environmental exposures to allergens, rapid urbanization, low vitamin D levels, low maternal omega-3 long-chain polyunsaturated fatty acid levels, maternal stress, and depression have also been highlighted.
It would seem that RSV and RV are a bit different. RV is thought to be associated with the development of asthma and wheezing, especially in people with a preexisting atopy or a reduced interferon immune response, while RSV, which occurs at a younger age and among the most vulnerable populations, seems to act independently of a person’s predisposition to allergies. RV stands out from other viral factors, owing to its tendency to create a Th2-biased inflammatory environment and its association with specific risk genes in people predisposed to asthma development (CDHR3).
Dr. Taillé has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.