The efficacy of the influenza vaccine when given to patients with multiple sclerosis (MS) is similar to that in healthy controls, Jackie Nguyen reported at the virtual annual meeting of the Consortium of Multiple Sclerosis Centers (CMSC). She presented a systematic review and meta-analysis of nine published cohort studies including 417 MS patients and more than 500 healthy controls, all of whom received inactivated seasonal influenza vaccine.

The impetus for this project was a recognition that the great majority of the research on the impact of influenza vaccine in patients with MS has focused on safety and MS relapse rates. In contrast, the nine studies included in the meta-analysis contained data on influenza vaccine efficacy as reflected in the ability to mount an adequate immune response. This was defined in standard fashion either by seroconversion, which required at least a fourfold increase in antibody titers following vaccination, or seroprotection, with a postvaccination antihemagglutination immunoglobulin G titer of at least 40. The analysis included patients with MS irrespective of disease duration or severity or treatment regimen, noted Ms. Nguyen, a third-year medical student at Nova Southeastern University College of Allopathic Medicine in Davie, Fla.

The researchers found that there was no significant difference between patients with MS and healthy controls in the rates of an adequate immune response for influenza H1N1, H3N2, or influenza B virus. “The vaccine should thus continue to be recommended for MS patients, as the data shows it to be efficacious,” she said.

Her conclusion is consistent with guidance provided in the American Academy of Neurology’s 2019 practice guideline update on immunization in MS, highlighted elsewhere at CMSC 2020 in a presentation by Marijean Buhse, PhD, of Stony Brook University in New York.

The guideline, updated for the first time in 17 years, states that all MS patients should be advised to receive influenza vaccine annually: “With known risks of exacerbation and other morbidity with influenza infection and no identified risks of exacerbation with influenza vaccines, benefits of influenza vaccination outweigh the risks in most scenarios. The exception involves the relatively few MS patients having a specific contraindication to the influenza vaccine, such as a previous severe reaction, noted Dr. Buhse, who wasn’t involved in developing the evidence-based guidelines.

The available evidence indicates that some but not all disease-modifying therapies for MS reduce the effectiveness of vaccination against influenza.

According to the guideline, “it is possible” that persons with MS being treated with glatiramer acetate have a reduced likelihood of seroprotection from influenza vaccine, a conclusion the guidelines committee drew with “low confidence in the evidence.” Further, the guideline states that “it is probable” MS patients on fingolimod have a lower likelihood of obtaining seroprotection from influenza vaccine than patients not on the drug, with moderate confidence in the evidence. Also, it is deemed probable that patients with MS who are taking mitoxantrone have a reduced likelihood of response to influenza vaccination, compared with healthy controls. But it is probable that patients with MS who are receiving interferon-beta have no diminution in the likelihood of seroprotection. According to the guideline, there is insufficient evidence to say whether patients with MS who are on natalizumab, teriflunomide, or methotrexate have a diminished response to influenza vaccination.

Dr. Buhse noted that rituximab is off-label therapy for MS, so there are no data available regarding the likelihood of seroprotection in response to influenza vaccination in that setting. However, rituximab profoundly decreases the immunogenicity of influenza and pneumococcal vaccines in rheumatoid arthritis patients. It is therefore recommended that inactivated influenza vaccine be given to patients with MS at least 2 weeks prior to starting rituximab or 6 months after the last dose in order to optimize the humoral results. Ms. Nguyen reported having no financial conflicts regarding her presentation. Dr. Buhse reported having received honoraria from Genzyme and Biogen.

bjancin@mdedge.com

The efficacy of the influenza vaccine when given to patients with multiple sclerosis (MS) is similar to that in healthy controls, Jackie Nguyen reported at the virtual annual meeting of the Consortium of Multiple Sclerosis Centers (CMSC). She presented a systematic review and meta-analysis of nine published cohort studies including 417 MS patients and more than 500 healthy controls, all of whom received inactivated seasonal influenza vaccine.

The impetus for this project was a recognition that the great majority of the research on the impact of influenza vaccine in patients with MS has focused on safety and MS relapse rates. In contrast, the nine studies included in the meta-analysis contained data on influenza vaccine efficacy as reflected in the ability to mount an adequate immune response. This was defined in standard fashion either by seroconversion, which required at least a fourfold increase in antibody titers following vaccination, or seroprotection, with a postvaccination antihemagglutination immunoglobulin G titer of at least 40. The analysis included patients with MS irrespective of disease duration or severity or treatment regimen, noted Ms. Nguyen, a third-year medical student at Nova Southeastern University College of Allopathic Medicine in Davie, Fla.

The researchers found that there was no significant difference between patients with MS and healthy controls in the rates of an adequate immune response for influenza H1N1, H3N2, or influenza B virus. “The vaccine should thus continue to be recommended for MS patients, as the data shows it to be efficacious,” she said.

Her conclusion is consistent with guidance provided in the American Academy of Neurology’s 2019 practice guideline update on immunization in MS, highlighted elsewhere at CMSC 2020 in a presentation by Marijean Buhse, PhD, of Stony Brook University in New York.

The guideline, updated for the first time in 17 years, states that all MS patients should be advised to receive influenza vaccine annually: “With known risks of exacerbation and other morbidity with influenza infection and no identified risks of exacerbation with influenza vaccines, benefits of influenza vaccination outweigh the risks in most scenarios. The exception involves the relatively few MS patients having a specific contraindication to the influenza vaccine, such as a previous severe reaction, noted Dr. Buhse, who wasn’t involved in developing the evidence-based guidelines.

The available evidence indicates that some but not all disease-modifying therapies for MS reduce the effectiveness of vaccination against influenza.

According to the guideline, “it is possible” that persons with MS being treated with glatiramer acetate have a reduced likelihood of seroprotection from influenza vaccine, a conclusion the guidelines committee drew with “low confidence in the evidence.” Further, the guideline states that “it is probable” MS patients on fingolimod have a lower likelihood of obtaining seroprotection from influenza vaccine than patients not on the drug, with moderate confidence in the evidence. Also, it is deemed probable that patients with MS who are taking mitoxantrone have a reduced likelihood of response to influenza vaccination, compared with healthy controls. But it is probable that patients with MS who are receiving interferon-beta have no diminution in the likelihood of seroprotection. According to the guideline, there is insufficient evidence to say whether patients with MS who are on natalizumab, teriflunomide, or methotrexate have a diminished response to influenza vaccination.

Dr. Buhse noted that rituximab is off-label therapy for MS, so there are no data available regarding the likelihood of seroprotection in response to influenza vaccination in that setting. However, rituximab profoundly decreases the immunogenicity of influenza and pneumococcal vaccines in rheumatoid arthritis patients. It is therefore recommended that inactivated influenza vaccine be given to patients with MS at least 2 weeks prior to starting rituximab or 6 months after the last dose in order to optimize the humoral results. Ms. Nguyen reported having no financial conflicts regarding her presentation. Dr. Buhse reported having received honoraria from Genzyme and Biogen.

bjancin@mdedge.com

The efficacy of the influenza vaccine when given to patients with multiple sclerosis (MS) is similar to that in healthy controls, Jackie Nguyen reported at the virtual annual meeting of the Consortium of Multiple Sclerosis Centers (CMSC). She presented a systematic review and meta-analysis of nine published cohort studies including 417 MS patients and more than 500 healthy controls, all of whom received inactivated seasonal influenza vaccine.

The impetus for this project was a recognition that the great majority of the research on the impact of influenza vaccine in patients with MS has focused on safety and MS relapse rates. In contrast, the nine studies included in the meta-analysis contained data on influenza vaccine efficacy as reflected in the ability to mount an adequate immune response. This was defined in standard fashion either by seroconversion, which required at least a fourfold increase in antibody titers following vaccination, or seroprotection, with a postvaccination antihemagglutination immunoglobulin G titer of at least 40. The analysis included patients with MS irrespective of disease duration or severity or treatment regimen, noted Ms. Nguyen, a third-year medical student at Nova Southeastern University College of Allopathic Medicine in Davie, Fla.

The researchers found that there was no significant difference between patients with MS and healthy controls in the rates of an adequate immune response for influenza H1N1, H3N2, or influenza B virus. “The vaccine should thus continue to be recommended for MS patients, as the data shows it to be efficacious,” she said.

Her conclusion is consistent with guidance provided in the American Academy of Neurology’s 2019 practice guideline update on immunization in MS, highlighted elsewhere at CMSC 2020 in a presentation by Marijean Buhse, PhD, of Stony Brook University in New York.

The guideline, updated for the first time in 17 years, states that all MS patients should be advised to receive influenza vaccine annually: “With known risks of exacerbation and other morbidity with influenza infection and no identified risks of exacerbation with influenza vaccines, benefits of influenza vaccination outweigh the risks in most scenarios. The exception involves the relatively few MS patients having a specific contraindication to the influenza vaccine, such as a previous severe reaction, noted Dr. Buhse, who wasn’t involved in developing the evidence-based guidelines.

The available evidence indicates that some but not all disease-modifying therapies for MS reduce the effectiveness of vaccination against influenza.

According to the guideline, “it is possible” that persons with MS being treated with glatiramer acetate have a reduced likelihood of seroprotection from influenza vaccine, a conclusion the guidelines committee drew with “low confidence in the evidence.” Further, the guideline states that “it is probable” MS patients on fingolimod have a lower likelihood of obtaining seroprotection from influenza vaccine than patients not on the drug, with moderate confidence in the evidence. Also, it is deemed probable that patients with MS who are taking mitoxantrone have a reduced likelihood of response to influenza vaccination, compared with healthy controls. But it is probable that patients with MS who are receiving interferon-beta have no diminution in the likelihood of seroprotection. According to the guideline, there is insufficient evidence to say whether patients with MS who are on natalizumab, teriflunomide, or methotrexate have a diminished response to influenza vaccination.

Dr. Buhse noted that rituximab is off-label therapy for MS, so there are no data available regarding the likelihood of seroprotection in response to influenza vaccination in that setting. However, rituximab profoundly decreases the immunogenicity of influenza and pneumococcal vaccines in rheumatoid arthritis patients. It is therefore recommended that inactivated influenza vaccine be given to patients with MS at least 2 weeks prior to starting rituximab or 6 months after the last dose in order to optimize the humoral results. Ms. Nguyen reported having no financial conflicts regarding her presentation. Dr. Buhse reported having received honoraria from Genzyme and Biogen.

bjancin@mdedge.com

Two studies published this week in BMJ provide support for eating more fruits, vegetables, and whole grain foods to lower the risk of developing diabetes.

Lisovskaya/iStock/Getty Images Plus

In a pooled analysis of three large prospective American cohorts, people with the highest versus lowest total consumption of whole grain foods had a significantly lower risk of type 2 diabetes.

“These findings provide further support for the current recommendations of increasing whole grain consumption as part of a healthy diet for the prevention of type 2 diabetes,” wrote the authors led by Yang Hu, a doctoral student at Harvard School of Public Health, Boston.

Similarly, in a large European case-cohort study, people with higher values for plasma vitamin C and carotenoids (fruit and vegetable intake) had a lower incidence of type 2 diabetes.

“This study suggests that even a modest increase in fruit and vegetable intake could help to prevent type 2 diabetes ... regardless of whether the increase is among people with initially low or high intake,” wrote Ju-Sheng Zheng, PhD, University of Cambridge (England), and colleagues.
 

Individual whole grain foods

Previous studies have shown that high consumption of whole grains is associated with a lower risk of developing chronic diseases, including type 2 diabetes, cardiovascular disease, obesity, and some types of cancer, Mr. Hu and colleagues wrote.

Although research has shown that whole grain breakfast cereal and brown rice are linked with a lower risk of type 2 diabetes, the effect of other commonly consumed whole grain foods – which contain different amounts of dietary fiber, antioxidants, magnesium, and phytochemicals – has not been established.

Mr. Hu and colleagues analyzed pooled data from 158,259 U.S. women who participated in the Nurses’ Health Study (1984-2014) or the Nurses’ Health Study II (1991-2017) and 36,525 U.S. men who took part in the Health Professionals Follow-Up Study (1986-2016), who were free of diabetes, cardiovascular disease, and cancer.

Participants’ baseline consumption of seven types of whole grain foods – whole grain breakfast cereal, oatmeal, dark bread, brown rice, added bran, wheat germ, and popcorn – was based on self-replies to food frequency questionnaires.

During an average 24-year follow-up, 18,629 participants developed type 2 diabetes.

After adjusting for body mass index, lifestyle, and dietary risk factors, participants in the highest quintile of total whole grain consumption had a 29% lower risk of incident type 2 diabetes than those in the lowest quintile.

The most commonly consumed whole grain foods were whole grain cold breakfast cereal, dark bread, and popcorn.

Compared with eating less than one serving a month of whole grain cold breakfast cereal or dark bread, eating one or more servings a day was associated with a 19% and 21% lower risk of developing diabetes, respectively.

For popcorn, a J-shaped association was found for intake, where the risk of type 2 diabetes was not significantly raised until consumption exceeded about one serving a day, which led to about an 8% increased risk of developing diabetes – likely related to fat and sugar added to the popcorn, the researchers wrote.

For the less frequently consumed whole grain foods, compared with eating less than one serving a month of oatmeal, brown rice, added bran, or wheat germ, participants who ate two or more servings a week had a 21%, 12%, 15%, and 12% lower risk of developing type 2 diabetes, respectively.

Lean or overweight individuals had a greater decreased risk of diabetes with increased consumption of whole grain foods; however, because individuals with obesity have a higher risk of diabetes, even a small decrease in risk is still meaningful.

Limitations include the study was observational and may have had unknown confounders, and the results may not be generalizable to other populations, the authors note.
 

‘Five a day’ fruits and vegetables

Only one previous small published study from the United Kingdom has examined how blood levels of vitamin C and carotenoids are associated with incident type 2 diabetes, Dr. Zheng and colleagues wrote.

They investigated the relationship in 9,754 adults who developed new-onset type 2 diabetes and a comparison group of 13,662 adults who remained diabetes free during an average 9.7-year follow-up, from 340,234 participants in the European Prospective Investigation Into Cancer and Nutrition–InterAct study.

Participants were from Denmark, France, Germany, Italy, the Netherlands, Spain, Sweden, and the United Kingdom, and incident type 2 diabetes occurred between 1991 and 2007.

The researchers used high-performance liquid chromatography–ultraviolet methods to determine participants’ plasma levels of vitamin C and six carotenoids (alphta-carotene, beta-carotene, lycopene, lutein, zeaxanthin, beta-cryptoxanthin), which they used to calculate a composite biomarker score.

The recommendation to eat at least five fruits and vegetables a day corresponds to eating ≥400 g/day, according to Dr. Zheng and colleagues. The self-reported median fruit and vegetable intake in the current study was 274, 357, 396, 452, and 508 g/day from lowest to highest quintile.

After multivariable adjustment, higher levels of plasma vitamin C and carotenoids were associated with an 18% and 25% lower risk of incident type 2 diabetes per standard deviation, respectively.

Compared with patients whose vitamin C and carotenoid composite biomarker scores were in the lowest 20%, those with scores in the top 20% had half the risk of incident diabetes. Increasing fruit and vegetable consumption by 66 g/day was associated with a 25% lower risk of developing diabetes.

“These findings provide strong evidence from objectively measured biomarkers for the recommendation that fruit and vegetable intake should be increased to prevent type 2 diabetes,” according to the researchers.

However, consumption of fruits and vegetables remains far below guideline recommendations, they observed. “Although five portions a day of fruit and vegetables have been recommended for decades, in 2014-2015, 69% of U.K. adults ate fewer than this number, and this proportion is even higher in European adults (86%).”

Dr. Zheng and colleagues acknowledged that study limitations include those that are inherent with observational studies.

Although they could not distinguish between juice, fortified products, or whole foods, the analyses “were adjusted for vitamin supplement use, and suggest that as biomarkers of fruit and vegetable intake these findings endorse the consumption of fruit and vegetables, not that of supplements,” they maintained.

The study by Mr. Hu and colleagues was funded by the National Institutes of Health. The InterAct project was funded by the EU FP6 program. Biomarker measurements for vitamin C and carotenoids were funded by the InterAct project, EPIC-CVD project, MRC Cambridge Initiative, European Commission Framework Program 7, European Research Council, and National Institute for Health Research. Dr. Zheng has reported receiving funding from Westlake University and the EU Horizon 2020 program.

A version of this article originally appeared on Medscape.com.

Two studies published this week in BMJ provide support for eating more fruits, vegetables, and whole grain foods to lower the risk of developing diabetes.

Lisovskaya/iStock/Getty Images Plus

In a pooled analysis of three large prospective American cohorts, people with the highest versus lowest total consumption of whole grain foods had a significantly lower risk of type 2 diabetes.

“These findings provide further support for the current recommendations of increasing whole grain consumption as part of a healthy diet for the prevention of type 2 diabetes,” wrote the authors led by Yang Hu, a doctoral student at Harvard School of Public Health, Boston.

Similarly, in a large European case-cohort study, people with higher values for plasma vitamin C and carotenoids (fruit and vegetable intake) had a lower incidence of type 2 diabetes.

“This study suggests that even a modest increase in fruit and vegetable intake could help to prevent type 2 diabetes ... regardless of whether the increase is among people with initially low or high intake,” wrote Ju-Sheng Zheng, PhD, University of Cambridge (England), and colleagues.
 

Individual whole grain foods

Previous studies have shown that high consumption of whole grains is associated with a lower risk of developing chronic diseases, including type 2 diabetes, cardiovascular disease, obesity, and some types of cancer, Mr. Hu and colleagues wrote.

Although research has shown that whole grain breakfast cereal and brown rice are linked with a lower risk of type 2 diabetes, the effect of other commonly consumed whole grain foods – which contain different amounts of dietary fiber, antioxidants, magnesium, and phytochemicals – has not been established.

Mr. Hu and colleagues analyzed pooled data from 158,259 U.S. women who participated in the Nurses’ Health Study (1984-2014) or the Nurses’ Health Study II (1991-2017) and 36,525 U.S. men who took part in the Health Professionals Follow-Up Study (1986-2016), who were free of diabetes, cardiovascular disease, and cancer.

Participants’ baseline consumption of seven types of whole grain foods – whole grain breakfast cereal, oatmeal, dark bread, brown rice, added bran, wheat germ, and popcorn – was based on self-replies to food frequency questionnaires.

During an average 24-year follow-up, 18,629 participants developed type 2 diabetes.

After adjusting for body mass index, lifestyle, and dietary risk factors, participants in the highest quintile of total whole grain consumption had a 29% lower risk of incident type 2 diabetes than those in the lowest quintile.

The most commonly consumed whole grain foods were whole grain cold breakfast cereal, dark bread, and popcorn.

Compared with eating less than one serving a month of whole grain cold breakfast cereal or dark bread, eating one or more servings a day was associated with a 19% and 21% lower risk of developing diabetes, respectively.

For popcorn, a J-shaped association was found for intake, where the risk of type 2 diabetes was not significantly raised until consumption exceeded about one serving a day, which led to about an 8% increased risk of developing diabetes – likely related to fat and sugar added to the popcorn, the researchers wrote.

For the less frequently consumed whole grain foods, compared with eating less than one serving a month of oatmeal, brown rice, added bran, or wheat germ, participants who ate two or more servings a week had a 21%, 12%, 15%, and 12% lower risk of developing type 2 diabetes, respectively.

Lean or overweight individuals had a greater decreased risk of diabetes with increased consumption of whole grain foods; however, because individuals with obesity have a higher risk of diabetes, even a small decrease in risk is still meaningful.

Limitations include the study was observational and may have had unknown confounders, and the results may not be generalizable to other populations, the authors note.
 

‘Five a day’ fruits and vegetables

Only one previous small published study from the United Kingdom has examined how blood levels of vitamin C and carotenoids are associated with incident type 2 diabetes, Dr. Zheng and colleagues wrote.

They investigated the relationship in 9,754 adults who developed new-onset type 2 diabetes and a comparison group of 13,662 adults who remained diabetes free during an average 9.7-year follow-up, from 340,234 participants in the European Prospective Investigation Into Cancer and Nutrition–InterAct study.

Participants were from Denmark, France, Germany, Italy, the Netherlands, Spain, Sweden, and the United Kingdom, and incident type 2 diabetes occurred between 1991 and 2007.

The researchers used high-performance liquid chromatography–ultraviolet methods to determine participants’ plasma levels of vitamin C and six carotenoids (alphta-carotene, beta-carotene, lycopene, lutein, zeaxanthin, beta-cryptoxanthin), which they used to calculate a composite biomarker score.

The recommendation to eat at least five fruits and vegetables a day corresponds to eating ≥400 g/day, according to Dr. Zheng and colleagues. The self-reported median fruit and vegetable intake in the current study was 274, 357, 396, 452, and 508 g/day from lowest to highest quintile.

After multivariable adjustment, higher levels of plasma vitamin C and carotenoids were associated with an 18% and 25% lower risk of incident type 2 diabetes per standard deviation, respectively.

Compared with patients whose vitamin C and carotenoid composite biomarker scores were in the lowest 20%, those with scores in the top 20% had half the risk of incident diabetes. Increasing fruit and vegetable consumption by 66 g/day was associated with a 25% lower risk of developing diabetes.

“These findings provide strong evidence from objectively measured biomarkers for the recommendation that fruit and vegetable intake should be increased to prevent type 2 diabetes,” according to the researchers.

However, consumption of fruits and vegetables remains far below guideline recommendations, they observed. “Although five portions a day of fruit and vegetables have been recommended for decades, in 2014-2015, 69% of U.K. adults ate fewer than this number, and this proportion is even higher in European adults (86%).”

Dr. Zheng and colleagues acknowledged that study limitations include those that are inherent with observational studies.

Although they could not distinguish between juice, fortified products, or whole foods, the analyses “were adjusted for vitamin supplement use, and suggest that as biomarkers of fruit and vegetable intake these findings endorse the consumption of fruit and vegetables, not that of supplements,” they maintained.

The study by Mr. Hu and colleagues was funded by the National Institutes of Health. The InterAct project was funded by the EU FP6 program. Biomarker measurements for vitamin C and carotenoids were funded by the InterAct project, EPIC-CVD project, MRC Cambridge Initiative, European Commission Framework Program 7, European Research Council, and National Institute for Health Research. Dr. Zheng has reported receiving funding from Westlake University and the EU Horizon 2020 program.

A version of this article originally appeared on Medscape.com.

Two studies published this week in BMJ provide support for eating more fruits, vegetables, and whole grain foods to lower the risk of developing diabetes.

Lisovskaya/iStock/Getty Images Plus

In a pooled analysis of three large prospective American cohorts, people with the highest versus lowest total consumption of whole grain foods had a significantly lower risk of type 2 diabetes.

“These findings provide further support for the current recommendations of increasing whole grain consumption as part of a healthy diet for the prevention of type 2 diabetes,” wrote the authors led by Yang Hu, a doctoral student at Harvard School of Public Health, Boston.

Similarly, in a large European case-cohort study, people with higher values for plasma vitamin C and carotenoids (fruit and vegetable intake) had a lower incidence of type 2 diabetes.

“This study suggests that even a modest increase in fruit and vegetable intake could help to prevent type 2 diabetes ... regardless of whether the increase is among people with initially low or high intake,” wrote Ju-Sheng Zheng, PhD, University of Cambridge (England), and colleagues.
 

Individual whole grain foods

Previous studies have shown that high consumption of whole grains is associated with a lower risk of developing chronic diseases, including type 2 diabetes, cardiovascular disease, obesity, and some types of cancer, Mr. Hu and colleagues wrote.

Although research has shown that whole grain breakfast cereal and brown rice are linked with a lower risk of type 2 diabetes, the effect of other commonly consumed whole grain foods – which contain different amounts of dietary fiber, antioxidants, magnesium, and phytochemicals – has not been established.

Mr. Hu and colleagues analyzed pooled data from 158,259 U.S. women who participated in the Nurses’ Health Study (1984-2014) or the Nurses’ Health Study II (1991-2017) and 36,525 U.S. men who took part in the Health Professionals Follow-Up Study (1986-2016), who were free of diabetes, cardiovascular disease, and cancer.

Participants’ baseline consumption of seven types of whole grain foods – whole grain breakfast cereal, oatmeal, dark bread, brown rice, added bran, wheat germ, and popcorn – was based on self-replies to food frequency questionnaires.

During an average 24-year follow-up, 18,629 participants developed type 2 diabetes.

After adjusting for body mass index, lifestyle, and dietary risk factors, participants in the highest quintile of total whole grain consumption had a 29% lower risk of incident type 2 diabetes than those in the lowest quintile.

The most commonly consumed whole grain foods were whole grain cold breakfast cereal, dark bread, and popcorn.

Compared with eating less than one serving a month of whole grain cold breakfast cereal or dark bread, eating one or more servings a day was associated with a 19% and 21% lower risk of developing diabetes, respectively.

For popcorn, a J-shaped association was found for intake, where the risk of type 2 diabetes was not significantly raised until consumption exceeded about one serving a day, which led to about an 8% increased risk of developing diabetes – likely related to fat and sugar added to the popcorn, the researchers wrote.

For the less frequently consumed whole grain foods, compared with eating less than one serving a month of oatmeal, brown rice, added bran, or wheat germ, participants who ate two or more servings a week had a 21%, 12%, 15%, and 12% lower risk of developing type 2 diabetes, respectively.

Lean or overweight individuals had a greater decreased risk of diabetes with increased consumption of whole grain foods; however, because individuals with obesity have a higher risk of diabetes, even a small decrease in risk is still meaningful.

Limitations include the study was observational and may have had unknown confounders, and the results may not be generalizable to other populations, the authors note.
 

‘Five a day’ fruits and vegetables

Only one previous small published study from the United Kingdom has examined how blood levels of vitamin C and carotenoids are associated with incident type 2 diabetes, Dr. Zheng and colleagues wrote.

They investigated the relationship in 9,754 adults who developed new-onset type 2 diabetes and a comparison group of 13,662 adults who remained diabetes free during an average 9.7-year follow-up, from 340,234 participants in the European Prospective Investigation Into Cancer and Nutrition–InterAct study.

Participants were from Denmark, France, Germany, Italy, the Netherlands, Spain, Sweden, and the United Kingdom, and incident type 2 diabetes occurred between 1991 and 2007.

The researchers used high-performance liquid chromatography–ultraviolet methods to determine participants’ plasma levels of vitamin C and six carotenoids (alphta-carotene, beta-carotene, lycopene, lutein, zeaxanthin, beta-cryptoxanthin), which they used to calculate a composite biomarker score.

The recommendation to eat at least five fruits and vegetables a day corresponds to eating ≥400 g/day, according to Dr. Zheng and colleagues. The self-reported median fruit and vegetable intake in the current study was 274, 357, 396, 452, and 508 g/day from lowest to highest quintile.

After multivariable adjustment, higher levels of plasma vitamin C and carotenoids were associated with an 18% and 25% lower risk of incident type 2 diabetes per standard deviation, respectively.

Compared with patients whose vitamin C and carotenoid composite biomarker scores were in the lowest 20%, those with scores in the top 20% had half the risk of incident diabetes. Increasing fruit and vegetable consumption by 66 g/day was associated with a 25% lower risk of developing diabetes.

“These findings provide strong evidence from objectively measured biomarkers for the recommendation that fruit and vegetable intake should be increased to prevent type 2 diabetes,” according to the researchers.

However, consumption of fruits and vegetables remains far below guideline recommendations, they observed. “Although five portions a day of fruit and vegetables have been recommended for decades, in 2014-2015, 69% of U.K. adults ate fewer than this number, and this proportion is even higher in European adults (86%).”

Dr. Zheng and colleagues acknowledged that study limitations include those that are inherent with observational studies.

Although they could not distinguish between juice, fortified products, or whole foods, the analyses “were adjusted for vitamin supplement use, and suggest that as biomarkers of fruit and vegetable intake these findings endorse the consumption of fruit and vegetables, not that of supplements,” they maintained.

The study by Mr. Hu and colleagues was funded by the National Institutes of Health. The InterAct project was funded by the EU FP6 program. Biomarker measurements for vitamin C and carotenoids were funded by the InterAct project, EPIC-CVD project, MRC Cambridge Initiative, European Commission Framework Program 7, European Research Council, and National Institute for Health Research. Dr. Zheng has reported receiving funding from Westlake University and the EU Horizon 2020 program.

A version of this article originally appeared on Medscape.com.

To the Editor: 

We read with interest the commentary by Srivastava et al,¹ "The Dayanara Effect: Increasing Skin Cancer Awareness in the Hispanic Community," concerning former Miss Universe Dayanara Torres and her diagnosis of metastatic melanoma; however, we believe it misses the mark. A quick Google search shows that Ms. Torres has fair skin and blue eyes. She has lived most of her life in Puerto Rico, the Philippines, and California--places where sun exposure is high and may have contributed to her diagnosis. Factors that have been linked to an increased risk for melanoma are fair skin, red or blonde hair, blue or green eyes, intense intermittent sun exposure and sunburns, a weakened immune system, and a family history of skin cancer.² Although we do not know her complete medical history, Ms. Torres' skin phenotype and likely chronic UV exposure made her a candidate for skin cancer. Although Srivastava et al¹ acknowledged that the Hispanic community encompasses a wide variety of individuals with varying levels of skin pigmentation and sun sensitivity, they overlooked Ms. Torres' risk for skin cancer because of her ethnic background. This form of generalization may negatively affect patient care and safety. By 2060, Hispanics are projected to account for almost 30% of the US population,³ and we must acknowledge the flaws that exist in our overall methodology for assessing skin cancer risk among this population to provide patients with unbiased care.  

In the early 1970s, the United States adopted the ethnonym Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America.⁴ The goal was to implement a common identifier that enabled the US Government to study the economic and social development of these groups. Nevertheless, considerable differences exist among distinct Hispanic communities, and variations in skin pigmentation and sun sensitivity are no exception. Although Hispanic countries are an amalgam of diverse races due to colonization, some have stronger European, African, or Amerindian influences, limiting the use of ethnicity during melanoma risk assessment. Another misconception reflected in the commentary by Srivastava et al¹ is the belief that the terms white and Hispanic are mutually exclusive. A study examining melanoma rates in the Chilean population supports this claim.⁵ The genetic composition of the Chilean high socioeconomic strata is 5% Amerindian and 95% white, while the low socioeconomic strata is approximately 40% Amerindian and 60% white. Patients from the low socioeconomic strata had higher rates of acral malignant melanoma, which typically is seen in patients with skin of color. On the other hand, males from the high socioeconomic strata had higher rates of truncal melanoma, which is more common among the white population.⁵ These results suggest that while both groups are considered Hispanic, it is ancestral origin that contributes to the differential rates and types of malignant melanoma.  

When analyzing data regarding melanoma rates in Hispanics, particularly data collected in the United States, we must question if the results are representative of the entire population. One point worth emphasizing is that melanoma data in the Hispanic community often is flawed. The North American Association of Central Cancer Registries considers Europeans such as Spaniards, as well as citizens of Andorra, the Canary Islands, and the Balearic Islands as Hispanic.⁶ Additionally, the Florida Cancer Data System uses data such as country of birth, ethnicity, and surname or maiden name recorded by the hospital tumor registry to identify Hispanic patients with melanoma.⁷ In 2006, Hu et al⁷ used the Florida Cancer Data System to analyze melanoma data in Miami-Dade County in South Florida, which has the second largest Hispanic community in the United States. One limitation to such data is that ethnicity often is self-reported by patients or assigned by a health care provider. In addition, women whose maiden names are not available may be misclassified through marriage depending on whether their husbands have Spanish or non-Spanish last names.⁷ Finally, with societal norms evolving, Americans are now more accepting of interracial marriages. In 2017, the Pew Research Center reported that 17% of all newlyweds in the United States were intermarried and 42% of these marriages were between a white individual and a Hispanic individual, comprising the most prevalent form of intermarriage reported.⁸ In 2015, 27% of newlywed Hispanics were intermarried. This percentage varied depending on whether they were born in the United States or abroad. Although 15% of Hispanic immigrants married a spouse from another race, 39% of Hispanics born in the United States married a non-Hispanic (eg, white, black, Asian, or Native American who is not Hispanic).⁸ This type of marriage and subsequent offspring might lead to an increase in the white genetic pool. As a result, the risk for melanoma development may be increased or misrepresented. Remaining aware of these changes in the population is crucial, as it exemplifies why the current methodology for gathering and reporting melanoma data is unreliable. 

Labeling Ms. Torres as Hispanic due to her Puerto Rican nationality did not tell us anything about her risk for developing melanoma. To correctly assess the risk for melanoma among Hispanics, it is imperative that we re-evaluate our approach. We agree with He et al⁹ that our efforts should be dedicated to better understanding the impact of pigmentation, race, genetics, and sunburn on the risk for melanoma. Until we know more about this possible correlation, we should reconsider how we study melanoma using Hispanics as an ethnicity. We may have it all wrong.  

1. Srivastava R, Wassef C, Rao BK. The Dayanara effect: increasing skin cancer awareness in the Hispanic community. Cutis. 2019;103:257-258. 
    
2. Curiel-Lewandrowski C. Risk factors for the development of melanoma. UpToDate. https://www.uptodate.com/contents/risk-factors-for-the-development-of-melanoma. Updated February 27, 2020. Accessed April 16, 2020. 
    
3. Colby SL, Ortman JM. Projections of the size and composition of the U.S. population: 2014 to 2060. United States Census Bureau website. https://www.census.gov/library/publications/2015/demo/p25-1143.html. Published March 3, 2015. Accessed April 16, 2020. 
    
4. National Research Council (US) Panel on Hispanics in the United States; Tienda M, Mitchell F, editors. Multiple Origins, Uncertain Destinies: Hispanics and the American Future. Washington (DC): National Academies Press (US); 2006. 3, Defining Hispanicity: E Pluribus Unum or E Pluribus Plures? Available from: https://www.ncbi.nlm.nih.gov/books/NBK19811/ 
    
5. Zemelman VB, Valenzuela CY, Sazunic I, et al. Malignant melanoma in Chile: different site distribution between private and state patients. Biol Res. 2014;47:34. 
    
6. NAACCR Race and Ethnicity Work Group. NAACCR guideline for enhancing Hispanic-Latino identification: revised NAACCR Hispanic/Latino identification algorithm [NHIA v2.2.1]. NAACCR website. https://www.naaccr.org/wp-content/uploads/2016/11/NHIA_v2_2_1_09122011.pdf. Revised September 12, 2011. Accessed April 15, 2020.  
    
7. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708. 
    
8. Livingston G, Brown A. Intermarriage in the U.S. 50 years after Loving v. Virginia. Pew Research Center website. https://www.pewsocialtrends.org/2017/05/18/intermarriage-in-the-u-s-50-years-after-loving-v-virginia/. Published May 18, 2017. Accessed April 15, 2020. 
    
9. He SY, McCulloch CE, Boscardin WJ, et al. Self-reported pigmentary phenotypes and race are significant but incomplete predictors of Fitzpatrick skin phototype in an ethnically diverse population. J Am Acad Dermatol. 2014;71:731-737. 

Authors' Response 

While Ms. Cruzval-O'Reilly and Dr. Lugo-Somolinos highlight many important points on conducting meaningful research for the Hispanic community, they seem to have misunderstood the overall purpose of our commentary,¹ which was to highlight the increased skin cancer awareness that a notable and vocal member of the Hispanic community brought to our academic dermatology clinic, rather than to discuss skin types within the Hispanic community. As the authors mentioned, the term Hispanic is a descriptor of ethnicity rather than race, and Hispanic patients may have varying levels of skin pigmentation and sun sensitivity. While Dayanara Torres may have risk factors for developing melanoma, minimizing her connection with the Hispanic community because of her fair skin and light eyes would be a mistake. It not only isolates members of the Hispanic community that are of skin types I and II, but it also discounts the power of her story and language in raising awareness. We observed an increase in Hispanic patients presenting to our clinic who were concerned about skin cancer after Ms. Torres shared her diagnosis of metastatic melanoma through social media, followed by Spanish language educational videos on melanoma.  

Several studies have described disparities among Hispanic patients diagnosed with melanoma as compared to their non-Hispanic white counterparts, including younger age at diagnosis, later stage of presentation, increased presence of regional involvement, and worse mortality.^2-6 Furthermore, a small study of high school students by Ma et al⁷ showed disparities in skin cancer knowledge, perceived risk, and sun-protective behaviors among Hispanic whites and non-Hispanic whites, which remained significant (P<.05) after controlling for skin pigmentation and sun sensitivity. We agree with the authors that further analysis of skin type, race, genetics, and other risk factors may help refine the research on skin cancer disparities within the Hispanic community. We suspect that disparities may persist even when examining these factors. There have been several studies showing that knowledge-based interventions, especially when delivered in Spanish, improve understanding of skin cancer, personal risk, and self-examinations, and we support Ms. Torres' efforts in utilizing her platform to provide information about melanoma in Spanish.^8-12  

Radhika Srivastava, MD; Cindy Wassef, MD; Babar K. Rao, MD 
 
From the Department of Dermatology, Rutgers Robert Wood Johnson Medical School, Somerset, New Jersey.  

The authors report no conflict of interest. 

Correspondence: Radhika Srivastava, MD, 1 World's Fair Dr, Ste 2400, Somerset, NJ 08873 (rsrivastavamd@gmail.com). 

References

1. Srivastava R, Wassef C, Rao BK. The Dayanara effect: increasing skin cancer awareness in the Hispanic community. Cutis. 2019;103:257-258. 
    
2. Perez MI. Skin cancer in Hispanics in the United States. J Drugs Dermatol. 2019;18:s117-s120.  
    
3. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. 
    
4. Harvey VM, Oldfield CW, Chen JT, et al. Melanoma disparities among US Hispanics: use of the social ecological model to contextualize reasons for inequitable outcomes and frame a research agenda [published online August 29, 2016]. J Skin Cancer. doi:10.1155/2016/4635740 
    
5. Garnett E, Townsend J, Steele B, et al. Characteristics, rates, and trends of melanoma incidence among Hispanics in the USA. Cancer Causes Control. 2016;27:647-659. 
    
6. Rouhani P, Hu S, Kirsner RS. Melanoma in Hispanic and black Americans. Cancer Control. 2008;15:248-253. 
    
7. Ma F, Collado-Mesa F, Hu S, et al. Skin cancer awareness and sun protection behaviors in white Hispanic and white non-Hispanic high school students in Miami, Florida. Arch Dermatol. 2007;143:983-988. 
    
8. Kundu RV, Kamaria M, Ortiz S, et al. Effectiveness of a knowledge-based intervention for melanoma among those with ethnic skin. J Am Acad Dermatol. 2010;62:777-784. 
    
9. Kailas A, Botwin AL, Pritchett EN, et al. Assessing the effectiveness of knowledge-based interventions in increasing skin cancer awareness, knowledge, and protective behaviors in skin of color populations. Cutis. 2017;100:235-240. 
    
10. Roman CJ, Guan X, Barnholtz-Sloan J, et al. A trial online educational melanoma program aimed at the Hispanic population improves knowledge and behaviors. Dermatol Surg. 2016;42:672-676. 
     
11. Hernandez C, Kim H, Mauleon G, et al. A pilot program in collaboration with community centers to increase awareness and participation in skin cancer screening among Latinos in Chicago. J Cancer Educ. 2013;28:342-345. 
     
12. Chung GY, Brown G, Gibson D. Increasing melanoma screening among Hispanic/Latino Americans: a community-based educational intervention. Health Educ Behav. 2015;42:627-632.

To the Editor: 

We read with interest the commentary by Srivastava et al,¹ "The Dayanara Effect: Increasing Skin Cancer Awareness in the Hispanic Community," concerning former Miss Universe Dayanara Torres and her diagnosis of metastatic melanoma; however, we believe it misses the mark. A quick Google search shows that Ms. Torres has fair skin and blue eyes. She has lived most of her life in Puerto Rico, the Philippines, and California--places where sun exposure is high and may have contributed to her diagnosis. Factors that have been linked to an increased risk for melanoma are fair skin, red or blonde hair, blue or green eyes, intense intermittent sun exposure and sunburns, a weakened immune system, and a family history of skin cancer.² Although we do not know her complete medical history, Ms. Torres' skin phenotype and likely chronic UV exposure made her a candidate for skin cancer. Although Srivastava et al¹ acknowledged that the Hispanic community encompasses a wide variety of individuals with varying levels of skin pigmentation and sun sensitivity, they overlooked Ms. Torres' risk for skin cancer because of her ethnic background. This form of generalization may negatively affect patient care and safety. By 2060, Hispanics are projected to account for almost 30% of the US population,³ and we must acknowledge the flaws that exist in our overall methodology for assessing skin cancer risk among this population to provide patients with unbiased care.  

In the early 1970s, the United States adopted the ethnonym Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America.⁴ The goal was to implement a common identifier that enabled the US Government to study the economic and social development of these groups. Nevertheless, considerable differences exist among distinct Hispanic communities, and variations in skin pigmentation and sun sensitivity are no exception. Although Hispanic countries are an amalgam of diverse races due to colonization, some have stronger European, African, or Amerindian influences, limiting the use of ethnicity during melanoma risk assessment. Another misconception reflected in the commentary by Srivastava et al¹ is the belief that the terms white and Hispanic are mutually exclusive. A study examining melanoma rates in the Chilean population supports this claim.⁵ The genetic composition of the Chilean high socioeconomic strata is 5% Amerindian and 95% white, while the low socioeconomic strata is approximately 40% Amerindian and 60% white. Patients from the low socioeconomic strata had higher rates of acral malignant melanoma, which typically is seen in patients with skin of color. On the other hand, males from the high socioeconomic strata had higher rates of truncal melanoma, which is more common among the white population.⁵ These results suggest that while both groups are considered Hispanic, it is ancestral origin that contributes to the differential rates and types of malignant melanoma.  

When analyzing data regarding melanoma rates in Hispanics, particularly data collected in the United States, we must question if the results are representative of the entire population. One point worth emphasizing is that melanoma data in the Hispanic community often is flawed. The North American Association of Central Cancer Registries considers Europeans such as Spaniards, as well as citizens of Andorra, the Canary Islands, and the Balearic Islands as Hispanic.⁶ Additionally, the Florida Cancer Data System uses data such as country of birth, ethnicity, and surname or maiden name recorded by the hospital tumor registry to identify Hispanic patients with melanoma.⁷ In 2006, Hu et al⁷ used the Florida Cancer Data System to analyze melanoma data in Miami-Dade County in South Florida, which has the second largest Hispanic community in the United States. One limitation to such data is that ethnicity often is self-reported by patients or assigned by a health care provider. In addition, women whose maiden names are not available may be misclassified through marriage depending on whether their husbands have Spanish or non-Spanish last names.⁷ Finally, with societal norms evolving, Americans are now more accepting of interracial marriages. In 2017, the Pew Research Center reported that 17% of all newlyweds in the United States were intermarried and 42% of these marriages were between a white individual and a Hispanic individual, comprising the most prevalent form of intermarriage reported.⁸ In 2015, 27% of newlywed Hispanics were intermarried. This percentage varied depending on whether they were born in the United States or abroad. Although 15% of Hispanic immigrants married a spouse from another race, 39% of Hispanics born in the United States married a non-Hispanic (eg, white, black, Asian, or Native American who is not Hispanic).⁸ This type of marriage and subsequent offspring might lead to an increase in the white genetic pool. As a result, the risk for melanoma development may be increased or misrepresented. Remaining aware of these changes in the population is crucial, as it exemplifies why the current methodology for gathering and reporting melanoma data is unreliable. 

Labeling Ms. Torres as Hispanic due to her Puerto Rican nationality did not tell us anything about her risk for developing melanoma. To correctly assess the risk for melanoma among Hispanics, it is imperative that we re-evaluate our approach. We agree with He et al⁹ that our efforts should be dedicated to better understanding the impact of pigmentation, race, genetics, and sunburn on the risk for melanoma. Until we know more about this possible correlation, we should reconsider how we study melanoma using Hispanics as an ethnicity. We may have it all wrong.  

1. Srivastava R, Wassef C, Rao BK. The Dayanara effect: increasing skin cancer awareness in the Hispanic community. Cutis. 2019;103:257-258. 
    
2. Curiel-Lewandrowski C. Risk factors for the development of melanoma. UpToDate. https://www.uptodate.com/contents/risk-factors-for-the-development-of-melanoma. Updated February 27, 2020. Accessed April 16, 2020. 
    
3. Colby SL, Ortman JM. Projections of the size and composition of the U.S. population: 2014 to 2060. United States Census Bureau website. https://www.census.gov/library/publications/2015/demo/p25-1143.html. Published March 3, 2015. Accessed April 16, 2020. 
    
4. National Research Council (US) Panel on Hispanics in the United States; Tienda M, Mitchell F, editors. Multiple Origins, Uncertain Destinies: Hispanics and the American Future. Washington (DC): National Academies Press (US); 2006. 3, Defining Hispanicity: E Pluribus Unum or E Pluribus Plures? Available from: https://www.ncbi.nlm.nih.gov/books/NBK19811/ 
    
5. Zemelman VB, Valenzuela CY, Sazunic I, et al. Malignant melanoma in Chile: different site distribution between private and state patients. Biol Res. 2014;47:34. 
    
6. NAACCR Race and Ethnicity Work Group. NAACCR guideline for enhancing Hispanic-Latino identification: revised NAACCR Hispanic/Latino identification algorithm [NHIA v2.2.1]. NAACCR website. https://www.naaccr.org/wp-content/uploads/2016/11/NHIA_v2_2_1_09122011.pdf. Revised September 12, 2011. Accessed April 15, 2020.  
    
7. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708. 
    
8. Livingston G, Brown A. Intermarriage in the U.S. 50 years after Loving v. Virginia. Pew Research Center website. https://www.pewsocialtrends.org/2017/05/18/intermarriage-in-the-u-s-50-years-after-loving-v-virginia/. Published May 18, 2017. Accessed April 15, 2020. 
    
9. He SY, McCulloch CE, Boscardin WJ, et al. Self-reported pigmentary phenotypes and race are significant but incomplete predictors of Fitzpatrick skin phototype in an ethnically diverse population. J Am Acad Dermatol. 2014;71:731-737. 

Authors' Response 

While Ms. Cruzval-O'Reilly and Dr. Lugo-Somolinos highlight many important points on conducting meaningful research for the Hispanic community, they seem to have misunderstood the overall purpose of our commentary,¹ which was to highlight the increased skin cancer awareness that a notable and vocal member of the Hispanic community brought to our academic dermatology clinic, rather than to discuss skin types within the Hispanic community. As the authors mentioned, the term Hispanic is a descriptor of ethnicity rather than race, and Hispanic patients may have varying levels of skin pigmentation and sun sensitivity. While Dayanara Torres may have risk factors for developing melanoma, minimizing her connection with the Hispanic community because of her fair skin and light eyes would be a mistake. It not only isolates members of the Hispanic community that are of skin types I and II, but it also discounts the power of her story and language in raising awareness. We observed an increase in Hispanic patients presenting to our clinic who were concerned about skin cancer after Ms. Torres shared her diagnosis of metastatic melanoma through social media, followed by Spanish language educational videos on melanoma.  

Several studies have described disparities among Hispanic patients diagnosed with melanoma as compared to their non-Hispanic white counterparts, including younger age at diagnosis, later stage of presentation, increased presence of regional involvement, and worse mortality.^2-6 Furthermore, a small study of high school students by Ma et al⁷ showed disparities in skin cancer knowledge, perceived risk, and sun-protective behaviors among Hispanic whites and non-Hispanic whites, which remained significant (P<.05) after controlling for skin pigmentation and sun sensitivity. We agree with the authors that further analysis of skin type, race, genetics, and other risk factors may help refine the research on skin cancer disparities within the Hispanic community. We suspect that disparities may persist even when examining these factors. There have been several studies showing that knowledge-based interventions, especially when delivered in Spanish, improve understanding of skin cancer, personal risk, and self-examinations, and we support Ms. Torres' efforts in utilizing her platform to provide information about melanoma in Spanish.^8-12  

Radhika Srivastava, MD; Cindy Wassef, MD; Babar K. Rao, MD 
 
From the Department of Dermatology, Rutgers Robert Wood Johnson Medical School, Somerset, New Jersey.  

The authors report no conflict of interest. 

Correspondence: Radhika Srivastava, MD, 1 World's Fair Dr, Ste 2400, Somerset, NJ 08873 (rsrivastavamd@gmail.com). 

References

1. Srivastava R, Wassef C, Rao BK. The Dayanara effect: increasing skin cancer awareness in the Hispanic community. Cutis. 2019;103:257-258. 
    
2. Perez MI. Skin cancer in Hispanics in the United States. J Drugs Dermatol. 2019;18:s117-s120.  
    
3. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. 
    
4. Harvey VM, Oldfield CW, Chen JT, et al. Melanoma disparities among US Hispanics: use of the social ecological model to contextualize reasons for inequitable outcomes and frame a research agenda [published online August 29, 2016]. J Skin Cancer. doi:10.1155/2016/4635740 
    
5. Garnett E, Townsend J, Steele B, et al. Characteristics, rates, and trends of melanoma incidence among Hispanics in the USA. Cancer Causes Control. 2016;27:647-659. 
    
6. Rouhani P, Hu S, Kirsner RS. Melanoma in Hispanic and black Americans. Cancer Control. 2008;15:248-253. 
    
7. Ma F, Collado-Mesa F, Hu S, et al. Skin cancer awareness and sun protection behaviors in white Hispanic and white non-Hispanic high school students in Miami, Florida. Arch Dermatol. 2007;143:983-988. 
    
8. Kundu RV, Kamaria M, Ortiz S, et al. Effectiveness of a knowledge-based intervention for melanoma among those with ethnic skin. J Am Acad Dermatol. 2010;62:777-784. 
    
9. Kailas A, Botwin AL, Pritchett EN, et al. Assessing the effectiveness of knowledge-based interventions in increasing skin cancer awareness, knowledge, and protective behaviors in skin of color populations. Cutis. 2017;100:235-240. 
    
10. Roman CJ, Guan X, Barnholtz-Sloan J, et al. A trial online educational melanoma program aimed at the Hispanic population improves knowledge and behaviors. Dermatol Surg. 2016;42:672-676. 
     
11. Hernandez C, Kim H, Mauleon G, et al. A pilot program in collaboration with community centers to increase awareness and participation in skin cancer screening among Latinos in Chicago. J Cancer Educ. 2013;28:342-345. 
     
12. Chung GY, Brown G, Gibson D. Increasing melanoma screening among Hispanic/Latino Americans: a community-based educational intervention. Health Educ Behav. 2015;42:627-632.

To the Editor: 

We read with interest the commentary by Srivastava et al,¹ "The Dayanara Effect: Increasing Skin Cancer Awareness in the Hispanic Community," concerning former Miss Universe Dayanara Torres and her diagnosis of metastatic melanoma; however, we believe it misses the mark. A quick Google search shows that Ms. Torres has fair skin and blue eyes. She has lived most of her life in Puerto Rico, the Philippines, and California--places where sun exposure is high and may have contributed to her diagnosis. Factors that have been linked to an increased risk for melanoma are fair skin, red or blonde hair, blue or green eyes, intense intermittent sun exposure and sunburns, a weakened immune system, and a family history of skin cancer.² Although we do not know her complete medical history, Ms. Torres' skin phenotype and likely chronic UV exposure made her a candidate for skin cancer. Although Srivastava et al¹ acknowledged that the Hispanic community encompasses a wide variety of individuals with varying levels of skin pigmentation and sun sensitivity, they overlooked Ms. Torres' risk for skin cancer because of her ethnic background. This form of generalization may negatively affect patient care and safety. By 2060, Hispanics are projected to account for almost 30% of the US population,³ and we must acknowledge the flaws that exist in our overall methodology for assessing skin cancer risk among this population to provide patients with unbiased care.  

In the early 1970s, the United States adopted the ethnonym Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America.⁴ The goal was to implement a common identifier that enabled the US Government to study the economic and social development of these groups. Nevertheless, considerable differences exist among distinct Hispanic communities, and variations in skin pigmentation and sun sensitivity are no exception. Although Hispanic countries are an amalgam of diverse races due to colonization, some have stronger European, African, or Amerindian influences, limiting the use of ethnicity during melanoma risk assessment. Another misconception reflected in the commentary by Srivastava et al¹ is the belief that the terms white and Hispanic are mutually exclusive. A study examining melanoma rates in the Chilean population supports this claim.⁵ The genetic composition of the Chilean high socioeconomic strata is 5% Amerindian and 95% white, while the low socioeconomic strata is approximately 40% Amerindian and 60% white. Patients from the low socioeconomic strata had higher rates of acral malignant melanoma, which typically is seen in patients with skin of color. On the other hand, males from the high socioeconomic strata had higher rates of truncal melanoma, which is more common among the white population.⁵ These results suggest that while both groups are considered Hispanic, it is ancestral origin that contributes to the differential rates and types of malignant melanoma.  

When analyzing data regarding melanoma rates in Hispanics, particularly data collected in the United States, we must question if the results are representative of the entire population. One point worth emphasizing is that melanoma data in the Hispanic community often is flawed. The North American Association of Central Cancer Registries considers Europeans such as Spaniards, as well as citizens of Andorra, the Canary Islands, and the Balearic Islands as Hispanic.⁶ Additionally, the Florida Cancer Data System uses data such as country of birth, ethnicity, and surname or maiden name recorded by the hospital tumor registry to identify Hispanic patients with melanoma.⁷ In 2006, Hu et al⁷ used the Florida Cancer Data System to analyze melanoma data in Miami-Dade County in South Florida, which has the second largest Hispanic community in the United States. One limitation to such data is that ethnicity often is self-reported by patients or assigned by a health care provider. In addition, women whose maiden names are not available may be misclassified through marriage depending on whether their husbands have Spanish or non-Spanish last names.⁷ Finally, with societal norms evolving, Americans are now more accepting of interracial marriages. In 2017, the Pew Research Center reported that 17% of all newlyweds in the United States were intermarried and 42% of these marriages were between a white individual and a Hispanic individual, comprising the most prevalent form of intermarriage reported.⁸ In 2015, 27% of newlywed Hispanics were intermarried. This percentage varied depending on whether they were born in the United States or abroad. Although 15% of Hispanic immigrants married a spouse from another race, 39% of Hispanics born in the United States married a non-Hispanic (eg, white, black, Asian, or Native American who is not Hispanic).⁸ This type of marriage and subsequent offspring might lead to an increase in the white genetic pool. As a result, the risk for melanoma development may be increased or misrepresented. Remaining aware of these changes in the population is crucial, as it exemplifies why the current methodology for gathering and reporting melanoma data is unreliable. 

Labeling Ms. Torres as Hispanic due to her Puerto Rican nationality did not tell us anything about her risk for developing melanoma. To correctly assess the risk for melanoma among Hispanics, it is imperative that we re-evaluate our approach. We agree with He et al⁹ that our efforts should be dedicated to better understanding the impact of pigmentation, race, genetics, and sunburn on the risk for melanoma. Until we know more about this possible correlation, we should reconsider how we study melanoma using Hispanics as an ethnicity. We may have it all wrong.  

1. Srivastava R, Wassef C, Rao BK. The Dayanara effect: increasing skin cancer awareness in the Hispanic community. Cutis. 2019;103:257-258. 
    
2. Curiel-Lewandrowski C. Risk factors for the development of melanoma. UpToDate. https://www.uptodate.com/contents/risk-factors-for-the-development-of-melanoma. Updated February 27, 2020. Accessed April 16, 2020. 
    
3. Colby SL, Ortman JM. Projections of the size and composition of the U.S. population: 2014 to 2060. United States Census Bureau website. https://www.census.gov/library/publications/2015/demo/p25-1143.html. Published March 3, 2015. Accessed April 16, 2020. 
    
4. National Research Council (US) Panel on Hispanics in the United States; Tienda M, Mitchell F, editors. Multiple Origins, Uncertain Destinies: Hispanics and the American Future. Washington (DC): National Academies Press (US); 2006. 3, Defining Hispanicity: E Pluribus Unum or E Pluribus Plures? Available from: https://www.ncbi.nlm.nih.gov/books/NBK19811/ 
    
5. Zemelman VB, Valenzuela CY, Sazunic I, et al. Malignant melanoma in Chile: different site distribution between private and state patients. Biol Res. 2014;47:34. 
    
6. NAACCR Race and Ethnicity Work Group. NAACCR guideline for enhancing Hispanic-Latino identification: revised NAACCR Hispanic/Latino identification algorithm [NHIA v2.2.1]. NAACCR website. https://www.naaccr.org/wp-content/uploads/2016/11/NHIA_v2_2_1_09122011.pdf. Revised September 12, 2011. Accessed April 15, 2020.  
    
7. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708. 
    
8. Livingston G, Brown A. Intermarriage in the U.S. 50 years after Loving v. Virginia. Pew Research Center website. https://www.pewsocialtrends.org/2017/05/18/intermarriage-in-the-u-s-50-years-after-loving-v-virginia/. Published May 18, 2017. Accessed April 15, 2020. 
    
9. He SY, McCulloch CE, Boscardin WJ, et al. Self-reported pigmentary phenotypes and race are significant but incomplete predictors of Fitzpatrick skin phototype in an ethnically diverse population. J Am Acad Dermatol. 2014;71:731-737. 

Authors' Response 

While Ms. Cruzval-O'Reilly and Dr. Lugo-Somolinos highlight many important points on conducting meaningful research for the Hispanic community, they seem to have misunderstood the overall purpose of our commentary,¹ which was to highlight the increased skin cancer awareness that a notable and vocal member of the Hispanic community brought to our academic dermatology clinic, rather than to discuss skin types within the Hispanic community. As the authors mentioned, the term Hispanic is a descriptor of ethnicity rather than race, and Hispanic patients may have varying levels of skin pigmentation and sun sensitivity. While Dayanara Torres may have risk factors for developing melanoma, minimizing her connection with the Hispanic community because of her fair skin and light eyes would be a mistake. It not only isolates members of the Hispanic community that are of skin types I and II, but it also discounts the power of her story and language in raising awareness. We observed an increase in Hispanic patients presenting to our clinic who were concerned about skin cancer after Ms. Torres shared her diagnosis of metastatic melanoma through social media, followed by Spanish language educational videos on melanoma.  

Several studies have described disparities among Hispanic patients diagnosed with melanoma as compared to their non-Hispanic white counterparts, including younger age at diagnosis, later stage of presentation, increased presence of regional involvement, and worse mortality.^2-6 Furthermore, a small study of high school students by Ma et al⁷ showed disparities in skin cancer knowledge, perceived risk, and sun-protective behaviors among Hispanic whites and non-Hispanic whites, which remained significant (P<.05) after controlling for skin pigmentation and sun sensitivity. We agree with the authors that further analysis of skin type, race, genetics, and other risk factors may help refine the research on skin cancer disparities within the Hispanic community. We suspect that disparities may persist even when examining these factors. There have been several studies showing that knowledge-based interventions, especially when delivered in Spanish, improve understanding of skin cancer, personal risk, and self-examinations, and we support Ms. Torres' efforts in utilizing her platform to provide information about melanoma in Spanish.^8-12  

Radhika Srivastava, MD; Cindy Wassef, MD; Babar K. Rao, MD 
 
From the Department of Dermatology, Rutgers Robert Wood Johnson Medical School, Somerset, New Jersey.  

The authors report no conflict of interest. 

Correspondence: Radhika Srivastava, MD, 1 World's Fair Dr, Ste 2400, Somerset, NJ 08873 (rsrivastavamd@gmail.com). 

References

1. Srivastava R, Wassef C, Rao BK. The Dayanara effect: increasing skin cancer awareness in the Hispanic community. Cutis. 2019;103:257-258. 
    
2. Perez MI. Skin cancer in Hispanics in the United States. J Drugs Dermatol. 2019;18:s117-s120.  
    
3. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. 
    
4. Harvey VM, Oldfield CW, Chen JT, et al. Melanoma disparities among US Hispanics: use of the social ecological model to contextualize reasons for inequitable outcomes and frame a research agenda [published online August 29, 2016]. J Skin Cancer. doi:10.1155/2016/4635740 
    
5. Garnett E, Townsend J, Steele B, et al. Characteristics, rates, and trends of melanoma incidence among Hispanics in the USA. Cancer Causes Control. 2016;27:647-659. 
    
6. Rouhani P, Hu S, Kirsner RS. Melanoma in Hispanic and black Americans. Cancer Control. 2008;15:248-253. 
    
7. Ma F, Collado-Mesa F, Hu S, et al. Skin cancer awareness and sun protection behaviors in white Hispanic and white non-Hispanic high school students in Miami, Florida. Arch Dermatol. 2007;143:983-988. 
    
8. Kundu RV, Kamaria M, Ortiz S, et al. Effectiveness of a knowledge-based intervention for melanoma among those with ethnic skin. J Am Acad Dermatol. 2010;62:777-784. 
    
9. Kailas A, Botwin AL, Pritchett EN, et al. Assessing the effectiveness of knowledge-based interventions in increasing skin cancer awareness, knowledge, and protective behaviors in skin of color populations. Cutis. 2017;100:235-240. 
    
10. Roman CJ, Guan X, Barnholtz-Sloan J, et al. A trial online educational melanoma program aimed at the Hispanic population improves knowledge and behaviors. Dermatol Surg. 2016;42:672-676. 
     
11. Hernandez C, Kim H, Mauleon G, et al. A pilot program in collaboration with community centers to increase awareness and participation in skin cancer screening among Latinos in Chicago. J Cancer Educ. 2013;28:342-345. 
     
12. Chung GY, Brown G, Gibson D. Increasing melanoma screening among Hispanic/Latino Americans: a community-based educational intervention. Health Educ Behav. 2015;42:627-632.

The way James R. Treat, MD, sees it, if there ever were a truism in the field of dermatology, it’s that everyone hates molluscum contagiosum.

“It tortures all of us,” Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “It’s very distressing to parents, but often more distressing to parents than to kids.”

A viral disorder of the skin and mucous membranes characterized by discrete single or multiple, flesh-colored papules, molluscum contagiosum (MC) lesions often appear on the face, neck, armpits, arms, and tops of the hands in children. The abdomen and inner thighs can also be affected. “When you look at inflamed molluscum it can be very difficult to recognize because it looks like a more complicated infection,” said Dr. Treat, who is also associate professor of clinical pediatrics and dermatology, at the University of Pennsylvania, Philadelphia.

An epidemiologic review of 302 MC cases found that 80% of patients were aged younger than 8 years, 63% had more than 15 lesions, and 24% had concomitant atopic dermatitis (J Am Acad Dermatol. 2006; 2006;54[1]:47-54). “Children with atopic dermatitis often have their molluscum last longer,” he said. “The average time course for molluscum is 18 months, but it can certainly be longer than that. So if you say, ‘it’s probably going to go away in a few months,’ that’s probably not going to happen.”

The telltale MC lesion is glossy and contains a white core in the center that can be revealed by shining an otoscope sideways on the lesion. “Umbilication doesn’t always occur, but if the center part looks white, that will help with diagnosis,” Dr. Treat said. “If they’re inflamed and they’re red and you’re worried that there’s a bacterial infection, do a culture, pop the lesion open, and get some of the pus out. If you’re concerned, start them on antibiotics. It’s always worse to miss an infection than to overtreat molluscum. But once you’ve done it a few times and you realize that the cultures are coming back negative, then you’ll probably have your threshold a little higher.”

The most useful clinical sign of MC is the so-called “BOTE” (beginning of the end) sign, which is characterized by erythema and swelling of MC skin lesions. “When the parents come to us in pediatric dermatology, often it’s because their kids have had molluscum for a while,” he said. “It spreads and becomes inflamed and the parents ask, ‘Is it infected?’ The answer is, yes, it’s an infection, but it’s not infected with what you think it is [which is Staphylococcus or Streptococcus], it’s the virus being recognized by the body. When the virus is recognized by the body, it creates a huge inflammatory reaction. That’s usually the time at which the body has had enough of the virus, and it eradicates the rest of it. It means the inflammatory response is finding the molluscum and it’s going to take care of it.”

MC brings its own eczematous response, which can complicate efforts to confirm the diagnosis. Dr. Treat spoke of a young patient he recently saw who had an eczematous reaction on the inner parts of the arms and the upper flank – with no such clinical history. “It kind of came out of the blue,” he said. “You think about contact allergies and other types of dermatitis, but molluscum brings its own eczema. Often what the parents recognize is the eczematous eruption and not the little dots of molluscum. So if you see someone with a new eruption in typical molluscum areas – the flank and your thighs and the back of the legs – and they’ve never had eczema in the past, or they’ve only had mild eczema, think about eczema as a response to molluscum.”

MC can also result in a Gianotti-Crosti syndrome-like reactions (Arch Dermatol. 2012;148[11]:1257-64). “These are angry, inflamed red papules on the knees and on the elbows and on the buttocks and on the cheeks,” Dr. Treat said. “It typically spares the trunk, and they look like molluscum.”

He went on to note that MC can present as cysts, and that MC in the gluteal cleft is a mimicker of condyloma. MC can also cause conjunctivitis, which is increased in HIV patients and in those with atopic dermatitis. “These are patients who should probably see an ophthalmologist” to make no damage has occurred, Dr. Treat said.

He closed his remarks by noting that rarely, MC can be the presenting sign of an immunodeficiency. “The immune system dysregulation that shows up this way is called a DOCK8 mutation, which have eczema and widespread viral disease including warts and molluscum,” Dr. Treat said.

He reported having no financial disclosures.

dbrunk@mdedge.com

The way James R. Treat, MD, sees it, if there ever were a truism in the field of dermatology, it’s that everyone hates molluscum contagiosum.

“It tortures all of us,” Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “It’s very distressing to parents, but often more distressing to parents than to kids.”

A viral disorder of the skin and mucous membranes characterized by discrete single or multiple, flesh-colored papules, molluscum contagiosum (MC) lesions often appear on the face, neck, armpits, arms, and tops of the hands in children. The abdomen and inner thighs can also be affected. “When you look at inflamed molluscum it can be very difficult to recognize because it looks like a more complicated infection,” said Dr. Treat, who is also associate professor of clinical pediatrics and dermatology, at the University of Pennsylvania, Philadelphia.

An epidemiologic review of 302 MC cases found that 80% of patients were aged younger than 8 years, 63% had more than 15 lesions, and 24% had concomitant atopic dermatitis (J Am Acad Dermatol. 2006; 2006;54[1]:47-54). “Children with atopic dermatitis often have their molluscum last longer,” he said. “The average time course for molluscum is 18 months, but it can certainly be longer than that. So if you say, ‘it’s probably going to go away in a few months,’ that’s probably not going to happen.”

The telltale MC lesion is glossy and contains a white core in the center that can be revealed by shining an otoscope sideways on the lesion. “Umbilication doesn’t always occur, but if the center part looks white, that will help with diagnosis,” Dr. Treat said. “If they’re inflamed and they’re red and you’re worried that there’s a bacterial infection, do a culture, pop the lesion open, and get some of the pus out. If you’re concerned, start them on antibiotics. It’s always worse to miss an infection than to overtreat molluscum. But once you’ve done it a few times and you realize that the cultures are coming back negative, then you’ll probably have your threshold a little higher.”

The most useful clinical sign of MC is the so-called “BOTE” (beginning of the end) sign, which is characterized by erythema and swelling of MC skin lesions. “When the parents come to us in pediatric dermatology, often it’s because their kids have had molluscum for a while,” he said. “It spreads and becomes inflamed and the parents ask, ‘Is it infected?’ The answer is, yes, it’s an infection, but it’s not infected with what you think it is [which is Staphylococcus or Streptococcus], it’s the virus being recognized by the body. When the virus is recognized by the body, it creates a huge inflammatory reaction. That’s usually the time at which the body has had enough of the virus, and it eradicates the rest of it. It means the inflammatory response is finding the molluscum and it’s going to take care of it.”

MC brings its own eczematous response, which can complicate efforts to confirm the diagnosis. Dr. Treat spoke of a young patient he recently saw who had an eczematous reaction on the inner parts of the arms and the upper flank – with no such clinical history. “It kind of came out of the blue,” he said. “You think about contact allergies and other types of dermatitis, but molluscum brings its own eczema. Often what the parents recognize is the eczematous eruption and not the little dots of molluscum. So if you see someone with a new eruption in typical molluscum areas – the flank and your thighs and the back of the legs – and they’ve never had eczema in the past, or they’ve only had mild eczema, think about eczema as a response to molluscum.”

MC can also result in a Gianotti-Crosti syndrome-like reactions (Arch Dermatol. 2012;148[11]:1257-64). “These are angry, inflamed red papules on the knees and on the elbows and on the buttocks and on the cheeks,” Dr. Treat said. “It typically spares the trunk, and they look like molluscum.”

He went on to note that MC can present as cysts, and that MC in the gluteal cleft is a mimicker of condyloma. MC can also cause conjunctivitis, which is increased in HIV patients and in those with atopic dermatitis. “These are patients who should probably see an ophthalmologist” to make no damage has occurred, Dr. Treat said.

He closed his remarks by noting that rarely, MC can be the presenting sign of an immunodeficiency. “The immune system dysregulation that shows up this way is called a DOCK8 mutation, which have eczema and widespread viral disease including warts and molluscum,” Dr. Treat said.

He reported having no financial disclosures.

dbrunk@mdedge.com

The way James R. Treat, MD, sees it, if there ever were a truism in the field of dermatology, it’s that everyone hates molluscum contagiosum.

“It tortures all of us,” Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia, said during the virtual Pediatric Dermatology 2020: Best Practices and Innovations Conference. “It’s very distressing to parents, but often more distressing to parents than to kids.”

A viral disorder of the skin and mucous membranes characterized by discrete single or multiple, flesh-colored papules, molluscum contagiosum (MC) lesions often appear on the face, neck, armpits, arms, and tops of the hands in children. The abdomen and inner thighs can also be affected. “When you look at inflamed molluscum it can be very difficult to recognize because it looks like a more complicated infection,” said Dr. Treat, who is also associate professor of clinical pediatrics and dermatology, at the University of Pennsylvania, Philadelphia.

An epidemiologic review of 302 MC cases found that 80% of patients were aged younger than 8 years, 63% had more than 15 lesions, and 24% had concomitant atopic dermatitis (J Am Acad Dermatol. 2006; 2006;54[1]:47-54). “Children with atopic dermatitis often have their molluscum last longer,” he said. “The average time course for molluscum is 18 months, but it can certainly be longer than that. So if you say, ‘it’s probably going to go away in a few months,’ that’s probably not going to happen.”

The telltale MC lesion is glossy and contains a white core in the center that can be revealed by shining an otoscope sideways on the lesion. “Umbilication doesn’t always occur, but if the center part looks white, that will help with diagnosis,” Dr. Treat said. “If they’re inflamed and they’re red and you’re worried that there’s a bacterial infection, do a culture, pop the lesion open, and get some of the pus out. If you’re concerned, start them on antibiotics. It’s always worse to miss an infection than to overtreat molluscum. But once you’ve done it a few times and you realize that the cultures are coming back negative, then you’ll probably have your threshold a little higher.”

The most useful clinical sign of MC is the so-called “BOTE” (beginning of the end) sign, which is characterized by erythema and swelling of MC skin lesions. “When the parents come to us in pediatric dermatology, often it’s because their kids have had molluscum for a while,” he said. “It spreads and becomes inflamed and the parents ask, ‘Is it infected?’ The answer is, yes, it’s an infection, but it’s not infected with what you think it is [which is Staphylococcus or Streptococcus], it’s the virus being recognized by the body. When the virus is recognized by the body, it creates a huge inflammatory reaction. That’s usually the time at which the body has had enough of the virus, and it eradicates the rest of it. It means the inflammatory response is finding the molluscum and it’s going to take care of it.”

MC brings its own eczematous response, which can complicate efforts to confirm the diagnosis. Dr. Treat spoke of a young patient he recently saw who had an eczematous reaction on the inner parts of the arms and the upper flank – with no such clinical history. “It kind of came out of the blue,” he said. “You think about contact allergies and other types of dermatitis, but molluscum brings its own eczema. Often what the parents recognize is the eczematous eruption and not the little dots of molluscum. So if you see someone with a new eruption in typical molluscum areas – the flank and your thighs and the back of the legs – and they’ve never had eczema in the past, or they’ve only had mild eczema, think about eczema as a response to molluscum.”

MC can also result in a Gianotti-Crosti syndrome-like reactions (Arch Dermatol. 2012;148[11]:1257-64). “These are angry, inflamed red papules on the knees and on the elbows and on the buttocks and on the cheeks,” Dr. Treat said. “It typically spares the trunk, and they look like molluscum.”

He went on to note that MC can present as cysts, and that MC in the gluteal cleft is a mimicker of condyloma. MC can also cause conjunctivitis, which is increased in HIV patients and in those with atopic dermatitis. “These are patients who should probably see an ophthalmologist” to make no damage has occurred, Dr. Treat said.

He closed his remarks by noting that rarely, MC can be the presenting sign of an immunodeficiency. “The immune system dysregulation that shows up this way is called a DOCK8 mutation, which have eczema and widespread viral disease including warts and molluscum,” Dr. Treat said.

He reported having no financial disclosures.

dbrunk@mdedge.com

This Acne and Rosacea supplement to Dermatology News includes commentary from Dr Hilary E. Baldwin

Topics Included:

Pathogenic Pathway As Target In Rosacea Treatment / 5
Acne In Skin Of Color / 6
Under FDA Review Of Novel Acne Treatment / 7
Chemical Peels For Acne / 8
Isotretinoin And Psychiatric Conditions / 10
Pregnancy Reports For Isotretinoin / 11
Rosacea Triggers / 12
Topical Treatment Of Demodex / 13
Social Media And Acne / 14

Read Here

This Acne and Rosacea supplement to Dermatology News includes commentary from Dr Hilary E. Baldwin

Topics Included:

Pathogenic Pathway As Target In Rosacea Treatment / 5
Acne In Skin Of Color / 6
Under FDA Review Of Novel Acne Treatment / 7
Chemical Peels For Acne / 8
Isotretinoin And Psychiatric Conditions / 10
Pregnancy Reports For Isotretinoin / 11
Rosacea Triggers / 12
Topical Treatment Of Demodex / 13
Social Media And Acne / 14

Read Here

This Acne and Rosacea supplement to Dermatology News includes commentary from Dr Hilary E. Baldwin

Topics Included:

Pathogenic Pathway As Target In Rosacea Treatment / 5
Acne In Skin Of Color / 6
Under FDA Review Of Novel Acne Treatment / 7
Chemical Peels For Acne / 8
Isotretinoin And Psychiatric Conditions / 10
Pregnancy Reports For Isotretinoin / 11
Rosacea Triggers / 12
Topical Treatment Of Demodex / 13
Social Media And Acne / 14

Read Here

There are several mechanisms by which the aging microenvironment can drive cancer and influence response to therapy, according to a plenary presentation at the AACR virtual meeting II.

Ashani T. Weeraratna, PhD, highlighted research showing how the aging microenvironment affects tumor cell metabolism, angiogenesis, and treatment resistance in melanoma.

Dr. Weeraratna, of Johns Hopkins Bloomberg School of Public Health in Baltimore, first described a study showing how fibroblasts in the aged microenvironment contribute to tumor progression in models of melanoma (Nature. 2016 Apr 14;532[7598]:250-4).

Dr. Weeraratna and colleagues isolated dermal fibroblasts from young human donors (aged 25-35 years) and older donors (55-65 years) and used these cells to produce artificial skin.

Melanoma cells placed in the artificial skin created with young fibroblasts remained “very tightly nested at the surface,” Dr. Weeraratna said. On the other hand, melanoma cells migrated “very rapidly” through the artificial dermis created from aged fibroblasts.

In mouse models of melanoma, tumors grew much faster in young mice (6-8 weeks) than in old mice (12-18 months). However, tumors metastasized to the lung at a “much greater rate in the aged mice than in the young mice,” Dr. Weeraratna said.
 

Angiogenesis, SFRP2, and VEGF

Dr. Weeraratna went on to explain how a member of her lab conducted proteomic analyses of young and aged lung fibroblasts. The results were compared with results from prior analyses of young and aged skin fibroblasts.

The results showed that aged skin fibroblasts promote noncanonical WNT signaling via expression of SFRP2, SERPINE2, DKK1, Wnt5A, and ROR2. On the other hand, aged lung fibroblasts promote canonical WNT signaling via some of the same family members, including SFRP1, DKK3, and ROR1.

Research by another group showed that SFRP2 stimulates angiogenesis via a calcineurin/NFAT signaling pathway (Cancer Res. 2009 Jun 1;69[11]:4621-8).

Research in Dr. Weeraratna’s lab showed that SFRP2 and VEGF are inversely correlated with aging. Tumors in aged mice had an abundance of SFRP2 but little VEGF. Tumors in young mice had an abundance of VEGF but little SFRP2.

Dr. Weeraratna’s team wanted to determine if results would be similar in melanoma patients, so the researchers analyzed data from the TCGA database. They found that VEGF and two of its key receptors are decreased in older melanoma patients, in comparison with younger melanoma patients.

The clinical relevancy of this finding is reflected in an analysis of data from the AVAST-M study (Ann Oncol. 2019;30[12]:2013-4). When compared with observation, bevacizumab did not improve survival overall or for older patients, but the EGFR inhibitor was associated with longer survival in patients younger than 45 years.

Dr. Weeraratna said this finding and her group’s prior findings suggest younger melanoma patients have more VEGF but less angiogenesis than older patients. The older patients have less VEGF and more SFRP2, which drives angiogenesis.

Dr. Weeraratna’s lab then conducted experiments in young mice, which suggested that an anti-VEGF antibody can reduce angiogenesis, but not in the presence of SFRP2.

Lipid metabolism and treatment resistance

A recently published study by Dr. Weeraratna and colleagues tied changes in aged fibroblast lipid metabolism to treatment resistance in melanoma (Cancer Discov. 2020 Jun 4;CD-20-0329).

The research showed that melanoma cells accumulate lipids when incubated with aged, rather than young, fibroblasts in vitro.

Lipid uptake is mediated by fatty acid transporters (FATPs), and the researchers found that most FATPs were unchanged by age. However, FATP2 was elevated in melanoma cells exposed to aged media, aged mice, and melanoma patients older than 50 years of age.

When melanoma cells were incubated with conditioned media from aged fibroblasts and a FATP2 inhibitor, they no longer took up lipids.

When FATP2 was knocked down in aged mice with melanoma, BRAF and MEK inhibitors (which are not very effective ordinarily) caused dramatic and prolonged tumor regression. These effects were not seen with FATP2 inhibition in young mice.

These results suggest FATP2 is a key transporter of lipids in the aged microenvironment, and inhibiting FATP2 can delay the onset of treatment resistance.

Striving to understand a complex system

For many years, the dogma was that cancer cells behaved like unwelcome invaders, co-opting the metabolic machinery of the sites of spread, with crowding of the normal structures within those organs.

To say that concept was primitive is an understatement. Clearly, the relationship between tumor cells and the surrounding stroma is complex. Changes that occur in an aging microenvironment can influence cancer outcomes in older adults.

Dr. Weeraratna’s presentation adds further impetus to efforts to broaden eligibility criteria for clinical trials so the median age and the metabolic milieu of trial participants more closely parallels the general population.

She highlighted the importance of data analysis by age cohorts and the need to design preclinical studies so that investigators can study the microenvironment of cancer cells in in vitro models and in young and older laboratory animals.

As management expert W. Edwards Deming is believed to have said, “Every system is perfectly designed to get the results it gets.” Cancer is likely not an independent, hostile invader, overtaking the failing machinery of aging cells. To understand the intersection of cancer and aging, we need a more perfect understanding of the system in which tumors develop and are treated.

Dr. Weeraratna reported having no disclosures.


Dr. Lyss was a community-based medical oncologist and clinical researcher for more than 35 years before his recent retirement. His clinical and research interests were focused on breast and lung cancers as well as expanding clinical trial access to medically underserved populations. He is based in St. Louis. He has no conflicts of interest.
 

SOURCE: Weeraratna A. AACR 2020. Age against the machine: How the aging microenvironment governs response to therapy.

There are several mechanisms by which the aging microenvironment can drive cancer and influence response to therapy, according to a plenary presentation at the AACR virtual meeting II.

Ashani T. Weeraratna, PhD, highlighted research showing how the aging microenvironment affects tumor cell metabolism, angiogenesis, and treatment resistance in melanoma.

Dr. Weeraratna, of Johns Hopkins Bloomberg School of Public Health in Baltimore, first described a study showing how fibroblasts in the aged microenvironment contribute to tumor progression in models of melanoma (Nature. 2016 Apr 14;532[7598]:250-4).

Dr. Weeraratna and colleagues isolated dermal fibroblasts from young human donors (aged 25-35 years) and older donors (55-65 years) and used these cells to produce artificial skin.

Melanoma cells placed in the artificial skin created with young fibroblasts remained “very tightly nested at the surface,” Dr. Weeraratna said. On the other hand, melanoma cells migrated “very rapidly” through the artificial dermis created from aged fibroblasts.

In mouse models of melanoma, tumors grew much faster in young mice (6-8 weeks) than in old mice (12-18 months). However, tumors metastasized to the lung at a “much greater rate in the aged mice than in the young mice,” Dr. Weeraratna said.
 

Angiogenesis, SFRP2, and VEGF

Dr. Weeraratna went on to explain how a member of her lab conducted proteomic analyses of young and aged lung fibroblasts. The results were compared with results from prior analyses of young and aged skin fibroblasts.

The results showed that aged skin fibroblasts promote noncanonical WNT signaling via expression of SFRP2, SERPINE2, DKK1, Wnt5A, and ROR2. On the other hand, aged lung fibroblasts promote canonical WNT signaling via some of the same family members, including SFRP1, DKK3, and ROR1.

Research by another group showed that SFRP2 stimulates angiogenesis via a calcineurin/NFAT signaling pathway (Cancer Res. 2009 Jun 1;69[11]:4621-8).

Research in Dr. Weeraratna’s lab showed that SFRP2 and VEGF are inversely correlated with aging. Tumors in aged mice had an abundance of SFRP2 but little VEGF. Tumors in young mice had an abundance of VEGF but little SFRP2.

Dr. Weeraratna’s team wanted to determine if results would be similar in melanoma patients, so the researchers analyzed data from the TCGA database. They found that VEGF and two of its key receptors are decreased in older melanoma patients, in comparison with younger melanoma patients.

The clinical relevancy of this finding is reflected in an analysis of data from the AVAST-M study (Ann Oncol. 2019;30[12]:2013-4). When compared with observation, bevacizumab did not improve survival overall or for older patients, but the EGFR inhibitor was associated with longer survival in patients younger than 45 years.

Dr. Weeraratna said this finding and her group’s prior findings suggest younger melanoma patients have more VEGF but less angiogenesis than older patients. The older patients have less VEGF and more SFRP2, which drives angiogenesis.

Dr. Weeraratna’s lab then conducted experiments in young mice, which suggested that an anti-VEGF antibody can reduce angiogenesis, but not in the presence of SFRP2.

Lipid metabolism and treatment resistance

A recently published study by Dr. Weeraratna and colleagues tied changes in aged fibroblast lipid metabolism to treatment resistance in melanoma (Cancer Discov. 2020 Jun 4;CD-20-0329).

The research showed that melanoma cells accumulate lipids when incubated with aged, rather than young, fibroblasts in vitro.

Lipid uptake is mediated by fatty acid transporters (FATPs), and the researchers found that most FATPs were unchanged by age. However, FATP2 was elevated in melanoma cells exposed to aged media, aged mice, and melanoma patients older than 50 years of age.

When melanoma cells were incubated with conditioned media from aged fibroblasts and a FATP2 inhibitor, they no longer took up lipids.

When FATP2 was knocked down in aged mice with melanoma, BRAF and MEK inhibitors (which are not very effective ordinarily) caused dramatic and prolonged tumor regression. These effects were not seen with FATP2 inhibition in young mice.

These results suggest FATP2 is a key transporter of lipids in the aged microenvironment, and inhibiting FATP2 can delay the onset of treatment resistance.

Striving to understand a complex system

For many years, the dogma was that cancer cells behaved like unwelcome invaders, co-opting the metabolic machinery of the sites of spread, with crowding of the normal structures within those organs.

To say that concept was primitive is an understatement. Clearly, the relationship between tumor cells and the surrounding stroma is complex. Changes that occur in an aging microenvironment can influence cancer outcomes in older adults.

Dr. Weeraratna’s presentation adds further impetus to efforts to broaden eligibility criteria for clinical trials so the median age and the metabolic milieu of trial participants more closely parallels the general population.

She highlighted the importance of data analysis by age cohorts and the need to design preclinical studies so that investigators can study the microenvironment of cancer cells in in vitro models and in young and older laboratory animals.

As management expert W. Edwards Deming is believed to have said, “Every system is perfectly designed to get the results it gets.” Cancer is likely not an independent, hostile invader, overtaking the failing machinery of aging cells. To understand the intersection of cancer and aging, we need a more perfect understanding of the system in which tumors develop and are treated.

Dr. Weeraratna reported having no disclosures.


Dr. Lyss was a community-based medical oncologist and clinical researcher for more than 35 years before his recent retirement. His clinical and research interests were focused on breast and lung cancers as well as expanding clinical trial access to medically underserved populations. He is based in St. Louis. He has no conflicts of interest.
 

SOURCE: Weeraratna A. AACR 2020. Age against the machine: How the aging microenvironment governs response to therapy.

There are several mechanisms by which the aging microenvironment can drive cancer and influence response to therapy, according to a plenary presentation at the AACR virtual meeting II.

Ashani T. Weeraratna, PhD, highlighted research showing how the aging microenvironment affects tumor cell metabolism, angiogenesis, and treatment resistance in melanoma.

Dr. Weeraratna, of Johns Hopkins Bloomberg School of Public Health in Baltimore, first described a study showing how fibroblasts in the aged microenvironment contribute to tumor progression in models of melanoma (Nature. 2016 Apr 14;532[7598]:250-4).

Dr. Weeraratna and colleagues isolated dermal fibroblasts from young human donors (aged 25-35 years) and older donors (55-65 years) and used these cells to produce artificial skin.

Melanoma cells placed in the artificial skin created with young fibroblasts remained “very tightly nested at the surface,” Dr. Weeraratna said. On the other hand, melanoma cells migrated “very rapidly” through the artificial dermis created from aged fibroblasts.

In mouse models of melanoma, tumors grew much faster in young mice (6-8 weeks) than in old mice (12-18 months). However, tumors metastasized to the lung at a “much greater rate in the aged mice than in the young mice,” Dr. Weeraratna said.
 

Angiogenesis, SFRP2, and VEGF

Dr. Weeraratna went on to explain how a member of her lab conducted proteomic analyses of young and aged lung fibroblasts. The results were compared with results from prior analyses of young and aged skin fibroblasts.

The results showed that aged skin fibroblasts promote noncanonical WNT signaling via expression of SFRP2, SERPINE2, DKK1, Wnt5A, and ROR2. On the other hand, aged lung fibroblasts promote canonical WNT signaling via some of the same family members, including SFRP1, DKK3, and ROR1.

Research by another group showed that SFRP2 stimulates angiogenesis via a calcineurin/NFAT signaling pathway (Cancer Res. 2009 Jun 1;69[11]:4621-8).

Research in Dr. Weeraratna’s lab showed that SFRP2 and VEGF are inversely correlated with aging. Tumors in aged mice had an abundance of SFRP2 but little VEGF. Tumors in young mice had an abundance of VEGF but little SFRP2.

Dr. Weeraratna’s team wanted to determine if results would be similar in melanoma patients, so the researchers analyzed data from the TCGA database. They found that VEGF and two of its key receptors are decreased in older melanoma patients, in comparison with younger melanoma patients.

The clinical relevancy of this finding is reflected in an analysis of data from the AVAST-M study (Ann Oncol. 2019;30[12]:2013-4). When compared with observation, bevacizumab did not improve survival overall or for older patients, but the EGFR inhibitor was associated with longer survival in patients younger than 45 years.

Dr. Weeraratna said this finding and her group’s prior findings suggest younger melanoma patients have more VEGF but less angiogenesis than older patients. The older patients have less VEGF and more SFRP2, which drives angiogenesis.

Dr. Weeraratna’s lab then conducted experiments in young mice, which suggested that an anti-VEGF antibody can reduce angiogenesis, but not in the presence of SFRP2.

Lipid metabolism and treatment resistance

A recently published study by Dr. Weeraratna and colleagues tied changes in aged fibroblast lipid metabolism to treatment resistance in melanoma (Cancer Discov. 2020 Jun 4;CD-20-0329).

The research showed that melanoma cells accumulate lipids when incubated with aged, rather than young, fibroblasts in vitro.

Lipid uptake is mediated by fatty acid transporters (FATPs), and the researchers found that most FATPs were unchanged by age. However, FATP2 was elevated in melanoma cells exposed to aged media, aged mice, and melanoma patients older than 50 years of age.

When melanoma cells were incubated with conditioned media from aged fibroblasts and a FATP2 inhibitor, they no longer took up lipids.

When FATP2 was knocked down in aged mice with melanoma, BRAF and MEK inhibitors (which are not very effective ordinarily) caused dramatic and prolonged tumor regression. These effects were not seen with FATP2 inhibition in young mice.

These results suggest FATP2 is a key transporter of lipids in the aged microenvironment, and inhibiting FATP2 can delay the onset of treatment resistance.

Striving to understand a complex system

For many years, the dogma was that cancer cells behaved like unwelcome invaders, co-opting the metabolic machinery of the sites of spread, with crowding of the normal structures within those organs.

To say that concept was primitive is an understatement. Clearly, the relationship between tumor cells and the surrounding stroma is complex. Changes that occur in an aging microenvironment can influence cancer outcomes in older adults.

Dr. Weeraratna’s presentation adds further impetus to efforts to broaden eligibility criteria for clinical trials so the median age and the metabolic milieu of trial participants more closely parallels the general population.

She highlighted the importance of data analysis by age cohorts and the need to design preclinical studies so that investigators can study the microenvironment of cancer cells in in vitro models and in young and older laboratory animals.

As management expert W. Edwards Deming is believed to have said, “Every system is perfectly designed to get the results it gets.” Cancer is likely not an independent, hostile invader, overtaking the failing machinery of aging cells. To understand the intersection of cancer and aging, we need a more perfect understanding of the system in which tumors develop and are treated.

Dr. Weeraratna reported having no disclosures.


Dr. Lyss was a community-based medical oncologist and clinical researcher for more than 35 years before his recent retirement. His clinical and research interests were focused on breast and lung cancers as well as expanding clinical trial access to medically underserved populations. He is based in St. Louis. He has no conflicts of interest.
 

SOURCE: Weeraratna A. AACR 2020. Age against the machine: How the aging microenvironment governs response to therapy.

The COVID-19 surge and pandemic have changed many things in medicine, from how we round on the wards to our increased use of telemedicine in outpatient and inpatient care. This not only changed our interactions with patients, but it also changed our learners’ education. From March to May 2020 during the COVID-19 pandemic, many Pediatric Hospital Medicine (PHM) fellowship directors were required to adjust clinical responsibilities and scholarly activities. These changes led to unique challenges and learning opportunities for fellows and faculty.

Many fellowships were asked to make changes to patient care for patient/provider safety. Because of low censuses, the University of Pittsburgh Medical Center’s Pittsburgh Children’s Hospital closed their observation unit; as a result, Elise Lu, MD, PhD, PHM fellow, spent time rounding on inpatient units instead of the observation unit. At the Children’s Hospital of Los Angeles, PHM fellow Brandon Palmer, MD, said his in-person child abuse elective was switched to a virtual elective. Dr. Adam Cohen, chief PHM fellow at Baylor College of Medicine/Texas Children’s Hospital, both in Houston, offered to care for adult patients and provide telehealth services to pediatric patients, but was never called to participate.

At other programs, fellows experienced greater changes to patient care and systems-based practice. Carlos Plancarte, MD, PHM fellow at Children’s Hospital of Montefiore, New York, provided care for patients up to the age of 30 years as his training hospital began admitting adult patients. Jeremiah Cleveland, MD, PHM fellowship director at Maimonides Children’s Hospital, New York, shared that his fellow’s “away elective” at a pediatric long-term acute care facility was canceled. Dr. Cleveland changed the fellow’s rotation to an infectious disease rotation, which gave her a unique opportunity to evaluate the clinical and nonclinical aspects of pandemic and disaster response.

PHM fellows also experienced changes to their scholarly activities. Matthew Shapiro, MD, a fellow at Anne and Robert H. Lurie Children’s Hospital in Chicago, had to place his quality improvement research on hold and is writing a commentary with his mentors. Marie Pfarr, MD, a fellow at Cincinnati Children’s Hospital and Medical Center, changed her plans from a simulation-based research project to studying compassion fatigue. Many fellows had workshops, platform and/or poster presentations at the Pediatric Academic Societies Meeting and/or the Pediatric Hospital Medicine Conference, both of which were canceled.

Some fellows felt the pandemic provided them an opportunity to learn communication and interpersonal skills. Dr. Shapiro observed his mentors effectively communicating while managing a crisis. Dr. Plancarte shared that he learned that saying “I don’t know” can be helpful when effectively leading a team.

Despite the changes, the COVID-19 pandemic’s most important lesson was the creation of a supportive community. Across the country, PHM fellows were supported by faculty, and faculty by their fellows. Dr. Plancarte observed how his colleagues united during a challenging situation to support each other. Ritu Patel, MD, PHM fellowship director at Kaiser Oakland shared that her fellowship’s weekly informal meetings helped bring her fellowship’s fellows and faculty closer. Joel Forman, MD, PHM fellowship director and vice chair of education at Mount Sinai Kravis Children’s Hospital in New York stressed the importance of camaraderie amongst faculty and learners.

While the pandemic continues, and long after it has passed, fellowship programs have learned that fostering community across training lines is important for both fellows and faculty.

Dr. Kumar is a pediatric hospitalist at Cleveland Clinic Children’s. She is a clinical assistant professor of pediatrics at Case Western Reserve University, Cleveland, and serves as the pediatrics editor for the Hospitalist.

The COVID-19 surge and pandemic have changed many things in medicine, from how we round on the wards to our increased use of telemedicine in outpatient and inpatient care. This not only changed our interactions with patients, but it also changed our learners’ education. From March to May 2020 during the COVID-19 pandemic, many Pediatric Hospital Medicine (PHM) fellowship directors were required to adjust clinical responsibilities and scholarly activities. These changes led to unique challenges and learning opportunities for fellows and faculty.

Many fellowships were asked to make changes to patient care for patient/provider safety. Because of low censuses, the University of Pittsburgh Medical Center’s Pittsburgh Children’s Hospital closed their observation unit; as a result, Elise Lu, MD, PhD, PHM fellow, spent time rounding on inpatient units instead of the observation unit. At the Children’s Hospital of Los Angeles, PHM fellow Brandon Palmer, MD, said his in-person child abuse elective was switched to a virtual elective. Dr. Adam Cohen, chief PHM fellow at Baylor College of Medicine/Texas Children’s Hospital, both in Houston, offered to care for adult patients and provide telehealth services to pediatric patients, but was never called to participate.

At other programs, fellows experienced greater changes to patient care and systems-based practice. Carlos Plancarte, MD, PHM fellow at Children’s Hospital of Montefiore, New York, provided care for patients up to the age of 30 years as his training hospital began admitting adult patients. Jeremiah Cleveland, MD, PHM fellowship director at Maimonides Children’s Hospital, New York, shared that his fellow’s “away elective” at a pediatric long-term acute care facility was canceled. Dr. Cleveland changed the fellow’s rotation to an infectious disease rotation, which gave her a unique opportunity to evaluate the clinical and nonclinical aspects of pandemic and disaster response.

PHM fellows also experienced changes to their scholarly activities. Matthew Shapiro, MD, a fellow at Anne and Robert H. Lurie Children’s Hospital in Chicago, had to place his quality improvement research on hold and is writing a commentary with his mentors. Marie Pfarr, MD, a fellow at Cincinnati Children’s Hospital and Medical Center, changed her plans from a simulation-based research project to studying compassion fatigue. Many fellows had workshops, platform and/or poster presentations at the Pediatric Academic Societies Meeting and/or the Pediatric Hospital Medicine Conference, both of which were canceled.

Some fellows felt the pandemic provided them an opportunity to learn communication and interpersonal skills. Dr. Shapiro observed his mentors effectively communicating while managing a crisis. Dr. Plancarte shared that he learned that saying “I don’t know” can be helpful when effectively leading a team.

Despite the changes, the COVID-19 pandemic’s most important lesson was the creation of a supportive community. Across the country, PHM fellows were supported by faculty, and faculty by their fellows. Dr. Plancarte observed how his colleagues united during a challenging situation to support each other. Ritu Patel, MD, PHM fellowship director at Kaiser Oakland shared that her fellowship’s weekly informal meetings helped bring her fellowship’s fellows and faculty closer. Joel Forman, MD, PHM fellowship director and vice chair of education at Mount Sinai Kravis Children’s Hospital in New York stressed the importance of camaraderie amongst faculty and learners.

While the pandemic continues, and long after it has passed, fellowship programs have learned that fostering community across training lines is important for both fellows and faculty.

Dr. Kumar is a pediatric hospitalist at Cleveland Clinic Children’s. She is a clinical assistant professor of pediatrics at Case Western Reserve University, Cleveland, and serves as the pediatrics editor for the Hospitalist.

The COVID-19 surge and pandemic have changed many things in medicine, from how we round on the wards to our increased use of telemedicine in outpatient and inpatient care. This not only changed our interactions with patients, but it also changed our learners’ education. From March to May 2020 during the COVID-19 pandemic, many Pediatric Hospital Medicine (PHM) fellowship directors were required to adjust clinical responsibilities and scholarly activities. These changes led to unique challenges and learning opportunities for fellows and faculty.

Many fellowships were asked to make changes to patient care for patient/provider safety. Because of low censuses, the University of Pittsburgh Medical Center’s Pittsburgh Children’s Hospital closed their observation unit; as a result, Elise Lu, MD, PhD, PHM fellow, spent time rounding on inpatient units instead of the observation unit. At the Children’s Hospital of Los Angeles, PHM fellow Brandon Palmer, MD, said his in-person child abuse elective was switched to a virtual elective. Dr. Adam Cohen, chief PHM fellow at Baylor College of Medicine/Texas Children’s Hospital, both in Houston, offered to care for adult patients and provide telehealth services to pediatric patients, but was never called to participate.

At other programs, fellows experienced greater changes to patient care and systems-based practice. Carlos Plancarte, MD, PHM fellow at Children’s Hospital of Montefiore, New York, provided care for patients up to the age of 30 years as his training hospital began admitting adult patients. Jeremiah Cleveland, MD, PHM fellowship director at Maimonides Children’s Hospital, New York, shared that his fellow’s “away elective” at a pediatric long-term acute care facility was canceled. Dr. Cleveland changed the fellow’s rotation to an infectious disease rotation, which gave her a unique opportunity to evaluate the clinical and nonclinical aspects of pandemic and disaster response.

PHM fellows also experienced changes to their scholarly activities. Matthew Shapiro, MD, a fellow at Anne and Robert H. Lurie Children’s Hospital in Chicago, had to place his quality improvement research on hold and is writing a commentary with his mentors. Marie Pfarr, MD, a fellow at Cincinnati Children’s Hospital and Medical Center, changed her plans from a simulation-based research project to studying compassion fatigue. Many fellows had workshops, platform and/or poster presentations at the Pediatric Academic Societies Meeting and/or the Pediatric Hospital Medicine Conference, both of which were canceled.

Some fellows felt the pandemic provided them an opportunity to learn communication and interpersonal skills. Dr. Shapiro observed his mentors effectively communicating while managing a crisis. Dr. Plancarte shared that he learned that saying “I don’t know” can be helpful when effectively leading a team.

Despite the changes, the COVID-19 pandemic’s most important lesson was the creation of a supportive community. Across the country, PHM fellows were supported by faculty, and faculty by their fellows. Dr. Plancarte observed how his colleagues united during a challenging situation to support each other. Ritu Patel, MD, PHM fellowship director at Kaiser Oakland shared that her fellowship’s weekly informal meetings helped bring her fellowship’s fellows and faculty closer. Joel Forman, MD, PHM fellowship director and vice chair of education at Mount Sinai Kravis Children’s Hospital in New York stressed the importance of camaraderie amongst faculty and learners.

While the pandemic continues, and long after it has passed, fellowship programs have learned that fostering community across training lines is important for both fellows and faculty.

Dr. Kumar is a pediatric hospitalist at Cleveland Clinic Children’s. She is a clinical assistant professor of pediatrics at Case Western Reserve University, Cleveland, and serves as the pediatrics editor for the Hospitalist.

To the Editor: 

We read with interest the excellent Cutis articles on cutaneous metastases by Tarantino et al¹ and Agnetta et al.² Tarantino et al¹ reported a 59-year-old man who developed cutaneous metastases on the scalp from an esophageal adenocarcinoma. Agnetta et al² described a 76-year-old woman with metastatic melanoma mimicking eruptive keratoacanthomas.  

Cutaneous metastases are not common. They may herald the unsuspected diagnosis of a solid tumor recurrence or progression of systemic disease in an oncology patient. Occasionally, they are the primary manifestation of a visceral tumor in a previously cancer-free patient. Less often, skin lesions are the manifestation of a new or recurrent hematologic malignancy.^3,4 

The morphology of cutaneous metastases is variable. Most commonly they appear as papules and nodules. However, they can mimic bacterial (eg, erysipelas) and viral (eg, herpes zoster) infections or present as scalp alopecia.^5-7

Cutaneous metastases also can mimic benign (eg, epidermoid cysts) or malignant (eg, keratoacanthoma) neoplasms. Keratoacanthomalike cutaneous metastases are rare.⁸ They can present as single or multiple tumors.^9,10 

In the case reported by Tarantino et al,¹ the patient had a history of metastatic adenocarcinoma of the esophagus. His unsuspected recurrence presented not only with a single keratoacanthomalike cutaneous metastasis on the scalp but also with another metastasis-related scalp lesion that appeared as a smooth pearly papule. We also observed a 53-year-old man whose metastatic esophageal adenocarcinoma presented with a keratoacanthomalike nodule on the right upper lip; additionally, the patient had other cutaneous metastases that appeared as an erythematous papule on the forehead and a cystic nodule on the scalp.⁸ Other investigators also observed a single keratoacanthomalike lesion on the left cheek of a 49-year-old man with metastatic esophageal adenocarcinoma.¹¹ 

Agnetta et al² described a patient with a history of malignant melanoma on the left upper back that had been excised 2 years prior. She presented with the eruptive onset of multiple keratoacanthomalike cutaneous metastases on the chest, back, and right arm.² The important observation of metastatic malignant melanoma presenting as multiple keratoacanthomalike cutaneous metastases pointed out by Agnetta et al2 confirms a similar occurrence reported by Reed et al¹² in a patient with metastatic malignant melanoma. 

We also previously reported the case of a 68-year-old man with metastatic laryngeal squamous cell carcinoma (SCC) who developed more than 10 keratoacanthomalike nodules within a radiation port that extended from the face to the mid chest.¹⁰ In addition, other researchers have noted a similar phenomenon of keratoacanthomalike cutaneous metastases mimicking eruptive keratoacanthomas.¹³ Gil et al¹⁴ described a 40-year-old woman whose metastatic epithelioid trophoblastic tumor initially presented as 11 keratoacanthomalike scalp nodules; interestingly, the first nodule spontaneously regressed. Araghi et al¹⁵ reported a 58-year-old woman--with a stable SCC of the larynx that had been diagnosed 2 years prior and treated with chemoradiotherapy--in whom cancer progression presented as multiple keratoacanthomalike lesions in an area of prior radiotherapy. 

In conclusion, cutaneous metastases presenting as new-onset solitary or multiple keratoacanthomalike nodules in either a cancer-free individual or a patient with a prior history of a visceral malignancy is uncommon. Although the clinical features mimic those of a single or eruptive keratoacanthomas, a biopsy will readily establish the diagnosis of cutaneous metastatic cancer. Metastatic esophageal carcinoma--either adenocarcinoma or SCC--can present, albeit rarely, with cutaneous lesions that can have various morphologies.⁸ Whether there is an increased predilection for patients with metastatic esophageal adenocarcinoma to present with single keratoacanthomalike cutaneous metastases with or without concurrent additional skin lesions of cutaneous metastases of other morphologies remains to be determined. 

To the Editor: 

We read with interest the excellent Cutis articles on cutaneous metastases by Tarantino et al¹ and Agnetta et al.² Tarantino et al¹ reported a 59-year-old man who developed cutaneous metastases on the scalp from an esophageal adenocarcinoma. Agnetta et al² described a 76-year-old woman with metastatic melanoma mimicking eruptive keratoacanthomas.  

Cutaneous metastases are not common. They may herald the unsuspected diagnosis of a solid tumor recurrence or progression of systemic disease in an oncology patient. Occasionally, they are the primary manifestation of a visceral tumor in a previously cancer-free patient. Less often, skin lesions are the manifestation of a new or recurrent hematologic malignancy.^3,4 

The morphology of cutaneous metastases is variable. Most commonly they appear as papules and nodules. However, they can mimic bacterial (eg, erysipelas) and viral (eg, herpes zoster) infections or present as scalp alopecia.^5-7

Cutaneous metastases also can mimic benign (eg, epidermoid cysts) or malignant (eg, keratoacanthoma) neoplasms. Keratoacanthomalike cutaneous metastases are rare.⁸ They can present as single or multiple tumors.^9,10 

In the case reported by Tarantino et al,¹ the patient had a history of metastatic adenocarcinoma of the esophagus. His unsuspected recurrence presented not only with a single keratoacanthomalike cutaneous metastasis on the scalp but also with another metastasis-related scalp lesion that appeared as a smooth pearly papule. We also observed a 53-year-old man whose metastatic esophageal adenocarcinoma presented with a keratoacanthomalike nodule on the right upper lip; additionally, the patient had other cutaneous metastases that appeared as an erythematous papule on the forehead and a cystic nodule on the scalp.⁸ Other investigators also observed a single keratoacanthomalike lesion on the left cheek of a 49-year-old man with metastatic esophageal adenocarcinoma.¹¹ 

Agnetta et al² described a patient with a history of malignant melanoma on the left upper back that had been excised 2 years prior. She presented with the eruptive onset of multiple keratoacanthomalike cutaneous metastases on the chest, back, and right arm.² The important observation of metastatic malignant melanoma presenting as multiple keratoacanthomalike cutaneous metastases pointed out by Agnetta et al2 confirms a similar occurrence reported by Reed et al¹² in a patient with metastatic malignant melanoma. 

We also previously reported the case of a 68-year-old man with metastatic laryngeal squamous cell carcinoma (SCC) who developed more than 10 keratoacanthomalike nodules within a radiation port that extended from the face to the mid chest.¹⁰ In addition, other researchers have noted a similar phenomenon of keratoacanthomalike cutaneous metastases mimicking eruptive keratoacanthomas.¹³ Gil et al¹⁴ described a 40-year-old woman whose metastatic epithelioid trophoblastic tumor initially presented as 11 keratoacanthomalike scalp nodules; interestingly, the first nodule spontaneously regressed. Araghi et al¹⁵ reported a 58-year-old woman--with a stable SCC of the larynx that had been diagnosed 2 years prior and treated with chemoradiotherapy--in whom cancer progression presented as multiple keratoacanthomalike lesions in an area of prior radiotherapy. 

In conclusion, cutaneous metastases presenting as new-onset solitary or multiple keratoacanthomalike nodules in either a cancer-free individual or a patient with a prior history of a visceral malignancy is uncommon. Although the clinical features mimic those of a single or eruptive keratoacanthomas, a biopsy will readily establish the diagnosis of cutaneous metastatic cancer. Metastatic esophageal carcinoma--either adenocarcinoma or SCC--can present, albeit rarely, with cutaneous lesions that can have various morphologies.⁸ Whether there is an increased predilection for patients with metastatic esophageal adenocarcinoma to present with single keratoacanthomalike cutaneous metastases with or without concurrent additional skin lesions of cutaneous metastases of other morphologies remains to be determined. 

To the Editor: 

We read with interest the excellent Cutis articles on cutaneous metastases by Tarantino et al¹ and Agnetta et al.² Tarantino et al¹ reported a 59-year-old man who developed cutaneous metastases on the scalp from an esophageal adenocarcinoma. Agnetta et al² described a 76-year-old woman with metastatic melanoma mimicking eruptive keratoacanthomas.  

Cutaneous metastases are not common. They may herald the unsuspected diagnosis of a solid tumor recurrence or progression of systemic disease in an oncology patient. Occasionally, they are the primary manifestation of a visceral tumor in a previously cancer-free patient. Less often, skin lesions are the manifestation of a new or recurrent hematologic malignancy.^3,4 

The morphology of cutaneous metastases is variable. Most commonly they appear as papules and nodules. However, they can mimic bacterial (eg, erysipelas) and viral (eg, herpes zoster) infections or present as scalp alopecia.^5-7

Cutaneous metastases also can mimic benign (eg, epidermoid cysts) or malignant (eg, keratoacanthoma) neoplasms. Keratoacanthomalike cutaneous metastases are rare.⁸ They can present as single or multiple tumors.^9,10 

In the case reported by Tarantino et al,¹ the patient had a history of metastatic adenocarcinoma of the esophagus. His unsuspected recurrence presented not only with a single keratoacanthomalike cutaneous metastasis on the scalp but also with another metastasis-related scalp lesion that appeared as a smooth pearly papule. We also observed a 53-year-old man whose metastatic esophageal adenocarcinoma presented with a keratoacanthomalike nodule on the right upper lip; additionally, the patient had other cutaneous metastases that appeared as an erythematous papule on the forehead and a cystic nodule on the scalp.⁸ Other investigators also observed a single keratoacanthomalike lesion on the left cheek of a 49-year-old man with metastatic esophageal adenocarcinoma.¹¹ 

Agnetta et al² described a patient with a history of malignant melanoma on the left upper back that had been excised 2 years prior. She presented with the eruptive onset of multiple keratoacanthomalike cutaneous metastases on the chest, back, and right arm.² The important observation of metastatic malignant melanoma presenting as multiple keratoacanthomalike cutaneous metastases pointed out by Agnetta et al2 confirms a similar occurrence reported by Reed et al¹² in a patient with metastatic malignant melanoma. 

We also previously reported the case of a 68-year-old man with metastatic laryngeal squamous cell carcinoma (SCC) who developed more than 10 keratoacanthomalike nodules within a radiation port that extended from the face to the mid chest.¹⁰ In addition, other researchers have noted a similar phenomenon of keratoacanthomalike cutaneous metastases mimicking eruptive keratoacanthomas.¹³ Gil et al¹⁴ described a 40-year-old woman whose metastatic epithelioid trophoblastic tumor initially presented as 11 keratoacanthomalike scalp nodules; interestingly, the first nodule spontaneously regressed. Araghi et al¹⁵ reported a 58-year-old woman--with a stable SCC of the larynx that had been diagnosed 2 years prior and treated with chemoradiotherapy--in whom cancer progression presented as multiple keratoacanthomalike lesions in an area of prior radiotherapy. 

In conclusion, cutaneous metastases presenting as new-onset solitary or multiple keratoacanthomalike nodules in either a cancer-free individual or a patient with a prior history of a visceral malignancy is uncommon. Although the clinical features mimic those of a single or eruptive keratoacanthomas, a biopsy will readily establish the diagnosis of cutaneous metastatic cancer. Metastatic esophageal carcinoma--either adenocarcinoma or SCC--can present, albeit rarely, with cutaneous lesions that can have various morphologies.⁸ Whether there is an increased predilection for patients with metastatic esophageal adenocarcinoma to present with single keratoacanthomalike cutaneous metastases with or without concurrent additional skin lesions of cutaneous metastases of other morphologies remains to be determined. 

BRCA carrier status alone should not influence screening recommendations for colorectal cancer or pancreatic ductal adenocarcinoma, according to an American Gastroenterological Association clinical practice update.

Relationships between BRCA carrier status and risks of pancreatic ductal adenocarcinoma (PDAC) and colorectal cancer (CRC) remain unclear, reported lead author Sonia S. Kupfer, MD, AGAF, of the University of Chicago, and colleagues.

“Pathogenic variants in BRCA1 and BRCA2 have ... been associated with variable risk of GI cancer, including CRC, PDAC, biliary, and gastric cancers,” the investigators wrote in Gastroenterology. “However, the magnitude of GI cancer risks is not well established and there is minimal evidence or guidance on screening for GI cancers among BRCA1 and BRCA2 carriers.”

According to the investigators, personalized screening for CRC is well supported by evidence, as higher-risk individuals, such as those with a family history of CRC, have been shown to benefit from earlier and more frequent colonoscopies. Although the value of risk-based screening is less clear for other types of GI cancer, the investigators cited a growing body of evidence that supports screening individuals at high risk of PDAC.

Still, data illuminating the role of BRCA carrier status are relatively scarce, which has led to variability in clinical practice.

“Lack of accurate CRC and PDAC risk estimates in BRCA1 and BRCA2 leave physicians and patients without guidance, and result in a range of screening recommendations and practices in this population,” wrote Dr. Kupfer and colleagues.

To offer some clarity, they drafted the present clinical practice update on behalf of the AGA. The recommendations are framed within a discussion of relevant publications.

Data from multiple studies, for instance, suggest that BRCA pathogenic variants are found in 1.3% of patients with early-onset CRC, 0.2% of those with high-risk CRC, and 1.0% of those with any type of CRC, all of which are higher rates “than would be expected by chance.

“However,” the investigators added, “this association is not proof that the observed BRCA1 and BRCA2 pathogenic variants play a causative role in CRC.”

The investigators went on to discuss a 2018 meta-analysis by Oho et al., which included 14 studies evaluating risk of CRC among BRCA carriers. The analysis found that BRCA carriers had a 24% increased risk of CRC, which Dr. Kupfer and colleagues described as “small but statistically significant.” Subgroup analysis suggested that BRCA1 carriers drove this association, with a 49% increased risk of CRC, whereas no significant link was found with BRCA2.

Dr. Kupfer and colleagues described the 49% increase as “very modest,” and therefore insufficient to warrant more intensive screening, particularly when considered in the context of other risk factors, such as Lynch syndrome, which may entail a 1,600% increased risk of CRC. For PDAC, no such meta-analysis has been conducted; however, multiple studies have pointed to associations between BRCA and risk of PDAC.

For example, a 2018 case-control study by Hu et al. showed that BRCA1 and BRCA2 had relative prevalence rates of 0.59% and 1.95% among patients with PDAC. These rates translated to a 158% increased risk of PDAC for BRCA1, and a 520% increase risk for BRCA2; but Dr. Kupfer and colleagues noted that the BRCA2 carriers were from high-risk families, so the findings may not extend to the general population.

In light of these findings, the update recommends PDAC screening for BRCA carriers only if they have a family history of PDAC, with the caveat that the association between risk and degree of family involvement remains unknown.

Ultimately, for both CRC and PDAC, the investigators called for further BRCA research, based on the conclusion that “results from published studies provide inconsistent levels of evidence.”

The investigators reported no conflicts of interest.

SOURCE: Kupfer SS et al. Gastroenterology. 2020 Apr 23. doi: 10.1053/j.gastro.2020.03.086.

BRCA carrier status alone should not influence screening recommendations for colorectal cancer or pancreatic ductal adenocarcinoma, according to an American Gastroenterological Association clinical practice update.

Relationships between BRCA carrier status and risks of pancreatic ductal adenocarcinoma (PDAC) and colorectal cancer (CRC) remain unclear, reported lead author Sonia S. Kupfer, MD, AGAF, of the University of Chicago, and colleagues.

“Pathogenic variants in BRCA1 and BRCA2 have ... been associated with variable risk of GI cancer, including CRC, PDAC, biliary, and gastric cancers,” the investigators wrote in Gastroenterology. “However, the magnitude of GI cancer risks is not well established and there is minimal evidence or guidance on screening for GI cancers among BRCA1 and BRCA2 carriers.”

According to the investigators, personalized screening for CRC is well supported by evidence, as higher-risk individuals, such as those with a family history of CRC, have been shown to benefit from earlier and more frequent colonoscopies. Although the value of risk-based screening is less clear for other types of GI cancer, the investigators cited a growing body of evidence that supports screening individuals at high risk of PDAC.

Still, data illuminating the role of BRCA carrier status are relatively scarce, which has led to variability in clinical practice.

“Lack of accurate CRC and PDAC risk estimates in BRCA1 and BRCA2 leave physicians and patients without guidance, and result in a range of screening recommendations and practices in this population,” wrote Dr. Kupfer and colleagues.

To offer some clarity, they drafted the present clinical practice update on behalf of the AGA. The recommendations are framed within a discussion of relevant publications.

Data from multiple studies, for instance, suggest that BRCA pathogenic variants are found in 1.3% of patients with early-onset CRC, 0.2% of those with high-risk CRC, and 1.0% of those with any type of CRC, all of which are higher rates “than would be expected by chance.

“However,” the investigators added, “this association is not proof that the observed BRCA1 and BRCA2 pathogenic variants play a causative role in CRC.”

The investigators went on to discuss a 2018 meta-analysis by Oho et al., which included 14 studies evaluating risk of CRC among BRCA carriers. The analysis found that BRCA carriers had a 24% increased risk of CRC, which Dr. Kupfer and colleagues described as “small but statistically significant.” Subgroup analysis suggested that BRCA1 carriers drove this association, with a 49% increased risk of CRC, whereas no significant link was found with BRCA2.

Dr. Kupfer and colleagues described the 49% increase as “very modest,” and therefore insufficient to warrant more intensive screening, particularly when considered in the context of other risk factors, such as Lynch syndrome, which may entail a 1,600% increased risk of CRC. For PDAC, no such meta-analysis has been conducted; however, multiple studies have pointed to associations between BRCA and risk of PDAC.

For example, a 2018 case-control study by Hu et al. showed that BRCA1 and BRCA2 had relative prevalence rates of 0.59% and 1.95% among patients with PDAC. These rates translated to a 158% increased risk of PDAC for BRCA1, and a 520% increase risk for BRCA2; but Dr. Kupfer and colleagues noted that the BRCA2 carriers were from high-risk families, so the findings may not extend to the general population.

In light of these findings, the update recommends PDAC screening for BRCA carriers only if they have a family history of PDAC, with the caveat that the association between risk and degree of family involvement remains unknown.

Ultimately, for both CRC and PDAC, the investigators called for further BRCA research, based on the conclusion that “results from published studies provide inconsistent levels of evidence.”

The investigators reported no conflicts of interest.

SOURCE: Kupfer SS et al. Gastroenterology. 2020 Apr 23. doi: 10.1053/j.gastro.2020.03.086.

BRCA carrier status alone should not influence screening recommendations for colorectal cancer or pancreatic ductal adenocarcinoma, according to an American Gastroenterological Association clinical practice update.

Relationships between BRCA carrier status and risks of pancreatic ductal adenocarcinoma (PDAC) and colorectal cancer (CRC) remain unclear, reported lead author Sonia S. Kupfer, MD, AGAF, of the University of Chicago, and colleagues.

“Pathogenic variants in BRCA1 and BRCA2 have ... been associated with variable risk of GI cancer, including CRC, PDAC, biliary, and gastric cancers,” the investigators wrote in Gastroenterology. “However, the magnitude of GI cancer risks is not well established and there is minimal evidence or guidance on screening for GI cancers among BRCA1 and BRCA2 carriers.”

According to the investigators, personalized screening for CRC is well supported by evidence, as higher-risk individuals, such as those with a family history of CRC, have been shown to benefit from earlier and more frequent colonoscopies. Although the value of risk-based screening is less clear for other types of GI cancer, the investigators cited a growing body of evidence that supports screening individuals at high risk of PDAC.

Still, data illuminating the role of BRCA carrier status are relatively scarce, which has led to variability in clinical practice.

“Lack of accurate CRC and PDAC risk estimates in BRCA1 and BRCA2 leave physicians and patients without guidance, and result in a range of screening recommendations and practices in this population,” wrote Dr. Kupfer and colleagues.

To offer some clarity, they drafted the present clinical practice update on behalf of the AGA. The recommendations are framed within a discussion of relevant publications.

Data from multiple studies, for instance, suggest that BRCA pathogenic variants are found in 1.3% of patients with early-onset CRC, 0.2% of those with high-risk CRC, and 1.0% of those with any type of CRC, all of which are higher rates “than would be expected by chance.

“However,” the investigators added, “this association is not proof that the observed BRCA1 and BRCA2 pathogenic variants play a causative role in CRC.”

The investigators went on to discuss a 2018 meta-analysis by Oho et al., which included 14 studies evaluating risk of CRC among BRCA carriers. The analysis found that BRCA carriers had a 24% increased risk of CRC, which Dr. Kupfer and colleagues described as “small but statistically significant.” Subgroup analysis suggested that BRCA1 carriers drove this association, with a 49% increased risk of CRC, whereas no significant link was found with BRCA2.

Dr. Kupfer and colleagues described the 49% increase as “very modest,” and therefore insufficient to warrant more intensive screening, particularly when considered in the context of other risk factors, such as Lynch syndrome, which may entail a 1,600% increased risk of CRC. For PDAC, no such meta-analysis has been conducted; however, multiple studies have pointed to associations between BRCA and risk of PDAC.

For example, a 2018 case-control study by Hu et al. showed that BRCA1 and BRCA2 had relative prevalence rates of 0.59% and 1.95% among patients with PDAC. These rates translated to a 158% increased risk of PDAC for BRCA1, and a 520% increase risk for BRCA2; but Dr. Kupfer and colleagues noted that the BRCA2 carriers were from high-risk families, so the findings may not extend to the general population.

In light of these findings, the update recommends PDAC screening for BRCA carriers only if they have a family history of PDAC, with the caveat that the association between risk and degree of family involvement remains unknown.

Ultimately, for both CRC and PDAC, the investigators called for further BRCA research, based on the conclusion that “results from published studies provide inconsistent levels of evidence.”

The investigators reported no conflicts of interest.

SOURCE: Kupfer SS et al. Gastroenterology. 2020 Apr 23. doi: 10.1053/j.gastro.2020.03.086.

The role of probiotics in the management of gastrointestinal disorders remains largely unclear, according to a clinical practice guideline published by the American Gastroenterological Association (AGA).

Out of eight disorders reviewed by the guideline panel, four had enough relevant data to support conditional recommendations, while the other four were associated with knowledge gaps that precluded guidance, reported lead author Grace L. Su, MD, AGAF, of the University of Michigan, Ann Arbor, and colleagues.

“It is estimated that 3.9 million American adults used some form of probiotics or prebiotics ... in 2015, an amount which is four times that in 2007,” the guideline panelists wrote. Their report is in Gastroenterology. “Given widespread use and often biased sources of information, it is essential that clinicians have objective guidance for their patients about the appropriate use of and indications for probiotics.”

The creation of such guidance, however, proved a challenging task for the panel, who faced an “extremely varied” evidence base.

Dr. Su and colleagues, who were selected by the AGA Governing Board and Clinical Guidelines Committee, encountered “differences in the strain of microbe(s) used, dose, and route of administration.”

They noted that such differences can significantly affect clinical outcomes.

“Within species, different strains can have widely different activities and biologic effects,” they wrote. “Many immunologic, neurologic, and biochemical effects of gut microbiota are likely not only to be strain specific, but also dose specific. Furthermore, combinations of different microbial strains may also have widely different activity as some microbial activities are dependent on interactions between different strains.”

Beyond differences in treatments, the investigators also reported wide variability in endpoints and outcomes, as well as relatively small study populations compared with pharmacological trials.

Still, data were sufficient to provide some conditional recommendations.

The guideline supports probiotics for patients with pouchitis, those receiving antibiotic therapy, and preterm/low-birthweight infants. In contrast, the panel recommended against probiotics for children with acute infectious gastroenteritis, noting that this recommendation differs from those made by other medical organizations.

“While other society guidelines have previously recommended the use of probiotics in [children with acute infectious gastroenteritis], these guidelines were developed without utilizing GRADE methodology and also relied on data outside of North America which became available after the recommendations were made,” wrote Dr. Su and colleagues. They described a moderate quality of evidence relevant to this indication.

In comparison, the quality of evidence was very low for patients with pouchitis, low for those receiving antibiotics, and moderate/high for preterm/low-birthweight infants.

For Clostridioides difficile infection, Crohn’s disease, ulcerative colitis, and irritable bowel syndrome, the panel recommended probiotics only in the context of a clinical trial, citing knowledge gaps in these areas.

They also noted that probiotics may not be suitable for those at high risk of infection.

“[F]or patients who place a high value on avoidance of potential harms, particularly those with severe illnesses or immunosuppression, it would be reasonable to select not to use probiotics,” the panelists wrote.

Concluding their discussion, Dr. Su and colleagues called for more high-quality research.

“We identified that significant knowledge gaps exist in this very promising and important area of research due to the significant heterogeneity between studies and variability in the probiotic strains studied,” they wrote. “The lack of consistent harms reporting makes it difficult to assess true harms. The lack of product manufacturing details prohibits true comparisons and decreases the feasibility of obtaining certain products by patients. Future high-quality studies are urgently needed which address these pitfalls.”

According to the panelists, the probiotic guideline will be updated in 3-5 years, or possibly earlier if practice-altering findings are published.

The investigators disclosed relationships with Nestex, AbbVie, Takeda, and others.

The role of probiotics in the management of gastrointestinal disorders remains largely unclear, according to a clinical practice guideline published by the American Gastroenterological Association (AGA).

Out of eight disorders reviewed by the guideline panel, four had enough relevant data to support conditional recommendations, while the other four were associated with knowledge gaps that precluded guidance, reported lead author Grace L. Su, MD, AGAF, of the University of Michigan, Ann Arbor, and colleagues.

“It is estimated that 3.9 million American adults used some form of probiotics or prebiotics ... in 2015, an amount which is four times that in 2007,” the guideline panelists wrote. Their report is in Gastroenterology. “Given widespread use and often biased sources of information, it is essential that clinicians have objective guidance for their patients about the appropriate use of and indications for probiotics.”

The creation of such guidance, however, proved a challenging task for the panel, who faced an “extremely varied” evidence base.

Dr. Su and colleagues, who were selected by the AGA Governing Board and Clinical Guidelines Committee, encountered “differences in the strain of microbe(s) used, dose, and route of administration.”

They noted that such differences can significantly affect clinical outcomes.

“Within species, different strains can have widely different activities and biologic effects,” they wrote. “Many immunologic, neurologic, and biochemical effects of gut microbiota are likely not only to be strain specific, but also dose specific. Furthermore, combinations of different microbial strains may also have widely different activity as some microbial activities are dependent on interactions between different strains.”

Beyond differences in treatments, the investigators also reported wide variability in endpoints and outcomes, as well as relatively small study populations compared with pharmacological trials.

Still, data were sufficient to provide some conditional recommendations.

The guideline supports probiotics for patients with pouchitis, those receiving antibiotic therapy, and preterm/low-birthweight infants. In contrast, the panel recommended against probiotics for children with acute infectious gastroenteritis, noting that this recommendation differs from those made by other medical organizations.

“While other society guidelines have previously recommended the use of probiotics in [children with acute infectious gastroenteritis], these guidelines were developed without utilizing GRADE methodology and also relied on data outside of North America which became available after the recommendations were made,” wrote Dr. Su and colleagues. They described a moderate quality of evidence relevant to this indication.

In comparison, the quality of evidence was very low for patients with pouchitis, low for those receiving antibiotics, and moderate/high for preterm/low-birthweight infants.

For Clostridioides difficile infection, Crohn’s disease, ulcerative colitis, and irritable bowel syndrome, the panel recommended probiotics only in the context of a clinical trial, citing knowledge gaps in these areas.

They also noted that probiotics may not be suitable for those at high risk of infection.

“[F]or patients who place a high value on avoidance of potential harms, particularly those with severe illnesses or immunosuppression, it would be reasonable to select not to use probiotics,” the panelists wrote.

Concluding their discussion, Dr. Su and colleagues called for more high-quality research.

“We identified that significant knowledge gaps exist in this very promising and important area of research due to the significant heterogeneity between studies and variability in the probiotic strains studied,” they wrote. “The lack of consistent harms reporting makes it difficult to assess true harms. The lack of product manufacturing details prohibits true comparisons and decreases the feasibility of obtaining certain products by patients. Future high-quality studies are urgently needed which address these pitfalls.”

According to the panelists, the probiotic guideline will be updated in 3-5 years, or possibly earlier if practice-altering findings are published.

The investigators disclosed relationships with Nestex, AbbVie, Takeda, and others.

The role of probiotics in the management of gastrointestinal disorders remains largely unclear, according to a clinical practice guideline published by the American Gastroenterological Association (AGA).

Out of eight disorders reviewed by the guideline panel, four had enough relevant data to support conditional recommendations, while the other four were associated with knowledge gaps that precluded guidance, reported lead author Grace L. Su, MD, AGAF, of the University of Michigan, Ann Arbor, and colleagues.

“It is estimated that 3.9 million American adults used some form of probiotics or prebiotics ... in 2015, an amount which is four times that in 2007,” the guideline panelists wrote. Their report is in Gastroenterology. “Given widespread use and often biased sources of information, it is essential that clinicians have objective guidance for their patients about the appropriate use of and indications for probiotics.”

The creation of such guidance, however, proved a challenging task for the panel, who faced an “extremely varied” evidence base.

Dr. Su and colleagues, who were selected by the AGA Governing Board and Clinical Guidelines Committee, encountered “differences in the strain of microbe(s) used, dose, and route of administration.”

They noted that such differences can significantly affect clinical outcomes.

“Within species, different strains can have widely different activities and biologic effects,” they wrote. “Many immunologic, neurologic, and biochemical effects of gut microbiota are likely not only to be strain specific, but also dose specific. Furthermore, combinations of different microbial strains may also have widely different activity as some microbial activities are dependent on interactions between different strains.”

Beyond differences in treatments, the investigators also reported wide variability in endpoints and outcomes, as well as relatively small study populations compared with pharmacological trials.

Still, data were sufficient to provide some conditional recommendations.

The guideline supports probiotics for patients with pouchitis, those receiving antibiotic therapy, and preterm/low-birthweight infants. In contrast, the panel recommended against probiotics for children with acute infectious gastroenteritis, noting that this recommendation differs from those made by other medical organizations.

“While other society guidelines have previously recommended the use of probiotics in [children with acute infectious gastroenteritis], these guidelines were developed without utilizing GRADE methodology and also relied on data outside of North America which became available after the recommendations were made,” wrote Dr. Su and colleagues. They described a moderate quality of evidence relevant to this indication.

In comparison, the quality of evidence was very low for patients with pouchitis, low for those receiving antibiotics, and moderate/high for preterm/low-birthweight infants.

For Clostridioides difficile infection, Crohn’s disease, ulcerative colitis, and irritable bowel syndrome, the panel recommended probiotics only in the context of a clinical trial, citing knowledge gaps in these areas.

They also noted that probiotics may not be suitable for those at high risk of infection.

“[F]or patients who place a high value on avoidance of potential harms, particularly those with severe illnesses or immunosuppression, it would be reasonable to select not to use probiotics,” the panelists wrote.

Concluding their discussion, Dr. Su and colleagues called for more high-quality research.

“We identified that significant knowledge gaps exist in this very promising and important area of research due to the significant heterogeneity between studies and variability in the probiotic strains studied,” they wrote. “The lack of consistent harms reporting makes it difficult to assess true harms. The lack of product manufacturing details prohibits true comparisons and decreases the feasibility of obtaining certain products by patients. Future high-quality studies are urgently needed which address these pitfalls.”

According to the panelists, the probiotic guideline will be updated in 3-5 years, or possibly earlier if practice-altering findings are published.

The investigators disclosed relationships with Nestex, AbbVie, Takeda, and others.