A new draft guideline for the diagnosis and management of thrombocytopenic purpura (TTP) was recently released by the International Society on Thrombosis and Hemostasis (ISTH).

Svisio/Thinkstock

According to the panel of experts involved, the ISTH guideline takes into account the latest TTP findings, offering a more up-to-date resource for clinicians than the two previously published guidelines in 2012 from the British Committee for Standards in Haematology and in 2017 from the TTP group of Japan’s Blood Coagulation Abnormalities Research Team.

“Since the publication of these guidelines, there have been significant developments in the diagnosis and treatment of TTP, and an increase in published data on how management strategies affect objective health outcomes,” the panel members wrote in the guideline, which is available at ISTH.org.

Despite these advancements, TTP remains a challenging condition for both clinicians and patients for a variety of reasons, the panel noted, which was led by clinical cochair X. Long Zheng, MD, PhD, of the University of Alabama in Birmingham and method cochair Sara K. Vesely, PhD, of the University of Oklahoma, Oklahoma City.

The ISTH guideline provides recommendations for adult patients with either immune or hereditary TTP, from acute events through remission, including diagnostic steps to determine if a case of thrombotic microangiopathy is in fact TTP.

Nearly all the recommendations are based on very-low-certainty evidence. Some of the key treatment recommendations include the following:

• For patients with immune TTP experiencing a first acute event, add corticosteroids to therapeutic plasma exchange (TPE), rather than treating with TPE alone. This is a strong recommendation.
• For patients with immune TTP experiencing a first acute event, add rituximab to corticosteroids and TPE, rather than corticosteroids and TPE alone. This is a conditional recommendation.
• For patients with immune TTP experiencing a relapse, add corticosteroids to TPE, rather than TPE alone. This is a strong recommendation.
• For patients with immune TTP experiencing a relapse, add rituximab to corticosteroids and TPE, rather than steroids and TPE alone. This is a conditional recommendation.
• For patients with immune TTP experiencing an acute event – either a first event or a relapse – use caplacizumab. This is a conditional recommendation based on moderate-certainty evidence.
• For patients with immune TTP who are in remission and have low plasma ADAMTS13 activity but no other symptoms of TMA, use rituximab for prophylaxis. This is a conditional recommendation.
• For patients with hereditary TTP who are in remission, plasma infusion or a watch-and-wait strategy is recommended. This is a conditional recommendation.
• For patients with hereditary TTP who are in remission, do not use factor VIII concentrate infusions. A watch-and-wait strategy is advised. This is a conditional recommendation.
• For patients with immune TTP who are pregnant and have decreased plasma ADAMTS13 activity but no symptoms of TMA, use prophylactic treatment. This is a strong recommendation.
• For patients with hereditary TTP who are pregnant, use prophylactic treatment. This is a strong recommendation. The panel further recommended treatment with plasma infusion rather than factor VIII products, which was a conditional recommendation.

The multidisciplinary expert panel included hematologists and pathologists with expertise in TTP, neurologists, nephrologists, intensive care specialists, and patient representatives. The panel followed the GRADE approach and the Population, Intervention, Comparison, Outcome (PICO) framework, and adhered to standards set forth by the Health and Medicine Division (HMD) of the National Academies of Sciences, Engineering, and Medicine and the GIN-McMaster Guideline Development Checklist.

Even with an experienced group of physicians and a structured plan, however, the creation of guidelines for rare diseases like TTP presents a unique set of obstacles, according to the panel members. Challenges include a small body of relevant evidence that is often inconsistent and lacking in high certainty and studies that do not address outcomes important to patients. These shortcomings can make it difficult for guideline developers to issue strong recommendations.

“However, well-developed clinical practice guidelines are vital in rare diseases; these conditions are, by their nature, encountered very infrequently by individual clinicians, who may feel unprepared to address their diagnosis and treatment,” the panelists wrote. “Well-synthesized evidence and clear recommendations play an important role in supporting clinical decision making. Systematically created guidelines can also highlight areas where evidence is uncertain, clinical judgement is required, and future research in the area is warranted.”

The guideline was supported by ISTH. Fifty percent of the panel members had no or minimal conflict of interest; those with conflicts of interest abstained from voting on recommendations relevant to their conflicts.

A new draft guideline for the diagnosis and management of thrombocytopenic purpura (TTP) was recently released by the International Society on Thrombosis and Hemostasis (ISTH).

Svisio/Thinkstock

According to the panel of experts involved, the ISTH guideline takes into account the latest TTP findings, offering a more up-to-date resource for clinicians than the two previously published guidelines in 2012 from the British Committee for Standards in Haematology and in 2017 from the TTP group of Japan’s Blood Coagulation Abnormalities Research Team.

“Since the publication of these guidelines, there have been significant developments in the diagnosis and treatment of TTP, and an increase in published data on how management strategies affect objective health outcomes,” the panel members wrote in the guideline, which is available at ISTH.org.

Despite these advancements, TTP remains a challenging condition for both clinicians and patients for a variety of reasons, the panel noted, which was led by clinical cochair X. Long Zheng, MD, PhD, of the University of Alabama in Birmingham and method cochair Sara K. Vesely, PhD, of the University of Oklahoma, Oklahoma City.

The ISTH guideline provides recommendations for adult patients with either immune or hereditary TTP, from acute events through remission, including diagnostic steps to determine if a case of thrombotic microangiopathy is in fact TTP.

Nearly all the recommendations are based on very-low-certainty evidence. Some of the key treatment recommendations include the following:

• For patients with immune TTP experiencing a first acute event, add corticosteroids to therapeutic plasma exchange (TPE), rather than treating with TPE alone. This is a strong recommendation.
• For patients with immune TTP experiencing a first acute event, add rituximab to corticosteroids and TPE, rather than corticosteroids and TPE alone. This is a conditional recommendation.
• For patients with immune TTP experiencing a relapse, add corticosteroids to TPE, rather than TPE alone. This is a strong recommendation.
• For patients with immune TTP experiencing a relapse, add rituximab to corticosteroids and TPE, rather than steroids and TPE alone. This is a conditional recommendation.
• For patients with immune TTP experiencing an acute event – either a first event or a relapse – use caplacizumab. This is a conditional recommendation based on moderate-certainty evidence.
• For patients with immune TTP who are in remission and have low plasma ADAMTS13 activity but no other symptoms of TMA, use rituximab for prophylaxis. This is a conditional recommendation.
• For patients with hereditary TTP who are in remission, plasma infusion or a watch-and-wait strategy is recommended. This is a conditional recommendation.
• For patients with hereditary TTP who are in remission, do not use factor VIII concentrate infusions. A watch-and-wait strategy is advised. This is a conditional recommendation.
• For patients with immune TTP who are pregnant and have decreased plasma ADAMTS13 activity but no symptoms of TMA, use prophylactic treatment. This is a strong recommendation.
• For patients with hereditary TTP who are pregnant, use prophylactic treatment. This is a strong recommendation. The panel further recommended treatment with plasma infusion rather than factor VIII products, which was a conditional recommendation.

The multidisciplinary expert panel included hematologists and pathologists with expertise in TTP, neurologists, nephrologists, intensive care specialists, and patient representatives. The panel followed the GRADE approach and the Population, Intervention, Comparison, Outcome (PICO) framework, and adhered to standards set forth by the Health and Medicine Division (HMD) of the National Academies of Sciences, Engineering, and Medicine and the GIN-McMaster Guideline Development Checklist.

Even with an experienced group of physicians and a structured plan, however, the creation of guidelines for rare diseases like TTP presents a unique set of obstacles, according to the panel members. Challenges include a small body of relevant evidence that is often inconsistent and lacking in high certainty and studies that do not address outcomes important to patients. These shortcomings can make it difficult for guideline developers to issue strong recommendations.

“However, well-developed clinical practice guidelines are vital in rare diseases; these conditions are, by their nature, encountered very infrequently by individual clinicians, who may feel unprepared to address their diagnosis and treatment,” the panelists wrote. “Well-synthesized evidence and clear recommendations play an important role in supporting clinical decision making. Systematically created guidelines can also highlight areas where evidence is uncertain, clinical judgement is required, and future research in the area is warranted.”

The guideline was supported by ISTH. Fifty percent of the panel members had no or minimal conflict of interest; those with conflicts of interest abstained from voting on recommendations relevant to their conflicts.

A new draft guideline for the diagnosis and management of thrombocytopenic purpura (TTP) was recently released by the International Society on Thrombosis and Hemostasis (ISTH).

Svisio/Thinkstock

According to the panel of experts involved, the ISTH guideline takes into account the latest TTP findings, offering a more up-to-date resource for clinicians than the two previously published guidelines in 2012 from the British Committee for Standards in Haematology and in 2017 from the TTP group of Japan’s Blood Coagulation Abnormalities Research Team.

“Since the publication of these guidelines, there have been significant developments in the diagnosis and treatment of TTP, and an increase in published data on how management strategies affect objective health outcomes,” the panel members wrote in the guideline, which is available at ISTH.org.

Despite these advancements, TTP remains a challenging condition for both clinicians and patients for a variety of reasons, the panel noted, which was led by clinical cochair X. Long Zheng, MD, PhD, of the University of Alabama in Birmingham and method cochair Sara K. Vesely, PhD, of the University of Oklahoma, Oklahoma City.

The ISTH guideline provides recommendations for adult patients with either immune or hereditary TTP, from acute events through remission, including diagnostic steps to determine if a case of thrombotic microangiopathy is in fact TTP.

Nearly all the recommendations are based on very-low-certainty evidence. Some of the key treatment recommendations include the following:

• For patients with immune TTP experiencing a first acute event, add corticosteroids to therapeutic plasma exchange (TPE), rather than treating with TPE alone. This is a strong recommendation.
• For patients with immune TTP experiencing a first acute event, add rituximab to corticosteroids and TPE, rather than corticosteroids and TPE alone. This is a conditional recommendation.
• For patients with immune TTP experiencing a relapse, add corticosteroids to TPE, rather than TPE alone. This is a strong recommendation.
• For patients with immune TTP experiencing a relapse, add rituximab to corticosteroids and TPE, rather than steroids and TPE alone. This is a conditional recommendation.
• For patients with immune TTP experiencing an acute event – either a first event or a relapse – use caplacizumab. This is a conditional recommendation based on moderate-certainty evidence.
• For patients with immune TTP who are in remission and have low plasma ADAMTS13 activity but no other symptoms of TMA, use rituximab for prophylaxis. This is a conditional recommendation.
• For patients with hereditary TTP who are in remission, plasma infusion or a watch-and-wait strategy is recommended. This is a conditional recommendation.
• For patients with hereditary TTP who are in remission, do not use factor VIII concentrate infusions. A watch-and-wait strategy is advised. This is a conditional recommendation.
• For patients with immune TTP who are pregnant and have decreased plasma ADAMTS13 activity but no symptoms of TMA, use prophylactic treatment. This is a strong recommendation.
• For patients with hereditary TTP who are pregnant, use prophylactic treatment. This is a strong recommendation. The panel further recommended treatment with plasma infusion rather than factor VIII products, which was a conditional recommendation.

The multidisciplinary expert panel included hematologists and pathologists with expertise in TTP, neurologists, nephrologists, intensive care specialists, and patient representatives. The panel followed the GRADE approach and the Population, Intervention, Comparison, Outcome (PICO) framework, and adhered to standards set forth by the Health and Medicine Division (HMD) of the National Academies of Sciences, Engineering, and Medicine and the GIN-McMaster Guideline Development Checklist.

Even with an experienced group of physicians and a structured plan, however, the creation of guidelines for rare diseases like TTP presents a unique set of obstacles, according to the panel members. Challenges include a small body of relevant evidence that is often inconsistent and lacking in high certainty and studies that do not address outcomes important to patients. These shortcomings can make it difficult for guideline developers to issue strong recommendations.

“However, well-developed clinical practice guidelines are vital in rare diseases; these conditions are, by their nature, encountered very infrequently by individual clinicians, who may feel unprepared to address their diagnosis and treatment,” the panelists wrote. “Well-synthesized evidence and clear recommendations play an important role in supporting clinical decision making. Systematically created guidelines can also highlight areas where evidence is uncertain, clinical judgement is required, and future research in the area is warranted.”

The guideline was supported by ISTH. Fifty percent of the panel members had no or minimal conflict of interest; those with conflicts of interest abstained from voting on recommendations relevant to their conflicts.

As the holiday shopping season approaches, the SVS Foundation would like to remind you to set up your AmazonSmile account and designate the SVS Foundation as your charity. It’s easy to begin. Start at smile.amazon.com and search ‘Society for Vascular Surgery Foundation.’ Once you choose the Foundation, start shopping! Amazon will donate 0.5% of the price of your eligible AmazonSmile purchases. Every little bit makes a difference. Questions? Reach out to SVSFoundation@vascularsociety.org.

As the holiday shopping season approaches, the SVS Foundation would like to remind you to set up your AmazonSmile account and designate the SVS Foundation as your charity. It’s easy to begin. Start at smile.amazon.com and search ‘Society for Vascular Surgery Foundation.’ Once you choose the Foundation, start shopping! Amazon will donate 0.5% of the price of your eligible AmazonSmile purchases. Every little bit makes a difference. Questions? Reach out to SVSFoundation@vascularsociety.org.

As the holiday shopping season approaches, the SVS Foundation would like to remind you to set up your AmazonSmile account and designate the SVS Foundation as your charity. It’s easy to begin. Start at smile.amazon.com and search ‘Society for Vascular Surgery Foundation.’ Once you choose the Foundation, start shopping! Amazon will donate 0.5% of the price of your eligible AmazonSmile purchases. Every little bit makes a difference. Questions? Reach out to SVSFoundation@vascularsociety.org.

By renewing your membership, you continue to support the critical work the Society does throughout the year, and you contribute directly to the ongoing improvement of vascular health. Renewing will also provide you continued access to all membership benefits, including access to peer-reviewed journals, your members-only community on SVSConnect, and discounts on meetings and educational products.

Avoid a lapse in your SVS membership and loss of benefits. Pay your open invoice online by logging on to your SVS member page. Pay your dues here.

By renewing your membership, you continue to support the critical work the Society does throughout the year, and you contribute directly to the ongoing improvement of vascular health. Renewing will also provide you continued access to all membership benefits, including access to peer-reviewed journals, your members-only community on SVSConnect, and discounts on meetings and educational products.

Avoid a lapse in your SVS membership and loss of benefits. Pay your open invoice online by logging on to your SVS member page. Pay your dues here.

By renewing your membership, you continue to support the critical work the Society does throughout the year, and you contribute directly to the ongoing improvement of vascular health. Renewing will also provide you continued access to all membership benefits, including access to peer-reviewed journals, your members-only community on SVSConnect, and discounts on meetings and educational products.

Avoid a lapse in your SVS membership and loss of benefits. Pay your open invoice online by logging on to your SVS member page. Pay your dues here.

Based on member needs assessment, SVS members have been asking for a more comprehensive, vascular surgery-specific leadership development program. The SVS, working in collaboration with the VESS and SCVS, is pleased to announce a unique program opportunity for vascular surgeons 5-10 years post-training. The focus of the program will be on the development of leadership skills identified by members as most relevant to accelerating their leadership efforts at their home institution or practice, society or community. Be on the lookout for the program application, and all the details, next week. Completed applications will be due November 22nd. There will be a limit of 20 vascular surgeons selected in the first program cohort.

Based on member needs assessment, SVS members have been asking for a more comprehensive, vascular surgery-specific leadership development program. The SVS, working in collaboration with the VESS and SCVS, is pleased to announce a unique program opportunity for vascular surgeons 5-10 years post-training. The focus of the program will be on the development of leadership skills identified by members as most relevant to accelerating their leadership efforts at their home institution or practice, society or community. Be on the lookout for the program application, and all the details, next week. Completed applications will be due November 22nd. There will be a limit of 20 vascular surgeons selected in the first program cohort.

Based on member needs assessment, SVS members have been asking for a more comprehensive, vascular surgery-specific leadership development program. The SVS, working in collaboration with the VESS and SCVS, is pleased to announce a unique program opportunity for vascular surgeons 5-10 years post-training. The focus of the program will be on the development of leadership skills identified by members as most relevant to accelerating their leadership efforts at their home institution or practice, society or community. Be on the lookout for the program application, and all the details, next week. Completed applications will be due November 22nd. There will be a limit of 20 vascular surgeons selected in the first program cohort.

PHILADELPHIA – Women with polycystic ovary syndrome (PCOS) are at a higher risk for metabolic and psychiatric comorbidities prior to pregnancy, cardiometabolic complications during pregnancy, and cardiometabolic and psychiatric complications in the postpartum period, according to results from a prize paper at the annual meeting of the American Society for Reproductive Medicine.

Jeff Craven/MDedge News

“Our findings do support the ACOG [American College of Obstetricians and Gynecologists] recommendations that women with PCOS should be considered a high-risk group, and during the postpartum period should be screened for cardiovascular as well as psychiatric comorbidities,” Anuja Dokras, MD, PhD, director of the Penn Polycystic Ovary Syndrome Center at the University of Pennsylvania, Philadelphia, said in her presentation.

Dr. Dokras and colleagues performed a retrospective cohort study during 2000-2016 of patients aged 18-50 years, in the Optum claims database, which comprised 42,391 women with PCOS and 795,480 women without PCOS in 50 U.S. states. Women were included in the analysis if there were data available for at least 6 months to 1 year before pregnancy and between 6 weeks and 1 year after pregnancy. The researchers looked at risk factors prior to pregnancy, such as depression, hypertension, hyperlipidemia, diabetes, obesity, smoking, and use of assisted reproductive technology. During pregnancy, Dr. Dokras and colleagues analyzed complications such as preterm birth, multiple gestation, cesarean section, gestational hypertension and diabetes, preeclampsia and eclampsia, and depression in addition to outcomes in the postpartum period, such as hypertensive complications, thrombotic disease, peripartum cardiomyopathy, heart failure, arterial complications, perinatal and postpartum depression.

“Realizing that PCOS is underreported in administrative data sets, we looked at not only the diagnosis of PCOS but also tried to combine any menstrual irregularity and hirsutism occurring simultaneously, and then doing a sensitivity analysis and looking at the population,” said Dr. Dokras. “Similarly, knowing that misclassification can be an issue in these datasets, we did the same thing amongst the controls, looking for a single diagnosis of irregular menses and hirsutism.”

Prior to pregnancy, women with PCOS in the dataset tended to have a higher rate of obesity (14.7% vs. 4.7%), hyperlipidemia (11.3% vs. 5.3%), hypertension (6.2% vs. 2.5%), diabetes (5.3% vs. 1.2%), and depression (4.3% vs. 3.1%) and were also more likely to use assisted reproductive technology (5.2% vs. 1.0%) than were patients without PCOS (all P less than .001). During pregnancy, there was a higher rate of gestational diabetes (13.7% vs. 7.7%), preeclampsia (5.0% vs. 2.6%), preterm birth (16.9% vs. 12.2%), multiple gestation (6.6% vs. 2.5%), and cesarean section (45.1% vs. 32.9%) in patients with PCOS, compared with those without PCOS (all P less than .001).

For patients in the postpartum period, women with PCOS were more likely to experience postpartum thrombotic disease (adjusted odds ratio, 1.60; 95% confidence interval, 1.23-2.09; P = .001), hypertensive heart disease (aOR, 1.45; 95% CI, 1.04-2.01; P = .027), eclampsia (aOR, 1.45; 95% CI, 1.14-1.86; P = .003), heart failure (aOR, 1.33; 95% CI, 1.08-1.64; P = .007), preeclampsia (aOR, 1.30; 95% CI, 1.17-1.45; P = than .001), and peripartum cardiomyopathy (aOR, 1.26; 95% CI, 1.03-1.54; P = .027).

With regard to depression, women with PCOS also were at greater risk of developing perinatal (aOR, 1.27; 95% CI, 1.22-1.33) and postpartum (aOR, 1.46; 95% CI, 1.36-1.57) depression, compared with women without PCOS (both P less than .001).

Dr. Dokras acknowledged the limitations of administrative datasets and noted that prospective studies need to be conducted to verify their findings.

This study was funded by a grant from the National Institutes of Health. Dr. Dokras reported being a consultant for Medtronic, AbbVie, and Ferring.

SOURCE: Dokras A, et al. ASRM 2019. Abstract O-93.

PHILADELPHIA – Women with polycystic ovary syndrome (PCOS) are at a higher risk for metabolic and psychiatric comorbidities prior to pregnancy, cardiometabolic complications during pregnancy, and cardiometabolic and psychiatric complications in the postpartum period, according to results from a prize paper at the annual meeting of the American Society for Reproductive Medicine.

Jeff Craven/MDedge News

“Our findings do support the ACOG [American College of Obstetricians and Gynecologists] recommendations that women with PCOS should be considered a high-risk group, and during the postpartum period should be screened for cardiovascular as well as psychiatric comorbidities,” Anuja Dokras, MD, PhD, director of the Penn Polycystic Ovary Syndrome Center at the University of Pennsylvania, Philadelphia, said in her presentation.

Dr. Dokras and colleagues performed a retrospective cohort study during 2000-2016 of patients aged 18-50 years, in the Optum claims database, which comprised 42,391 women with PCOS and 795,480 women without PCOS in 50 U.S. states. Women were included in the analysis if there were data available for at least 6 months to 1 year before pregnancy and between 6 weeks and 1 year after pregnancy. The researchers looked at risk factors prior to pregnancy, such as depression, hypertension, hyperlipidemia, diabetes, obesity, smoking, and use of assisted reproductive technology. During pregnancy, Dr. Dokras and colleagues analyzed complications such as preterm birth, multiple gestation, cesarean section, gestational hypertension and diabetes, preeclampsia and eclampsia, and depression in addition to outcomes in the postpartum period, such as hypertensive complications, thrombotic disease, peripartum cardiomyopathy, heart failure, arterial complications, perinatal and postpartum depression.

“Realizing that PCOS is underreported in administrative data sets, we looked at not only the diagnosis of PCOS but also tried to combine any menstrual irregularity and hirsutism occurring simultaneously, and then doing a sensitivity analysis and looking at the population,” said Dr. Dokras. “Similarly, knowing that misclassification can be an issue in these datasets, we did the same thing amongst the controls, looking for a single diagnosis of irregular menses and hirsutism.”

Prior to pregnancy, women with PCOS in the dataset tended to have a higher rate of obesity (14.7% vs. 4.7%), hyperlipidemia (11.3% vs. 5.3%), hypertension (6.2% vs. 2.5%), diabetes (5.3% vs. 1.2%), and depression (4.3% vs. 3.1%) and were also more likely to use assisted reproductive technology (5.2% vs. 1.0%) than were patients without PCOS (all P less than .001). During pregnancy, there was a higher rate of gestational diabetes (13.7% vs. 7.7%), preeclampsia (5.0% vs. 2.6%), preterm birth (16.9% vs. 12.2%), multiple gestation (6.6% vs. 2.5%), and cesarean section (45.1% vs. 32.9%) in patients with PCOS, compared with those without PCOS (all P less than .001).

For patients in the postpartum period, women with PCOS were more likely to experience postpartum thrombotic disease (adjusted odds ratio, 1.60; 95% confidence interval, 1.23-2.09; P = .001), hypertensive heart disease (aOR, 1.45; 95% CI, 1.04-2.01; P = .027), eclampsia (aOR, 1.45; 95% CI, 1.14-1.86; P = .003), heart failure (aOR, 1.33; 95% CI, 1.08-1.64; P = .007), preeclampsia (aOR, 1.30; 95% CI, 1.17-1.45; P = than .001), and peripartum cardiomyopathy (aOR, 1.26; 95% CI, 1.03-1.54; P = .027).

With regard to depression, women with PCOS also were at greater risk of developing perinatal (aOR, 1.27; 95% CI, 1.22-1.33) and postpartum (aOR, 1.46; 95% CI, 1.36-1.57) depression, compared with women without PCOS (both P less than .001).

Dr. Dokras acknowledged the limitations of administrative datasets and noted that prospective studies need to be conducted to verify their findings.

This study was funded by a grant from the National Institutes of Health. Dr. Dokras reported being a consultant for Medtronic, AbbVie, and Ferring.

SOURCE: Dokras A, et al. ASRM 2019. Abstract O-93.

PHILADELPHIA – Women with polycystic ovary syndrome (PCOS) are at a higher risk for metabolic and psychiatric comorbidities prior to pregnancy, cardiometabolic complications during pregnancy, and cardiometabolic and psychiatric complications in the postpartum period, according to results from a prize paper at the annual meeting of the American Society for Reproductive Medicine.

Jeff Craven/MDedge News

“Our findings do support the ACOG [American College of Obstetricians and Gynecologists] recommendations that women with PCOS should be considered a high-risk group, and during the postpartum period should be screened for cardiovascular as well as psychiatric comorbidities,” Anuja Dokras, MD, PhD, director of the Penn Polycystic Ovary Syndrome Center at the University of Pennsylvania, Philadelphia, said in her presentation.

Dr. Dokras and colleagues performed a retrospective cohort study during 2000-2016 of patients aged 18-50 years, in the Optum claims database, which comprised 42,391 women with PCOS and 795,480 women without PCOS in 50 U.S. states. Women were included in the analysis if there were data available for at least 6 months to 1 year before pregnancy and between 6 weeks and 1 year after pregnancy. The researchers looked at risk factors prior to pregnancy, such as depression, hypertension, hyperlipidemia, diabetes, obesity, smoking, and use of assisted reproductive technology. During pregnancy, Dr. Dokras and colleagues analyzed complications such as preterm birth, multiple gestation, cesarean section, gestational hypertension and diabetes, preeclampsia and eclampsia, and depression in addition to outcomes in the postpartum period, such as hypertensive complications, thrombotic disease, peripartum cardiomyopathy, heart failure, arterial complications, perinatal and postpartum depression.

“Realizing that PCOS is underreported in administrative data sets, we looked at not only the diagnosis of PCOS but also tried to combine any menstrual irregularity and hirsutism occurring simultaneously, and then doing a sensitivity analysis and looking at the population,” said Dr. Dokras. “Similarly, knowing that misclassification can be an issue in these datasets, we did the same thing amongst the controls, looking for a single diagnosis of irregular menses and hirsutism.”

Prior to pregnancy, women with PCOS in the dataset tended to have a higher rate of obesity (14.7% vs. 4.7%), hyperlipidemia (11.3% vs. 5.3%), hypertension (6.2% vs. 2.5%), diabetes (5.3% vs. 1.2%), and depression (4.3% vs. 3.1%) and were also more likely to use assisted reproductive technology (5.2% vs. 1.0%) than were patients without PCOS (all P less than .001). During pregnancy, there was a higher rate of gestational diabetes (13.7% vs. 7.7%), preeclampsia (5.0% vs. 2.6%), preterm birth (16.9% vs. 12.2%), multiple gestation (6.6% vs. 2.5%), and cesarean section (45.1% vs. 32.9%) in patients with PCOS, compared with those without PCOS (all P less than .001).

For patients in the postpartum period, women with PCOS were more likely to experience postpartum thrombotic disease (adjusted odds ratio, 1.60; 95% confidence interval, 1.23-2.09; P = .001), hypertensive heart disease (aOR, 1.45; 95% CI, 1.04-2.01; P = .027), eclampsia (aOR, 1.45; 95% CI, 1.14-1.86; P = .003), heart failure (aOR, 1.33; 95% CI, 1.08-1.64; P = .007), preeclampsia (aOR, 1.30; 95% CI, 1.17-1.45; P = than .001), and peripartum cardiomyopathy (aOR, 1.26; 95% CI, 1.03-1.54; P = .027).

With regard to depression, women with PCOS also were at greater risk of developing perinatal (aOR, 1.27; 95% CI, 1.22-1.33) and postpartum (aOR, 1.46; 95% CI, 1.36-1.57) depression, compared with women without PCOS (both P less than .001).

Dr. Dokras acknowledged the limitations of administrative datasets and noted that prospective studies need to be conducted to verify their findings.

This study was funded by a grant from the National Institutes of Health. Dr. Dokras reported being a consultant for Medtronic, AbbVie, and Ferring.

SOURCE: Dokras A, et al. ASRM 2019. Abstract O-93.

Regular low-level alcohol consumption may be a bigger risk factor for new-onset atrial fibrillation than binge drinking, according to a paper published online in EP Europace.

Nikada/iStockphoto

Alcohol consumption is known to have a dose-dependent association with the risk of new-onset atrial fibrillation (AFib), but the mechanism underlying this association was not clear, according to Yun Gi Kim, MD, from the Seoul National University (South Korea), and coauthors.

They analyzed data from the Korean National Health Insurance Service database for 9,776,956 individuals without atrial fibrillation at baseline, including health survey information about their alcohol consumption.

Overall, 51.3% of the study population were classified as nondrinkers, 32.1% were mild drinkers – defined as up to 105 g of alcohol consumed per week ­– 9.7% were moderate drinkers consuming 105-210 g/week, and 6.9% were heavy drinkers consuming 210 g or more per week.

The analysis revealed that heavy drinkers had the highest risk for new-onset AFib – 21.5% higher than mild drinkers – while nondrinkers had an 8.6% higher risk and moderate drinkers had a 7.7% higher risk, compared with mild drinkers.

It also showed an association between the number of drinking sessions per week and the development of new-onset atrial fibrillation. Individuals who only drank once per week had the lowest risk of AFib while those who drank every day had the highest.

“Although weekly alcohol intake was associated with the risk of new-onset [AFib], such association was lost when drinking frequency was included in the multivariate model,” the authors wrote.

They found a significant inverse relationship between the amount of alcohol consumed per drinking session, and the risk of new-onset AFib, such that individuals who consumed low amounts of alcohol per session had a higher risk, and the risk decreased as higher amounts were consumed.

“Regardless of whether weekly alcohol intake exceeded 210 g, the frequency of drinking was significantly associated with risk of new-onset [AFib],” they reported. “Patients who drink everyday represented the highest-risk group and those who drink once per week were the lowest-risk group for new-onset [AFib] in this investigation, respectively.”

The authors speculated that if alcohol consumption can trigger AFib, then multiple drinking episodes per week, regardless of amount, might trigger more episodes of AFib and potentially lead to the development of overt, new-onset disease. They also suggested that frequent drinking could lead to regular sleep disturbance, which might also contribute to the link with atrial fibrillation.

The study was supported by Korea University, Korea University Anam Hospital, Republic of Korea, the National Research Foundation of Korea, the Ministry of Education and the Ministry of Science, ICT, and Future Planning. No conflicts of interest were declared.

SOURCE: Kim YG et al. EP Europace. 2019 Oct 17. doi: 10.1093/europace/euz256.

Regular low-level alcohol consumption may be a bigger risk factor for new-onset atrial fibrillation than binge drinking, according to a paper published online in EP Europace.

Nikada/iStockphoto

Alcohol consumption is known to have a dose-dependent association with the risk of new-onset atrial fibrillation (AFib), but the mechanism underlying this association was not clear, according to Yun Gi Kim, MD, from the Seoul National University (South Korea), and coauthors.

They analyzed data from the Korean National Health Insurance Service database for 9,776,956 individuals without atrial fibrillation at baseline, including health survey information about their alcohol consumption.

Overall, 51.3% of the study population were classified as nondrinkers, 32.1% were mild drinkers – defined as up to 105 g of alcohol consumed per week ­– 9.7% were moderate drinkers consuming 105-210 g/week, and 6.9% were heavy drinkers consuming 210 g or more per week.

The analysis revealed that heavy drinkers had the highest risk for new-onset AFib – 21.5% higher than mild drinkers – while nondrinkers had an 8.6% higher risk and moderate drinkers had a 7.7% higher risk, compared with mild drinkers.

It also showed an association between the number of drinking sessions per week and the development of new-onset atrial fibrillation. Individuals who only drank once per week had the lowest risk of AFib while those who drank every day had the highest.

“Although weekly alcohol intake was associated with the risk of new-onset [AFib], such association was lost when drinking frequency was included in the multivariate model,” the authors wrote.

They found a significant inverse relationship between the amount of alcohol consumed per drinking session, and the risk of new-onset AFib, such that individuals who consumed low amounts of alcohol per session had a higher risk, and the risk decreased as higher amounts were consumed.

“Regardless of whether weekly alcohol intake exceeded 210 g, the frequency of drinking was significantly associated with risk of new-onset [AFib],” they reported. “Patients who drink everyday represented the highest-risk group and those who drink once per week were the lowest-risk group for new-onset [AFib] in this investigation, respectively.”

The authors speculated that if alcohol consumption can trigger AFib, then multiple drinking episodes per week, regardless of amount, might trigger more episodes of AFib and potentially lead to the development of overt, new-onset disease. They also suggested that frequent drinking could lead to regular sleep disturbance, which might also contribute to the link with atrial fibrillation.

The study was supported by Korea University, Korea University Anam Hospital, Republic of Korea, the National Research Foundation of Korea, the Ministry of Education and the Ministry of Science, ICT, and Future Planning. No conflicts of interest were declared.

SOURCE: Kim YG et al. EP Europace. 2019 Oct 17. doi: 10.1093/europace/euz256.

Regular low-level alcohol consumption may be a bigger risk factor for new-onset atrial fibrillation than binge drinking, according to a paper published online in EP Europace.

Nikada/iStockphoto

Alcohol consumption is known to have a dose-dependent association with the risk of new-onset atrial fibrillation (AFib), but the mechanism underlying this association was not clear, according to Yun Gi Kim, MD, from the Seoul National University (South Korea), and coauthors.

They analyzed data from the Korean National Health Insurance Service database for 9,776,956 individuals without atrial fibrillation at baseline, including health survey information about their alcohol consumption.

Overall, 51.3% of the study population were classified as nondrinkers, 32.1% were mild drinkers – defined as up to 105 g of alcohol consumed per week ­– 9.7% were moderate drinkers consuming 105-210 g/week, and 6.9% were heavy drinkers consuming 210 g or more per week.

The analysis revealed that heavy drinkers had the highest risk for new-onset AFib – 21.5% higher than mild drinkers – while nondrinkers had an 8.6% higher risk and moderate drinkers had a 7.7% higher risk, compared with mild drinkers.

It also showed an association between the number of drinking sessions per week and the development of new-onset atrial fibrillation. Individuals who only drank once per week had the lowest risk of AFib while those who drank every day had the highest.

“Although weekly alcohol intake was associated with the risk of new-onset [AFib], such association was lost when drinking frequency was included in the multivariate model,” the authors wrote.

They found a significant inverse relationship between the amount of alcohol consumed per drinking session, and the risk of new-onset AFib, such that individuals who consumed low amounts of alcohol per session had a higher risk, and the risk decreased as higher amounts were consumed.

“Regardless of whether weekly alcohol intake exceeded 210 g, the frequency of drinking was significantly associated with risk of new-onset [AFib],” they reported. “Patients who drink everyday represented the highest-risk group and those who drink once per week were the lowest-risk group for new-onset [AFib] in this investigation, respectively.”

The authors speculated that if alcohol consumption can trigger AFib, then multiple drinking episodes per week, regardless of amount, might trigger more episodes of AFib and potentially lead to the development of overt, new-onset disease. They also suggested that frequent drinking could lead to regular sleep disturbance, which might also contribute to the link with atrial fibrillation.

The study was supported by Korea University, Korea University Anam Hospital, Republic of Korea, the National Research Foundation of Korea, the Ministry of Education and the Ministry of Science, ICT, and Future Planning. No conflicts of interest were declared.

SOURCE: Kim YG et al. EP Europace. 2019 Oct 17. doi: 10.1093/europace/euz256.

A new study has found that beta-blocker treatment did not prevent exacerbations in patients with moderate or severe chronic obstructive pulmonary disease (COPD).

decade3d/Thinkstock

“These results differ from previously reported findings from observational studies suggesting that beta-blockers reduce the risks of exacerbation and death from any cause in patients with COPD,” wrote Mark T. Dransfield, MD, of the University of Alabama at Birmingham and coauthors. Their findings were presented at the annual meeting of the American College of Chest Physicians and also were published simultaneously in the New England Journal of Medicine.

To determine the value of beta-blockers as a potential treatment for COPD, the researchers launched a prospective randomized trial called BLOCK COPD, consisting of 532 patients with moderate or severe COPD. They were assigned to two groups: those receiving extended-release metoprolol (n = 268) and those receiving placebo (n = 264). The mean age of all patients was 65 years.

The groups saw no significant difference in median time until the first exacerbation, which was 202 days (95% confidence interval, 162-282) in the metoprolol group and 222 days (95% CI, 189-295) in the placebo group (hazard ratio, 1.05; 95% CI, 0.84-1.32; P = .66). Metoprolol was associated with a higher risk of severe or very severe exacerbations leading to hospitalization (HR, 1.91; 95% CI, 1.29-2.83). During treatment, there were 11 deaths in the metoprolol group and 5 deaths in the placebo group.

Though there was no evidence of increases in patient-reported adverse events related to metoprolol, more discontinuations did occur in the metoprolol group compared with placebo (11.2% vs. 6.1%).

The authors acknowledged their study’s limitations, chiefly including the fact that the trial was ended early “on the basis of the conditional power analyses and concern about safety.” In addition, the reduction of heart rate and blood pressure in the metoprolol group made it impossible to fully blind the study. Finally, many patients in the trial had already suffered the effects of moderate to severe COPD, including previous hospitalization and the need for supplemental oxygen, leading to uncertainty as to “whether our results would apply to patients with mild airflow obstruction or a lower exacerbation risk.”

The study was supported by a grant from the Department of Defense. The authors reported numerous potential conflicts of interest, including receiving grants, personal fees and research funds from various pharmaceutical companies and government entities.
 

SOURCE: Dransfield MT et al. CHEST 2019. 2019 Oct 20. doi: 10.1056/NEJMoa1908142.

A new study has found that beta-blocker treatment did not prevent exacerbations in patients with moderate or severe chronic obstructive pulmonary disease (COPD).

decade3d/Thinkstock

“These results differ from previously reported findings from observational studies suggesting that beta-blockers reduce the risks of exacerbation and death from any cause in patients with COPD,” wrote Mark T. Dransfield, MD, of the University of Alabama at Birmingham and coauthors. Their findings were presented at the annual meeting of the American College of Chest Physicians and also were published simultaneously in the New England Journal of Medicine.

To determine the value of beta-blockers as a potential treatment for COPD, the researchers launched a prospective randomized trial called BLOCK COPD, consisting of 532 patients with moderate or severe COPD. They were assigned to two groups: those receiving extended-release metoprolol (n = 268) and those receiving placebo (n = 264). The mean age of all patients was 65 years.

The groups saw no significant difference in median time until the first exacerbation, which was 202 days (95% confidence interval, 162-282) in the metoprolol group and 222 days (95% CI, 189-295) in the placebo group (hazard ratio, 1.05; 95% CI, 0.84-1.32; P = .66). Metoprolol was associated with a higher risk of severe or very severe exacerbations leading to hospitalization (HR, 1.91; 95% CI, 1.29-2.83). During treatment, there were 11 deaths in the metoprolol group and 5 deaths in the placebo group.

Though there was no evidence of increases in patient-reported adverse events related to metoprolol, more discontinuations did occur in the metoprolol group compared with placebo (11.2% vs. 6.1%).

The authors acknowledged their study’s limitations, chiefly including the fact that the trial was ended early “on the basis of the conditional power analyses and concern about safety.” In addition, the reduction of heart rate and blood pressure in the metoprolol group made it impossible to fully blind the study. Finally, many patients in the trial had already suffered the effects of moderate to severe COPD, including previous hospitalization and the need for supplemental oxygen, leading to uncertainty as to “whether our results would apply to patients with mild airflow obstruction or a lower exacerbation risk.”

The study was supported by a grant from the Department of Defense. The authors reported numerous potential conflicts of interest, including receiving grants, personal fees and research funds from various pharmaceutical companies and government entities.
 

SOURCE: Dransfield MT et al. CHEST 2019. 2019 Oct 20. doi: 10.1056/NEJMoa1908142.

A new study has found that beta-blocker treatment did not prevent exacerbations in patients with moderate or severe chronic obstructive pulmonary disease (COPD).

decade3d/Thinkstock

“These results differ from previously reported findings from observational studies suggesting that beta-blockers reduce the risks of exacerbation and death from any cause in patients with COPD,” wrote Mark T. Dransfield, MD, of the University of Alabama at Birmingham and coauthors. Their findings were presented at the annual meeting of the American College of Chest Physicians and also were published simultaneously in the New England Journal of Medicine.

To determine the value of beta-blockers as a potential treatment for COPD, the researchers launched a prospective randomized trial called BLOCK COPD, consisting of 532 patients with moderate or severe COPD. They were assigned to two groups: those receiving extended-release metoprolol (n = 268) and those receiving placebo (n = 264). The mean age of all patients was 65 years.

The groups saw no significant difference in median time until the first exacerbation, which was 202 days (95% confidence interval, 162-282) in the metoprolol group and 222 days (95% CI, 189-295) in the placebo group (hazard ratio, 1.05; 95% CI, 0.84-1.32; P = .66). Metoprolol was associated with a higher risk of severe or very severe exacerbations leading to hospitalization (HR, 1.91; 95% CI, 1.29-2.83). During treatment, there were 11 deaths in the metoprolol group and 5 deaths in the placebo group.

Though there was no evidence of increases in patient-reported adverse events related to metoprolol, more discontinuations did occur in the metoprolol group compared with placebo (11.2% vs. 6.1%).

The authors acknowledged their study’s limitations, chiefly including the fact that the trial was ended early “on the basis of the conditional power analyses and concern about safety.” In addition, the reduction of heart rate and blood pressure in the metoprolol group made it impossible to fully blind the study. Finally, many patients in the trial had already suffered the effects of moderate to severe COPD, including previous hospitalization and the need for supplemental oxygen, leading to uncertainty as to “whether our results would apply to patients with mild airflow obstruction or a lower exacerbation risk.”

The study was supported by a grant from the Department of Defense. The authors reported numerous potential conflicts of interest, including receiving grants, personal fees and research funds from various pharmaceutical companies and government entities.
 

SOURCE: Dransfield MT et al. CHEST 2019. 2019 Oct 20. doi: 10.1056/NEJMoa1908142.

AUSTIN, TEX. – Patients with peripheral neuropathy may benefit from genetic testing to determine of the cause of their neuropathy even if they do not have a family history of the condition, according to new research.

The same research identified more than 80 genetic variants in patients with neuropathy who lacked any other known genetic mutations, potentially representing not-yet-identified pathogenic mutations.

Sasa Zivkovic, MD, PhD, of the University of Pittsburgh Medical Center (UPMC), and associates shared a poster of their findings at the annual meeting of the American Association for Neuromuscular and Electrodiagnostic Medicine.

The researchers conducted next-generation sequencing (NGS) on 85 adult patients with peripheral neuropathy at the UPMC Neuromuscular Clinic during May 2017–Feb. 2019. The targeted NGS panel included 70 genes. The patients, aged 60 years on average, were primarily from Allegheny County, Pa., and had neuropathy either suspected to be hereditary or of unknown etiology.

Among the 19% of patients (n = 16) who tested positive for a known pathogenic mutation, half had Charcot-Marie-Tooth disease type 1A (CMT1A). Two patients – 13% of those with pathogenic variants – had hereditary neuropathy with liability to pressure palsies, and two had CMT1X. The remaining four patients had CMT1B, CMT2B1, CMT2E, and hereditary sensory and autonomic neuropathy mutations.

Another 4% of the overall patient sample (n = 3) had likely pathogenic mutations in genes associated with CMT2S, CMT4C and CMT4F. A third of the patients (32%) tested negative for the full NGS panel, and, comprising the largest proportion of patients, 46% had variants of unknown significance.

“The high occurrence of variants of unknown significance has uncertain significance but some variations may represent unrecognized pathogenic mutations,” the authors noted.

They identified 81 of these variants, with the DST, PLEKHG5, and SPG11 genes most commonly affected, each found in six patients. Four patients had a variant in the next most commonly affected gene, SBF2. The following variants occurred in three people each: BICD2, NEFL3, PRX, SCN11A, SCN9A, SLC52A2, and WNK1.

Among the 73 patients who underwent electrodiagnostic testing, 44 had sporadic axonal neuropathy, 17 had sporadic demyelinating neuropathy, and 11 had mixed neuropathies; the 1 remaining patient was not accounted for. Positive genetic testing occurred in a third (32%) of those with familial neuropathy (n = 28) and in 12% of those with sporadic neuropathy (n = 57).

No external funding was noted, and the authors had no disclosures.

SOURCE: Zivkovic S et al. AANEM 2019. Abstract 160. Targeted genetic testing in the evaluation of neuropathy .

AUSTIN, TEX. – Patients with peripheral neuropathy may benefit from genetic testing to determine of the cause of their neuropathy even if they do not have a family history of the condition, according to new research.

The same research identified more than 80 genetic variants in patients with neuropathy who lacked any other known genetic mutations, potentially representing not-yet-identified pathogenic mutations.

Sasa Zivkovic, MD, PhD, of the University of Pittsburgh Medical Center (UPMC), and associates shared a poster of their findings at the annual meeting of the American Association for Neuromuscular and Electrodiagnostic Medicine.

The researchers conducted next-generation sequencing (NGS) on 85 adult patients with peripheral neuropathy at the UPMC Neuromuscular Clinic during May 2017–Feb. 2019. The targeted NGS panel included 70 genes. The patients, aged 60 years on average, were primarily from Allegheny County, Pa., and had neuropathy either suspected to be hereditary or of unknown etiology.

Among the 19% of patients (n = 16) who tested positive for a known pathogenic mutation, half had Charcot-Marie-Tooth disease type 1A (CMT1A). Two patients – 13% of those with pathogenic variants – had hereditary neuropathy with liability to pressure palsies, and two had CMT1X. The remaining four patients had CMT1B, CMT2B1, CMT2E, and hereditary sensory and autonomic neuropathy mutations.

Another 4% of the overall patient sample (n = 3) had likely pathogenic mutations in genes associated with CMT2S, CMT4C and CMT4F. A third of the patients (32%) tested negative for the full NGS panel, and, comprising the largest proportion of patients, 46% had variants of unknown significance.

“The high occurrence of variants of unknown significance has uncertain significance but some variations may represent unrecognized pathogenic mutations,” the authors noted.

They identified 81 of these variants, with the DST, PLEKHG5, and SPG11 genes most commonly affected, each found in six patients. Four patients had a variant in the next most commonly affected gene, SBF2. The following variants occurred in three people each: BICD2, NEFL3, PRX, SCN11A, SCN9A, SLC52A2, and WNK1.

Among the 73 patients who underwent electrodiagnostic testing, 44 had sporadic axonal neuropathy, 17 had sporadic demyelinating neuropathy, and 11 had mixed neuropathies; the 1 remaining patient was not accounted for. Positive genetic testing occurred in a third (32%) of those with familial neuropathy (n = 28) and in 12% of those with sporadic neuropathy (n = 57).

No external funding was noted, and the authors had no disclosures.

SOURCE: Zivkovic S et al. AANEM 2019. Abstract 160. Targeted genetic testing in the evaluation of neuropathy .

AUSTIN, TEX. – Patients with peripheral neuropathy may benefit from genetic testing to determine of the cause of their neuropathy even if they do not have a family history of the condition, according to new research.

The same research identified more than 80 genetic variants in patients with neuropathy who lacked any other known genetic mutations, potentially representing not-yet-identified pathogenic mutations.

Sasa Zivkovic, MD, PhD, of the University of Pittsburgh Medical Center (UPMC), and associates shared a poster of their findings at the annual meeting of the American Association for Neuromuscular and Electrodiagnostic Medicine.

The researchers conducted next-generation sequencing (NGS) on 85 adult patients with peripheral neuropathy at the UPMC Neuromuscular Clinic during May 2017–Feb. 2019. The targeted NGS panel included 70 genes. The patients, aged 60 years on average, were primarily from Allegheny County, Pa., and had neuropathy either suspected to be hereditary or of unknown etiology.

Among the 19% of patients (n = 16) who tested positive for a known pathogenic mutation, half had Charcot-Marie-Tooth disease type 1A (CMT1A). Two patients – 13% of those with pathogenic variants – had hereditary neuropathy with liability to pressure palsies, and two had CMT1X. The remaining four patients had CMT1B, CMT2B1, CMT2E, and hereditary sensory and autonomic neuropathy mutations.

Another 4% of the overall patient sample (n = 3) had likely pathogenic mutations in genes associated with CMT2S, CMT4C and CMT4F. A third of the patients (32%) tested negative for the full NGS panel, and, comprising the largest proportion of patients, 46% had variants of unknown significance.

“The high occurrence of variants of unknown significance has uncertain significance but some variations may represent unrecognized pathogenic mutations,” the authors noted.

They identified 81 of these variants, with the DST, PLEKHG5, and SPG11 genes most commonly affected, each found in six patients. Four patients had a variant in the next most commonly affected gene, SBF2. The following variants occurred in three people each: BICD2, NEFL3, PRX, SCN11A, SCN9A, SLC52A2, and WNK1.

Among the 73 patients who underwent electrodiagnostic testing, 44 had sporadic axonal neuropathy, 17 had sporadic demyelinating neuropathy, and 11 had mixed neuropathies; the 1 remaining patient was not accounted for. Positive genetic testing occurred in a third (32%) of those with familial neuropathy (n = 28) and in 12% of those with sporadic neuropathy (n = 57).

No external funding was noted, and the authors had no disclosures.

SOURCE: Zivkovic S et al. AANEM 2019. Abstract 160. Targeted genetic testing in the evaluation of neuropathy .

Lung function appears to continue to decline even decades after smoking cessation, according to new data from the National Heart, Lung, and Blood Institute Pooled Cohort Study. Compared with never-smokers, former smokers had a decline in forced expiratory volume in 1 second (FEV₁) about 20% as severe as current smokers, but nevertheless higher than never-smokers. Low-intensity smokers also fared worse than never-smokers, suggesting that no amount of smoke exposure should be considered safe.

bilderbox/fotolia.com

The increased decline occurred even decades after smoking cessation, according to the study published in Lancet Respiratory Medicine, which was led by Elizabeth Oelsner, MD, MPH, of Columbia University, New York. Smoking prevalence has decreased from 42% to 16% in the past 50 years, and many smokers report that they smoke fewer cigarettes per day, from an average of 21 to 14, according to the authors. Despite those trends, the prevalence of chronic obstructive pulmonary disease has continued to increase, and is now the third-leading cause of death worldwide.

A meta-analysis of 47 studies and 88,887 adults found no association between smoking and FEV₁ decline, but many of the studies were small or focused on nonrepresentative populations, and they used variably standardized spirometry.

The study pooled data from nine individual U.S. cohorts, with 25,352 participants recruited during 1983-2016. Subjects included those who underwent at least two prebronchodilator spirometry tests following American Thoracic Society standards. After adjustment, former smokers had increased FEV₁ decline of 1.82 mL/year (P less than .0001), compared with never-smokers. Current smokers had an increased decline of 9.21 mL/year (P less than .0001).

Even after decades of abstinence, the effects of smoking appeared to linger: 20-30 years later, FEV₁ loss was accelerated by 2.50 mL/year (P less than .0001), and by 0.93 mL/year (P = .0104) after 30 years, compared with never-smokers.

Even low-intensity smokers (cumulative less than 10 pack-years) had an significantly accelerated FEV₁ decline (0.87 mL; P = .0153).

The researchers also found a relationship between FEV₁ decline and intensity of current smoking: Those smoking fewer than 5 cigarettes per day had a lower decline than those smoking 30 or more (7.65 mL; 95% confidence interval, 6.21-9.09 vs. 11.24 mL; 95% CI, 9.86-12.62).

The study is limited by the fact that smoking status and daily tobacco reporting were self-reported, which could result in information bias.

The study was funded by the National Institutes of Health, National Heart Lung and Blood Institute, and U.S. Environmental Protection Agency. The authors report personal fees, consultancy fees, or grants from a wide variety of pharmaceutical companies.
 

SOURCE: Oelsner EC et al. Lancet Respir Med. 2019 Oct 9. doi: 10.1016/S2213-2600(19)30276-0.

Lung function appears to continue to decline even decades after smoking cessation, according to new data from the National Heart, Lung, and Blood Institute Pooled Cohort Study. Compared with never-smokers, former smokers had a decline in forced expiratory volume in 1 second (FEV₁) about 20% as severe as current smokers, but nevertheless higher than never-smokers. Low-intensity smokers also fared worse than never-smokers, suggesting that no amount of smoke exposure should be considered safe.

bilderbox/fotolia.com

The increased decline occurred even decades after smoking cessation, according to the study published in Lancet Respiratory Medicine, which was led by Elizabeth Oelsner, MD, MPH, of Columbia University, New York. Smoking prevalence has decreased from 42% to 16% in the past 50 years, and many smokers report that they smoke fewer cigarettes per day, from an average of 21 to 14, according to the authors. Despite those trends, the prevalence of chronic obstructive pulmonary disease has continued to increase, and is now the third-leading cause of death worldwide.

A meta-analysis of 47 studies and 88,887 adults found no association between smoking and FEV₁ decline, but many of the studies were small or focused on nonrepresentative populations, and they used variably standardized spirometry.

The study pooled data from nine individual U.S. cohorts, with 25,352 participants recruited during 1983-2016. Subjects included those who underwent at least two prebronchodilator spirometry tests following American Thoracic Society standards. After adjustment, former smokers had increased FEV₁ decline of 1.82 mL/year (P less than .0001), compared with never-smokers. Current smokers had an increased decline of 9.21 mL/year (P less than .0001).

Even after decades of abstinence, the effects of smoking appeared to linger: 20-30 years later, FEV₁ loss was accelerated by 2.50 mL/year (P less than .0001), and by 0.93 mL/year (P = .0104) after 30 years, compared with never-smokers.

Even low-intensity smokers (cumulative less than 10 pack-years) had an significantly accelerated FEV₁ decline (0.87 mL; P = .0153).

The researchers also found a relationship between FEV₁ decline and intensity of current smoking: Those smoking fewer than 5 cigarettes per day had a lower decline than those smoking 30 or more (7.65 mL; 95% confidence interval, 6.21-9.09 vs. 11.24 mL; 95% CI, 9.86-12.62).

The study is limited by the fact that smoking status and daily tobacco reporting were self-reported, which could result in information bias.

The study was funded by the National Institutes of Health, National Heart Lung and Blood Institute, and U.S. Environmental Protection Agency. The authors report personal fees, consultancy fees, or grants from a wide variety of pharmaceutical companies.
 

SOURCE: Oelsner EC et al. Lancet Respir Med. 2019 Oct 9. doi: 10.1016/S2213-2600(19)30276-0.

Lung function appears to continue to decline even decades after smoking cessation, according to new data from the National Heart, Lung, and Blood Institute Pooled Cohort Study. Compared with never-smokers, former smokers had a decline in forced expiratory volume in 1 second (FEV₁) about 20% as severe as current smokers, but nevertheless higher than never-smokers. Low-intensity smokers also fared worse than never-smokers, suggesting that no amount of smoke exposure should be considered safe.

bilderbox/fotolia.com

The increased decline occurred even decades after smoking cessation, according to the study published in Lancet Respiratory Medicine, which was led by Elizabeth Oelsner, MD, MPH, of Columbia University, New York. Smoking prevalence has decreased from 42% to 16% in the past 50 years, and many smokers report that they smoke fewer cigarettes per day, from an average of 21 to 14, according to the authors. Despite those trends, the prevalence of chronic obstructive pulmonary disease has continued to increase, and is now the third-leading cause of death worldwide.

A meta-analysis of 47 studies and 88,887 adults found no association between smoking and FEV₁ decline, but many of the studies were small or focused on nonrepresentative populations, and they used variably standardized spirometry.

The study pooled data from nine individual U.S. cohorts, with 25,352 participants recruited during 1983-2016. Subjects included those who underwent at least two prebronchodilator spirometry tests following American Thoracic Society standards. After adjustment, former smokers had increased FEV₁ decline of 1.82 mL/year (P less than .0001), compared with never-smokers. Current smokers had an increased decline of 9.21 mL/year (P less than .0001).

Even after decades of abstinence, the effects of smoking appeared to linger: 20-30 years later, FEV₁ loss was accelerated by 2.50 mL/year (P less than .0001), and by 0.93 mL/year (P = .0104) after 30 years, compared with never-smokers.

Even low-intensity smokers (cumulative less than 10 pack-years) had an significantly accelerated FEV₁ decline (0.87 mL; P = .0153).

The researchers also found a relationship between FEV₁ decline and intensity of current smoking: Those smoking fewer than 5 cigarettes per day had a lower decline than those smoking 30 or more (7.65 mL; 95% confidence interval, 6.21-9.09 vs. 11.24 mL; 95% CI, 9.86-12.62).

The study is limited by the fact that smoking status and daily tobacco reporting were self-reported, which could result in information bias.

The study was funded by the National Institutes of Health, National Heart Lung and Blood Institute, and U.S. Environmental Protection Agency. The authors report personal fees, consultancy fees, or grants from a wide variety of pharmaceutical companies.
 

SOURCE: Oelsner EC et al. Lancet Respir Med. 2019 Oct 9. doi: 10.1016/S2213-2600(19)30276-0.

Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.

“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.

In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A_1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.

Although FBG and HbA_1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.

The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.

However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.

The researchers had no financial conflicts to disclose.
 

SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.

Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.

“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.

In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A_1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.

Although FBG and HbA_1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.

The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.

However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.

The researchers had no financial conflicts to disclose.
 

SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.

Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.

“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.

In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A_1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.

Although FBG and HbA_1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.

The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.

However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.

The researchers had no financial conflicts to disclose.
 

SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.