Jim Kling

Exposure during pregnancy to a specific per- and polyfluoroalkyl substance (PFAS), combined with a low cholesterol level, is linked to a heightened risk of abdominal and whole-body obesity in granddaughters, according to a new analysis of the Child Health and Development Studies, which have been ongoing since the 1960s.

Researchers directly measured levels of N-ethyl-perfluorooctane sulfonamido acetic acid (EtFOSAA) in blood samples from the grandmothers, which had been taken shortly after delivery, and then analyzed measures of obesity and other metabolic factors in their daughters at ages 30 years and 50 years, and their granddaughters at age 20.

PFASs are synthetic compounds commonly used as oil and water repellents; coatings for cookware, carpets, and textiles; and as firefighting foams. The compounds do not break down in the environment or the human body and accumulate over time. They are known to disrupt the endocrine system.

EtFOSAA is a metabolite of a raw material used in the manufacturing of packaging and paper products, and itself gets converted to perfluorooctane sulfonic acid (PFOS), which is extremely stable in the environment and within organisms, leading to bioaccumulation that has the potential to span generations, Barbara A. Cohn, PhD, director of child health and development studies at the Public Health Institute in Berkeley, Calif., said during a virtual press conference held by The Endocrine Society. The study was slated for presentation during ENDO 2020, the society’s annual meeting, which was canceled because of the COVID-19 pandemic.

Abdominal obesity was defined as a waist circumference of more than 34.6 inches (88 cm), and whole-body obesity was defined as a body mass index of more than 30 kg/m². Findings from a previous study drawn from the same cohort showed that exposure to EtFOSAA, combined with high maternal cholesterol levels, was linked to increased risk of breast cancer in daughters.

“I want to emphasize that we don’t understand the mechanism, but we do know that this finding [from the current study], if it is confirmed, has implications for the current epidemic of obesity. Exposure to these compounds is very widespread, [having] started in the 1940s and 50s, and is consistent with the timing of the obesity epidemic,” said Dr. Cohn, during the virtual press conference.

Robert Sargis, MD, professor of endocrinology, diabetes, and metabolism at the University of Illinois at Chicago, said the mechanistic connection could be complex. “It’s a combination of the possibility that the chemicals themselves are passed down either through breast milk or across the placenta, or that the biological impact is somehow coded epigenetically, and then that epigenetic code is somehow passed on to subsequent generations,” he said in an interview. He was not associated with the research.

Dr. Cohn said her team is investigating both of those possibilities through analysis of the existing blood samples. “There are implications for PFAS clean-up if [these findings are] confirmed, and there’s an opportunity for setting up precautions for pregnant women on how they can try to avoid this contamination to [offset] a rekindling of this generational effect 60 years down the road,” Dr. Cohn added.

Daughters of the original participants (now grandmothers) were measured at an average age of 50, and the granddaughters, at an average of 20 (219 dyads, 657 women in total). Daughters also reported their weight at age 30, which was close to the mean age at which they had given birth. This allowed the researchers to control for obesity present during gestation of the granddaughters.

The researchers analyzed EtFOSAA, PFOS, and cholesterol levels from archived blood samples taken from grandmothers within 3 days of delivery. There was an association between EtFOSAA and self-reported obesity at age 30 in daughters, as well as measured abdominal, whole-body obesity, and blood pressure at age 20 in granddaughters, and all were modified by low cholesterol levels (25% interquartile) in grandmothers (P < .05).

In granddaughters, the combined risk of abdominal and whole-body obesity was 2.3-fold higher in those whose grandmothers were in the top 25% of EtFOSAA exposure, compared with those whose grandmothers were in the lowest 25% (95% confidence interval, 1.1-4.8). Those associations remained after adjustments for race, being overweight in early pregnancy (BMI, >25 kg/m²), and serum PFOS levels.

Although the weight of daughters did not affect the association between the granddaughters’ risk for obesity risk and EtFOSAA levels in grandmothers, it did predict high metabolic risk in granddaughters. That suggests that the burden may be building over generations. “Independently, their mothers themselves are heavier and fatter, and that heaviness of the mother is also a source of increasing body size for the granddaughter. We have a multiplying, very ugly situation that may be helping us to understand this really quick rise of obesity,” said Dr. Cohn.

She also emphasized that PFAS may not be the only culprit in fueling obesity. “Most of us believe that there is sufficient data in the animal studies and, now, growing data in human studies, to suggest that these obesogens exist and are contributing to the health problems that are going to be following the obesity epidemic in young people now.”

Dr. Cohn noted that the study is limited by its lack of a control group.

The California Breast Research Foundation, the National Institutes of Health, and the State of California funded the study. Dr. Cohn and Dr. Sargis reported no relevant financial disclosures.

The study abstract will be published in the Journal of the Endocrine Society. In addition to a series of news conferences held on March 30-31, the society will host ENDO Online 2020 during June 8-22 with programming for clinicians and researchers.
 

SOURCE: Cohn B et al. ENDO 2020, Abstract LB132.

Exposure during pregnancy to a specific per- and polyfluoroalkyl substance (PFAS), combined with a low cholesterol level, is linked to a heightened risk of abdominal and whole-body obesity in granddaughters, according to a new analysis of the Child Health and Development Studies, which have been ongoing since the 1960s.

Researchers directly measured levels of N-ethyl-perfluorooctane sulfonamido acetic acid (EtFOSAA) in blood samples from the grandmothers, which had been taken shortly after delivery, and then analyzed measures of obesity and other metabolic factors in their daughters at ages 30 years and 50 years, and their granddaughters at age 20.

PFASs are synthetic compounds commonly used as oil and water repellents; coatings for cookware, carpets, and textiles; and as firefighting foams. The compounds do not break down in the environment or the human body and accumulate over time. They are known to disrupt the endocrine system.

EtFOSAA is a metabolite of a raw material used in the manufacturing of packaging and paper products, and itself gets converted to perfluorooctane sulfonic acid (PFOS), which is extremely stable in the environment and within organisms, leading to bioaccumulation that has the potential to span generations, Barbara A. Cohn, PhD, director of child health and development studies at the Public Health Institute in Berkeley, Calif., said during a virtual press conference held by The Endocrine Society. The study was slated for presentation during ENDO 2020, the society’s annual meeting, which was canceled because of the COVID-19 pandemic.

Abdominal obesity was defined as a waist circumference of more than 34.6 inches (88 cm), and whole-body obesity was defined as a body mass index of more than 30 kg/m². Findings from a previous study drawn from the same cohort showed that exposure to EtFOSAA, combined with high maternal cholesterol levels, was linked to increased risk of breast cancer in daughters.

“I want to emphasize that we don’t understand the mechanism, but we do know that this finding [from the current study], if it is confirmed, has implications for the current epidemic of obesity. Exposure to these compounds is very widespread, [having] started in the 1940s and 50s, and is consistent with the timing of the obesity epidemic,” said Dr. Cohn, during the virtual press conference.

Robert Sargis, MD, professor of endocrinology, diabetes, and metabolism at the University of Illinois at Chicago, said the mechanistic connection could be complex. “It’s a combination of the possibility that the chemicals themselves are passed down either through breast milk or across the placenta, or that the biological impact is somehow coded epigenetically, and then that epigenetic code is somehow passed on to subsequent generations,” he said in an interview. He was not associated with the research.

Dr. Cohn said her team is investigating both of those possibilities through analysis of the existing blood samples. “There are implications for PFAS clean-up if [these findings are] confirmed, and there’s an opportunity for setting up precautions for pregnant women on how they can try to avoid this contamination to [offset] a rekindling of this generational effect 60 years down the road,” Dr. Cohn added.

Daughters of the original participants (now grandmothers) were measured at an average age of 50, and the granddaughters, at an average of 20 (219 dyads, 657 women in total). Daughters also reported their weight at age 30, which was close to the mean age at which they had given birth. This allowed the researchers to control for obesity present during gestation of the granddaughters.

The researchers analyzed EtFOSAA, PFOS, and cholesterol levels from archived blood samples taken from grandmothers within 3 days of delivery. There was an association between EtFOSAA and self-reported obesity at age 30 in daughters, as well as measured abdominal, whole-body obesity, and blood pressure at age 20 in granddaughters, and all were modified by low cholesterol levels (25% interquartile) in grandmothers (P < .05).

In granddaughters, the combined risk of abdominal and whole-body obesity was 2.3-fold higher in those whose grandmothers were in the top 25% of EtFOSAA exposure, compared with those whose grandmothers were in the lowest 25% (95% confidence interval, 1.1-4.8). Those associations remained after adjustments for race, being overweight in early pregnancy (BMI, >25 kg/m²), and serum PFOS levels.

Although the weight of daughters did not affect the association between the granddaughters’ risk for obesity risk and EtFOSAA levels in grandmothers, it did predict high metabolic risk in granddaughters. That suggests that the burden may be building over generations. “Independently, their mothers themselves are heavier and fatter, and that heaviness of the mother is also a source of increasing body size for the granddaughter. We have a multiplying, very ugly situation that may be helping us to understand this really quick rise of obesity,” said Dr. Cohn.

She also emphasized that PFAS may not be the only culprit in fueling obesity. “Most of us believe that there is sufficient data in the animal studies and, now, growing data in human studies, to suggest that these obesogens exist and are contributing to the health problems that are going to be following the obesity epidemic in young people now.”

Dr. Cohn noted that the study is limited by its lack of a control group.

The California Breast Research Foundation, the National Institutes of Health, and the State of California funded the study. Dr. Cohn and Dr. Sargis reported no relevant financial disclosures.

The study abstract will be published in the Journal of the Endocrine Society. In addition to a series of news conferences held on March 30-31, the society will host ENDO Online 2020 during June 8-22 with programming for clinicians and researchers.
 

SOURCE: Cohn B et al. ENDO 2020, Abstract LB132.

Exposure during pregnancy to a specific per- and polyfluoroalkyl substance (PFAS), combined with a low cholesterol level, is linked to a heightened risk of abdominal and whole-body obesity in granddaughters, according to a new analysis of the Child Health and Development Studies, which have been ongoing since the 1960s.

Researchers directly measured levels of N-ethyl-perfluorooctane sulfonamido acetic acid (EtFOSAA) in blood samples from the grandmothers, which had been taken shortly after delivery, and then analyzed measures of obesity and other metabolic factors in their daughters at ages 30 years and 50 years, and their granddaughters at age 20.

PFASs are synthetic compounds commonly used as oil and water repellents; coatings for cookware, carpets, and textiles; and as firefighting foams. The compounds do not break down in the environment or the human body and accumulate over time. They are known to disrupt the endocrine system.

EtFOSAA is a metabolite of a raw material used in the manufacturing of packaging and paper products, and itself gets converted to perfluorooctane sulfonic acid (PFOS), which is extremely stable in the environment and within organisms, leading to bioaccumulation that has the potential to span generations, Barbara A. Cohn, PhD, director of child health and development studies at the Public Health Institute in Berkeley, Calif., said during a virtual press conference held by The Endocrine Society. The study was slated for presentation during ENDO 2020, the society’s annual meeting, which was canceled because of the COVID-19 pandemic.

Abdominal obesity was defined as a waist circumference of more than 34.6 inches (88 cm), and whole-body obesity was defined as a body mass index of more than 30 kg/m². Findings from a previous study drawn from the same cohort showed that exposure to EtFOSAA, combined with high maternal cholesterol levels, was linked to increased risk of breast cancer in daughters.

“I want to emphasize that we don’t understand the mechanism, but we do know that this finding [from the current study], if it is confirmed, has implications for the current epidemic of obesity. Exposure to these compounds is very widespread, [having] started in the 1940s and 50s, and is consistent with the timing of the obesity epidemic,” said Dr. Cohn, during the virtual press conference.

Robert Sargis, MD, professor of endocrinology, diabetes, and metabolism at the University of Illinois at Chicago, said the mechanistic connection could be complex. “It’s a combination of the possibility that the chemicals themselves are passed down either through breast milk or across the placenta, or that the biological impact is somehow coded epigenetically, and then that epigenetic code is somehow passed on to subsequent generations,” he said in an interview. He was not associated with the research.

Dr. Cohn said her team is investigating both of those possibilities through analysis of the existing blood samples. “There are implications for PFAS clean-up if [these findings are] confirmed, and there’s an opportunity for setting up precautions for pregnant women on how they can try to avoid this contamination to [offset] a rekindling of this generational effect 60 years down the road,” Dr. Cohn added.

Daughters of the original participants (now grandmothers) were measured at an average age of 50, and the granddaughters, at an average of 20 (219 dyads, 657 women in total). Daughters also reported their weight at age 30, which was close to the mean age at which they had given birth. This allowed the researchers to control for obesity present during gestation of the granddaughters.

The researchers analyzed EtFOSAA, PFOS, and cholesterol levels from archived blood samples taken from grandmothers within 3 days of delivery. There was an association between EtFOSAA and self-reported obesity at age 30 in daughters, as well as measured abdominal, whole-body obesity, and blood pressure at age 20 in granddaughters, and all were modified by low cholesterol levels (25% interquartile) in grandmothers (P < .05).

In granddaughters, the combined risk of abdominal and whole-body obesity was 2.3-fold higher in those whose grandmothers were in the top 25% of EtFOSAA exposure, compared with those whose grandmothers were in the lowest 25% (95% confidence interval, 1.1-4.8). Those associations remained after adjustments for race, being overweight in early pregnancy (BMI, >25 kg/m²), and serum PFOS levels.

Although the weight of daughters did not affect the association between the granddaughters’ risk for obesity risk and EtFOSAA levels in grandmothers, it did predict high metabolic risk in granddaughters. That suggests that the burden may be building over generations. “Independently, their mothers themselves are heavier and fatter, and that heaviness of the mother is also a source of increasing body size for the granddaughter. We have a multiplying, very ugly situation that may be helping us to understand this really quick rise of obesity,” said Dr. Cohn.

She also emphasized that PFAS may not be the only culprit in fueling obesity. “Most of us believe that there is sufficient data in the animal studies and, now, growing data in human studies, to suggest that these obesogens exist and are contributing to the health problems that are going to be following the obesity epidemic in young people now.”

Dr. Cohn noted that the study is limited by its lack of a control group.

The California Breast Research Foundation, the National Institutes of Health, and the State of California funded the study. Dr. Cohn and Dr. Sargis reported no relevant financial disclosures.

The study abstract will be published in the Journal of the Endocrine Society. In addition to a series of news conferences held on March 30-31, the society will host ENDO Online 2020 during June 8-22 with programming for clinicians and researchers.
 

SOURCE: Cohn B et al. ENDO 2020, Abstract LB132.

The novel coronavirus (2019-nCoV) shows evidence of causing gastrointestinal symptoms and has the potential to be transmitted by the fecal-oral route, according to a new report from physicians at Shanghai Jiao Tong University, published online (Gastroenterology. 2020 March 3. doi: 10.1053/j.gastro.2020.02.054).

The virus’s respiratory symptoms are well documented and suggest primary transmission by droplet or contact, while other symptoms such as diarrhea, nausea, vomiting, and abdominal discomfort are less common and appear to vary between populations. The SARS coronavirus showed up in stool, even sometimes in patients discharged from the hospital. In a study of hospitalized patients in Wuhan, China, 10.1% of coronavirus patients had diarrhea and nausea in the 1-2 days before onset of fever and dyspnea. The first U.S. patient to be diagnosed had a 2-day history of nausea and vomiting, and had a loose bowel movement on the second day in the hospital. Clinicians later confirmed the presence of viral RNA in both the patient’s stool and airway.

The authors say that researchers in China have isolated viral RNA from the stool of two patients (unpublished), and it has been found in saliva, suggesting the possibility of the salivary gland as an infection or transmission route.

The authors maintain that previous studies likely overlooked or neglected patients who had mild intestinal symptoms. “Many efforts should be made to be alert on the initial digestive symptoms of COVID-19 for early detection, early diagnosis, early isolation and early intervention,” the authors wrote.

Like other coronaviruses, it appears that 2019-nCoV infects cells through an interaction between viral transmembrane spike glycoprotein (S-protein) receptor-binding domain, and the cell receptors angiotensin-converting enzyme 2 (ACE-2) and host cellular transmembrane serine protease (TMPRSS). Transcriptome analysis has shown that human lung AT2 cells express ACE-2 and TMPRSS, but esophagus upper and stratified epithelial cells also express both factors, as do stratified epithelial cells and absorptive enterocytes in the ileum and colon.

The researchers call for investigation into ACE-2 fusion proteins and TMPRSS inhibitors for diagnosis, prophylaxis, or treatment of COVID-19.

The authors also noted that COVID-19 has been linked to mild to moderate liver injury as revealed by elevated aminotransferases, hypoproteinemia and prothrombin time prolongation. This also has precedent in that the SARS coronavirus can infect the liver, and biopsies revealed mitoses and apoptosis, along with other abnormalities. SARS-associated hepatitis may be the result of viral hepatitis, immune overreaction, or a secondary effect of antiviral medications or other drugs. Little is known to date about the ability of 2019-nCoV to infect the liver, but single-cell RNA sequencing data from two distinct cohorts showed more ACE-2 expression in cholangiocytes (59.7%) than hepatocytes (2.6%), which indicates that the virus might directly affect intrahepatic bile ducts.

The authors had no sources of funding or financial conflicts.

SOURCE: GU J et al. Gastroenterology. 2020 March 3. doi: 10.1053/j.gastro.2020.02.054.

*This story was updated on 4/10.2020.

The novel coronavirus (2019-nCoV) shows evidence of causing gastrointestinal symptoms and has the potential to be transmitted by the fecal-oral route, according to a new report from physicians at Shanghai Jiao Tong University, published online (Gastroenterology. 2020 March 3. doi: 10.1053/j.gastro.2020.02.054).

The virus’s respiratory symptoms are well documented and suggest primary transmission by droplet or contact, while other symptoms such as diarrhea, nausea, vomiting, and abdominal discomfort are less common and appear to vary between populations. The SARS coronavirus showed up in stool, even sometimes in patients discharged from the hospital. In a study of hospitalized patients in Wuhan, China, 10.1% of coronavirus patients had diarrhea and nausea in the 1-2 days before onset of fever and dyspnea. The first U.S. patient to be diagnosed had a 2-day history of nausea and vomiting, and had a loose bowel movement on the second day in the hospital. Clinicians later confirmed the presence of viral RNA in both the patient’s stool and airway.

The authors say that researchers in China have isolated viral RNA from the stool of two patients (unpublished), and it has been found in saliva, suggesting the possibility of the salivary gland as an infection or transmission route.

The authors maintain that previous studies likely overlooked or neglected patients who had mild intestinal symptoms. “Many efforts should be made to be alert on the initial digestive symptoms of COVID-19 for early detection, early diagnosis, early isolation and early intervention,” the authors wrote.

Like other coronaviruses, it appears that 2019-nCoV infects cells through an interaction between viral transmembrane spike glycoprotein (S-protein) receptor-binding domain, and the cell receptors angiotensin-converting enzyme 2 (ACE-2) and host cellular transmembrane serine protease (TMPRSS). Transcriptome analysis has shown that human lung AT2 cells express ACE-2 and TMPRSS, but esophagus upper and stratified epithelial cells also express both factors, as do stratified epithelial cells and absorptive enterocytes in the ileum and colon.

The researchers call for investigation into ACE-2 fusion proteins and TMPRSS inhibitors for diagnosis, prophylaxis, or treatment of COVID-19.

The authors also noted that COVID-19 has been linked to mild to moderate liver injury as revealed by elevated aminotransferases, hypoproteinemia and prothrombin time prolongation. This also has precedent in that the SARS coronavirus can infect the liver, and biopsies revealed mitoses and apoptosis, along with other abnormalities. SARS-associated hepatitis may be the result of viral hepatitis, immune overreaction, or a secondary effect of antiviral medications or other drugs. Little is known to date about the ability of 2019-nCoV to infect the liver, but single-cell RNA sequencing data from two distinct cohorts showed more ACE-2 expression in cholangiocytes (59.7%) than hepatocytes (2.6%), which indicates that the virus might directly affect intrahepatic bile ducts.

The authors had no sources of funding or financial conflicts.

SOURCE: GU J et al. Gastroenterology. 2020 March 3. doi: 10.1053/j.gastro.2020.02.054.

*This story was updated on 4/10.2020.

The novel coronavirus (2019-nCoV) shows evidence of causing gastrointestinal symptoms and has the potential to be transmitted by the fecal-oral route, according to a new report from physicians at Shanghai Jiao Tong University, published online (Gastroenterology. 2020 March 3. doi: 10.1053/j.gastro.2020.02.054).

The virus’s respiratory symptoms are well documented and suggest primary transmission by droplet or contact, while other symptoms such as diarrhea, nausea, vomiting, and abdominal discomfort are less common and appear to vary between populations. The SARS coronavirus showed up in stool, even sometimes in patients discharged from the hospital. In a study of hospitalized patients in Wuhan, China, 10.1% of coronavirus patients had diarrhea and nausea in the 1-2 days before onset of fever and dyspnea. The first U.S. patient to be diagnosed had a 2-day history of nausea and vomiting, and had a loose bowel movement on the second day in the hospital. Clinicians later confirmed the presence of viral RNA in both the patient’s stool and airway.

The authors say that researchers in China have isolated viral RNA from the stool of two patients (unpublished), and it has been found in saliva, suggesting the possibility of the salivary gland as an infection or transmission route.

The authors maintain that previous studies likely overlooked or neglected patients who had mild intestinal symptoms. “Many efforts should be made to be alert on the initial digestive symptoms of COVID-19 for early detection, early diagnosis, early isolation and early intervention,” the authors wrote.

Like other coronaviruses, it appears that 2019-nCoV infects cells through an interaction between viral transmembrane spike glycoprotein (S-protein) receptor-binding domain, and the cell receptors angiotensin-converting enzyme 2 (ACE-2) and host cellular transmembrane serine protease (TMPRSS). Transcriptome analysis has shown that human lung AT2 cells express ACE-2 and TMPRSS, but esophagus upper and stratified epithelial cells also express both factors, as do stratified epithelial cells and absorptive enterocytes in the ileum and colon.

The researchers call for investigation into ACE-2 fusion proteins and TMPRSS inhibitors for diagnosis, prophylaxis, or treatment of COVID-19.

The authors also noted that COVID-19 has been linked to mild to moderate liver injury as revealed by elevated aminotransferases, hypoproteinemia and prothrombin time prolongation. This also has precedent in that the SARS coronavirus can infect the liver, and biopsies revealed mitoses and apoptosis, along with other abnormalities. SARS-associated hepatitis may be the result of viral hepatitis, immune overreaction, or a secondary effect of antiviral medications or other drugs. Little is known to date about the ability of 2019-nCoV to infect the liver, but single-cell RNA sequencing data from two distinct cohorts showed more ACE-2 expression in cholangiocytes (59.7%) than hepatocytes (2.6%), which indicates that the virus might directly affect intrahepatic bile ducts.

The authors had no sources of funding or financial conflicts.

SOURCE: GU J et al. Gastroenterology. 2020 March 3. doi: 10.1053/j.gastro.2020.02.054.

*This story was updated on 4/10.2020.

Two observational studies link better cardiovascular health (CVH) in childhood and midlife to reduced CV mortality and subclinical atherosclerosis in later life. Though many studies have examined CVH and CV mortality in later life, the two studies, published in JAMA Cardiology, examine longitudinal CVH and could inform lifestyle modification.

Together, the studies lend support to the American Heart Association 2010 Strategic Initiative, which put an emphasis on health promotion in children rather than CV disease prevention, Erica Spatz, MD, of Yale University, New Haven, Conn., wrote in an accompanying editorial.

Dr. Spatz pointed out that CV disease prevention can be a tough sell, especially in younger patients for whom the threat of heart disease is distant. These studies and others like them could capture evolving risk factors through patients’ lives, and connect them to current lifestyle and experiences. Such data could overcome barriers to behavioral change and lead to more personalized interventions, she wrote.
 

Framingham Offspring Study

One study, led by Vanessa Xanthakis, PhD, of Boston University, examined the relationship between the length of time during midlife spent in ideal CVH and various CV disease and mortality outcomes at the final examination.

The prospective study included 1,445 participants (mean age 60 years, 52% women) from a Framingham Heart Study Offspring investigation based in Massachusetts. The subjects had completed seven examinations. The current study ranged from 1991 to 2015, and encompassed the fifth, sixth, and seventh examinations. Researchers calculated CVH scores based on resting blood pressure, height, weight, total cholesterol level, fasting blood glucose level, smoking status, diet, and physical activity.

At the seventh examination, 39% of participants had poor CVH scores and 54% had intermediate scores. For each 5-year period of intermediate or ideal CVH (compared with poor) measured in previous examinations, during the follow-up period after the seventh examination, there was an associated reduction in risk for adverse outcomes including incident hypertension (hazard ratio, 0.67; 95% confidence interval, 056-0.80), diabetes (HR, 0.73; 95% CI, 0.57-0.93), chronic kidney disease (HR, 0.75; 95% CI, 0.63-0.89), CV disease (HR, 0.73; 95% CI, 0.63-0.85), and all-cause mortality (HR, 0.86; 95% CI, 0.76-0.97).

“Our results indicated that living longer in adulthood with better CVH may be potentially beneficial regardless of age because we did not observe statistically significant effect modification by age of the associations between duration in a given CVH score category and any outcome. Overall, our findings support the importance of promoting healthy behaviors throughout the life course,” the authors wrote.

The study was limited by several factors. Diet and physical activity were self-reported, and about half of participants were excluded after missing an examination, which could introduce bias.
 

International cohort study

The second study analyzed data from 9,388 individuals in five prospective cohorts in the United States and Finland. During 1973-2015, it tracked participants from childhood through middle age (age 8-55 years), linking CVH measures to subclinical atherosclerosis as measured by carotid intima-media thickness (cIMT) in middle age. Led by Norrina Allen, PhD, of the Northwestern University, Chicago, the researchers measured body mass index, total cholesterol level, blood pressure, glucose level, diet, physical activity, and smoking status during a minimum of three examinations. Based on those data, they classified participants as having ideal, intermediate, or poor CVH.

The researchers grouped the participants into five CVH trajectories: High-late decline, which started with high CVH scores at age 8 and maintained them through early adulthood (16%); high-moderate decline (high early scores, moderate decline; 26%); high-early decline (high early scores, early-life decline; 32%); intermediate-late decline (intermediate initial scores, late decline; 16%); and intermediate-early decline (10%). CVH stratification began early: At age 8, 25% of individuals had intermediate CVH scores.

After adjustment for demographics and baseline smoking, diet, and physical activity, the high-late decline CVH group had the smallest mean cIMT value (0.64 mm; 95 % CI, 0.63-0.65 mm), while the intermediate-early decline group, which had the poorest CVH, had the largest (0.72 mm; 95% CI, 0.69-0.76 mm; P less than .001). The relationship was the same even after adjustment for baseline or proximal CVH scores, showing that the trajectory of CVH scores was driving the measure of subclinical atherosclerosis.

“Although it remains important to provide treatment to individuals with elevated risk factor levels, the most effective way to reduce the burden of future CV disease may be to prevent the development of those CV disease risk factors, an approach termed primordial prevention. There is a large body of literature showing effective interventions that may help individuals maintain ideal CV health. Our findings suggest that these interventions are critical and should be implemented early in life to prevent the loss of CVH and future CV [disease] development,” the authors wrote.

The study’s limitations include the fact that analyzed cohorts were drawn from studies with varying protocols and CVH measurement methods. It is also limited by its observational nature.

The two studies were funded by a range of nonindustry sources.

SOURCES: Allen N et al. JAMA Cardiol. 2020 Mar 11. doi: 10.1001/jamacardio.2020.0140; Corlin N et al. JAMA Cardiol. 2020 Mar 11. doi: 10.1001/jamacardio.2020.0109.

Two observational studies link better cardiovascular health (CVH) in childhood and midlife to reduced CV mortality and subclinical atherosclerosis in later life. Though many studies have examined CVH and CV mortality in later life, the two studies, published in JAMA Cardiology, examine longitudinal CVH and could inform lifestyle modification.

Together, the studies lend support to the American Heart Association 2010 Strategic Initiative, which put an emphasis on health promotion in children rather than CV disease prevention, Erica Spatz, MD, of Yale University, New Haven, Conn., wrote in an accompanying editorial.

Dr. Spatz pointed out that CV disease prevention can be a tough sell, especially in younger patients for whom the threat of heart disease is distant. These studies and others like them could capture evolving risk factors through patients’ lives, and connect them to current lifestyle and experiences. Such data could overcome barriers to behavioral change and lead to more personalized interventions, she wrote.
 

Framingham Offspring Study

One study, led by Vanessa Xanthakis, PhD, of Boston University, examined the relationship between the length of time during midlife spent in ideal CVH and various CV disease and mortality outcomes at the final examination.

The prospective study included 1,445 participants (mean age 60 years, 52% women) from a Framingham Heart Study Offspring investigation based in Massachusetts. The subjects had completed seven examinations. The current study ranged from 1991 to 2015, and encompassed the fifth, sixth, and seventh examinations. Researchers calculated CVH scores based on resting blood pressure, height, weight, total cholesterol level, fasting blood glucose level, smoking status, diet, and physical activity.

At the seventh examination, 39% of participants had poor CVH scores and 54% had intermediate scores. For each 5-year period of intermediate or ideal CVH (compared with poor) measured in previous examinations, during the follow-up period after the seventh examination, there was an associated reduction in risk for adverse outcomes including incident hypertension (hazard ratio, 0.67; 95% confidence interval, 056-0.80), diabetes (HR, 0.73; 95% CI, 0.57-0.93), chronic kidney disease (HR, 0.75; 95% CI, 0.63-0.89), CV disease (HR, 0.73; 95% CI, 0.63-0.85), and all-cause mortality (HR, 0.86; 95% CI, 0.76-0.97).

“Our results indicated that living longer in adulthood with better CVH may be potentially beneficial regardless of age because we did not observe statistically significant effect modification by age of the associations between duration in a given CVH score category and any outcome. Overall, our findings support the importance of promoting healthy behaviors throughout the life course,” the authors wrote.

The study was limited by several factors. Diet and physical activity were self-reported, and about half of participants were excluded after missing an examination, which could introduce bias.
 

International cohort study

The second study analyzed data from 9,388 individuals in five prospective cohorts in the United States and Finland. During 1973-2015, it tracked participants from childhood through middle age (age 8-55 years), linking CVH measures to subclinical atherosclerosis as measured by carotid intima-media thickness (cIMT) in middle age. Led by Norrina Allen, PhD, of the Northwestern University, Chicago, the researchers measured body mass index, total cholesterol level, blood pressure, glucose level, diet, physical activity, and smoking status during a minimum of three examinations. Based on those data, they classified participants as having ideal, intermediate, or poor CVH.

The researchers grouped the participants into five CVH trajectories: High-late decline, which started with high CVH scores at age 8 and maintained them through early adulthood (16%); high-moderate decline (high early scores, moderate decline; 26%); high-early decline (high early scores, early-life decline; 32%); intermediate-late decline (intermediate initial scores, late decline; 16%); and intermediate-early decline (10%). CVH stratification began early: At age 8, 25% of individuals had intermediate CVH scores.

After adjustment for demographics and baseline smoking, diet, and physical activity, the high-late decline CVH group had the smallest mean cIMT value (0.64 mm; 95 % CI, 0.63-0.65 mm), while the intermediate-early decline group, which had the poorest CVH, had the largest (0.72 mm; 95% CI, 0.69-0.76 mm; P less than .001). The relationship was the same even after adjustment for baseline or proximal CVH scores, showing that the trajectory of CVH scores was driving the measure of subclinical atherosclerosis.

“Although it remains important to provide treatment to individuals with elevated risk factor levels, the most effective way to reduce the burden of future CV disease may be to prevent the development of those CV disease risk factors, an approach termed primordial prevention. There is a large body of literature showing effective interventions that may help individuals maintain ideal CV health. Our findings suggest that these interventions are critical and should be implemented early in life to prevent the loss of CVH and future CV [disease] development,” the authors wrote.

The study’s limitations include the fact that analyzed cohorts were drawn from studies with varying protocols and CVH measurement methods. It is also limited by its observational nature.

The two studies were funded by a range of nonindustry sources.

SOURCES: Allen N et al. JAMA Cardiol. 2020 Mar 11. doi: 10.1001/jamacardio.2020.0140; Corlin N et al. JAMA Cardiol. 2020 Mar 11. doi: 10.1001/jamacardio.2020.0109.

Two observational studies link better cardiovascular health (CVH) in childhood and midlife to reduced CV mortality and subclinical atherosclerosis in later life. Though many studies have examined CVH and CV mortality in later life, the two studies, published in JAMA Cardiology, examine longitudinal CVH and could inform lifestyle modification.

Together, the studies lend support to the American Heart Association 2010 Strategic Initiative, which put an emphasis on health promotion in children rather than CV disease prevention, Erica Spatz, MD, of Yale University, New Haven, Conn., wrote in an accompanying editorial.

Dr. Spatz pointed out that CV disease prevention can be a tough sell, especially in younger patients for whom the threat of heart disease is distant. These studies and others like them could capture evolving risk factors through patients’ lives, and connect them to current lifestyle and experiences. Such data could overcome barriers to behavioral change and lead to more personalized interventions, she wrote.
 

Framingham Offspring Study

One study, led by Vanessa Xanthakis, PhD, of Boston University, examined the relationship between the length of time during midlife spent in ideal CVH and various CV disease and mortality outcomes at the final examination.

The prospective study included 1,445 participants (mean age 60 years, 52% women) from a Framingham Heart Study Offspring investigation based in Massachusetts. The subjects had completed seven examinations. The current study ranged from 1991 to 2015, and encompassed the fifth, sixth, and seventh examinations. Researchers calculated CVH scores based on resting blood pressure, height, weight, total cholesterol level, fasting blood glucose level, smoking status, diet, and physical activity.

At the seventh examination, 39% of participants had poor CVH scores and 54% had intermediate scores. For each 5-year period of intermediate or ideal CVH (compared with poor) measured in previous examinations, during the follow-up period after the seventh examination, there was an associated reduction in risk for adverse outcomes including incident hypertension (hazard ratio, 0.67; 95% confidence interval, 056-0.80), diabetes (HR, 0.73; 95% CI, 0.57-0.93), chronic kidney disease (HR, 0.75; 95% CI, 0.63-0.89), CV disease (HR, 0.73; 95% CI, 0.63-0.85), and all-cause mortality (HR, 0.86; 95% CI, 0.76-0.97).

“Our results indicated that living longer in adulthood with better CVH may be potentially beneficial regardless of age because we did not observe statistically significant effect modification by age of the associations between duration in a given CVH score category and any outcome. Overall, our findings support the importance of promoting healthy behaviors throughout the life course,” the authors wrote.

The study was limited by several factors. Diet and physical activity were self-reported, and about half of participants were excluded after missing an examination, which could introduce bias.
 

International cohort study

The second study analyzed data from 9,388 individuals in five prospective cohorts in the United States and Finland. During 1973-2015, it tracked participants from childhood through middle age (age 8-55 years), linking CVH measures to subclinical atherosclerosis as measured by carotid intima-media thickness (cIMT) in middle age. Led by Norrina Allen, PhD, of the Northwestern University, Chicago, the researchers measured body mass index, total cholesterol level, blood pressure, glucose level, diet, physical activity, and smoking status during a minimum of three examinations. Based on those data, they classified participants as having ideal, intermediate, or poor CVH.

The researchers grouped the participants into five CVH trajectories: High-late decline, which started with high CVH scores at age 8 and maintained them through early adulthood (16%); high-moderate decline (high early scores, moderate decline; 26%); high-early decline (high early scores, early-life decline; 32%); intermediate-late decline (intermediate initial scores, late decline; 16%); and intermediate-early decline (10%). CVH stratification began early: At age 8, 25% of individuals had intermediate CVH scores.

After adjustment for demographics and baseline smoking, diet, and physical activity, the high-late decline CVH group had the smallest mean cIMT value (0.64 mm; 95 % CI, 0.63-0.65 mm), while the intermediate-early decline group, which had the poorest CVH, had the largest (0.72 mm; 95% CI, 0.69-0.76 mm; P less than .001). The relationship was the same even after adjustment for baseline or proximal CVH scores, showing that the trajectory of CVH scores was driving the measure of subclinical atherosclerosis.

“Although it remains important to provide treatment to individuals with elevated risk factor levels, the most effective way to reduce the burden of future CV disease may be to prevent the development of those CV disease risk factors, an approach termed primordial prevention. There is a large body of literature showing effective interventions that may help individuals maintain ideal CV health. Our findings suggest that these interventions are critical and should be implemented early in life to prevent the loss of CVH and future CV [disease] development,” the authors wrote.

The study’s limitations include the fact that analyzed cohorts were drawn from studies with varying protocols and CVH measurement methods. It is also limited by its observational nature.

The two studies were funded by a range of nonindustry sources.

SOURCES: Allen N et al. JAMA Cardiol. 2020 Mar 11. doi: 10.1001/jamacardio.2020.0140; Corlin N et al. JAMA Cardiol. 2020 Mar 11. doi: 10.1001/jamacardio.2020.0109.

The novel coronavirus (2019-nCoV) is presenting a severe challenge to global health care, but its impact isn’t just felt in the emergency department. Specialists, including dermatologists, must also navigate the presence of the virus and its impact on patients and practices.

Courtesy CDC

A new report from dermatologists in China’s Wuhan province, where the 2019-nCoV outbreak began, outlines initial experiences and provides a blueprint for triaging potential cases before they reach the dermatology clinic. Despite its presence in the epicenter of the outbreak, the hospital has not detected any 2019-nCoV-infected patients in any of its departments.

The commentary appeared in the British Journal of Dermatology and was authored by a group led by Juan Tao of Huazhong University of Science and Technology (Br J Dermatol. 2020 Mar 5. doi: 10.1111/bjd.19011).

The hospital triages all patients at the hospital entrance. Those who are suspected of having 2019-nCoV infection are sent to a designated department. Those with a skin condition who are not suspected of being infected are allowed to go to a dermatology triage center, where they are examined again. If the second examination raises suspicion, they are sent to the designated 2019-nCoV department. If no infection is suspected, or a patient from the 2019-nCoV department is cleared, they are allowed access to the dermatology clinic.

The team also suggested that skin lesions associated with dermatological conditions could lead to increased risk of 2019-nCoV infection. Contacted by email, Dr. Tao outlined a theoretical risk that the virus could lead to infection through contact with subcutaneous tissues, mucosal surfaces, or blood vessels. He did not respond to a request for evidence that such a route of transmission had occurred.

However, Adam Friedman, MD, professor of dermatology at George Washington University, Washington, said he doubted any such transmission would occur since the virus does not infect keratinocytes, and expressed concern that the suggestion could add to the stigma experienced by dermatological patients, whose noticeable rashes can sometimes lead to social avoidance. “I don’t want to add to that,” said Dr. Friedman in an interview.

A critical aspect of dermatology is the immunosuppressive agents often used in dermatology patients. Such drugs could make them more susceptible to infections, or to worse outcomes in the event of disease. Dr. Friedman recounted sending a letter to one patient on an immunosuppressive medication, suggesting that she work remotely. “I think that’s something we have to think about in at-risk individuals. I know there’s such a focus on the elderly, but there’s a large population of individuals on medications that lower their immune system who are going to be at risk for more severe infections,” said Dr. Friedman.

To reduce patient exposure, the commentary recommended that dermatologists perform online consultation for mild and nonemergency cases.

The authors also covered hospitalized patients with primary or secondary skin conditions. A dermatologist is on site at the dermatology triage station to conduct in-depth assessments if needed. If a patient has a fever that is believed to be caused by a dermatologic condition, the on-site dermatologist assists in the consult.

Because some patients may only become symptomatic after admission to a ward, the authors recommend hospitals have a COVID-19 trained contingency group on hand to prevent and control outbreaks within the institution. The team should be in communication with respiratory intensive care and radiology departments to exclude 2019-nCoV when cases develop in-hospital, and to ensure proper care infected patients who require it.

When a hospitalized 2019-nCoV-infected patient has a skin condition requiring treatment, the authors recommend that pictures be sent to the dermatologist for evaluation, along with teleconferences to further assess the patient. If necessary, the dermatologist should go to the patient’s bedside, with as much information as possible related in advance in order to minimize bedside exposure.

There was no funding source. Dr. Tao and Dr. Friedman have no relevant financial conflicts.

The novel coronavirus (2019-nCoV) is presenting a severe challenge to global health care, but its impact isn’t just felt in the emergency department. Specialists, including dermatologists, must also navigate the presence of the virus and its impact on patients and practices.

Courtesy CDC

A new report from dermatologists in China’s Wuhan province, where the 2019-nCoV outbreak began, outlines initial experiences and provides a blueprint for triaging potential cases before they reach the dermatology clinic. Despite its presence in the epicenter of the outbreak, the hospital has not detected any 2019-nCoV-infected patients in any of its departments.

The commentary appeared in the British Journal of Dermatology and was authored by a group led by Juan Tao of Huazhong University of Science and Technology (Br J Dermatol. 2020 Mar 5. doi: 10.1111/bjd.19011).

The hospital triages all patients at the hospital entrance. Those who are suspected of having 2019-nCoV infection are sent to a designated department. Those with a skin condition who are not suspected of being infected are allowed to go to a dermatology triage center, where they are examined again. If the second examination raises suspicion, they are sent to the designated 2019-nCoV department. If no infection is suspected, or a patient from the 2019-nCoV department is cleared, they are allowed access to the dermatology clinic.

The team also suggested that skin lesions associated with dermatological conditions could lead to increased risk of 2019-nCoV infection. Contacted by email, Dr. Tao outlined a theoretical risk that the virus could lead to infection through contact with subcutaneous tissues, mucosal surfaces, or blood vessels. He did not respond to a request for evidence that such a route of transmission had occurred.

However, Adam Friedman, MD, professor of dermatology at George Washington University, Washington, said he doubted any such transmission would occur since the virus does not infect keratinocytes, and expressed concern that the suggestion could add to the stigma experienced by dermatological patients, whose noticeable rashes can sometimes lead to social avoidance. “I don’t want to add to that,” said Dr. Friedman in an interview.

A critical aspect of dermatology is the immunosuppressive agents often used in dermatology patients. Such drugs could make them more susceptible to infections, or to worse outcomes in the event of disease. Dr. Friedman recounted sending a letter to one patient on an immunosuppressive medication, suggesting that she work remotely. “I think that’s something we have to think about in at-risk individuals. I know there’s such a focus on the elderly, but there’s a large population of individuals on medications that lower their immune system who are going to be at risk for more severe infections,” said Dr. Friedman.

To reduce patient exposure, the commentary recommended that dermatologists perform online consultation for mild and nonemergency cases.

The authors also covered hospitalized patients with primary or secondary skin conditions. A dermatologist is on site at the dermatology triage station to conduct in-depth assessments if needed. If a patient has a fever that is believed to be caused by a dermatologic condition, the on-site dermatologist assists in the consult.

Because some patients may only become symptomatic after admission to a ward, the authors recommend hospitals have a COVID-19 trained contingency group on hand to prevent and control outbreaks within the institution. The team should be in communication with respiratory intensive care and radiology departments to exclude 2019-nCoV when cases develop in-hospital, and to ensure proper care infected patients who require it.

When a hospitalized 2019-nCoV-infected patient has a skin condition requiring treatment, the authors recommend that pictures be sent to the dermatologist for evaluation, along with teleconferences to further assess the patient. If necessary, the dermatologist should go to the patient’s bedside, with as much information as possible related in advance in order to minimize bedside exposure.

There was no funding source. Dr. Tao and Dr. Friedman have no relevant financial conflicts.

The novel coronavirus (2019-nCoV) is presenting a severe challenge to global health care, but its impact isn’t just felt in the emergency department. Specialists, including dermatologists, must also navigate the presence of the virus and its impact on patients and practices.

Courtesy CDC

A new report from dermatologists in China’s Wuhan province, where the 2019-nCoV outbreak began, outlines initial experiences and provides a blueprint for triaging potential cases before they reach the dermatology clinic. Despite its presence in the epicenter of the outbreak, the hospital has not detected any 2019-nCoV-infected patients in any of its departments.

The commentary appeared in the British Journal of Dermatology and was authored by a group led by Juan Tao of Huazhong University of Science and Technology (Br J Dermatol. 2020 Mar 5. doi: 10.1111/bjd.19011).

The hospital triages all patients at the hospital entrance. Those who are suspected of having 2019-nCoV infection are sent to a designated department. Those with a skin condition who are not suspected of being infected are allowed to go to a dermatology triage center, where they are examined again. If the second examination raises suspicion, they are sent to the designated 2019-nCoV department. If no infection is suspected, or a patient from the 2019-nCoV department is cleared, they are allowed access to the dermatology clinic.

The team also suggested that skin lesions associated with dermatological conditions could lead to increased risk of 2019-nCoV infection. Contacted by email, Dr. Tao outlined a theoretical risk that the virus could lead to infection through contact with subcutaneous tissues, mucosal surfaces, or blood vessels. He did not respond to a request for evidence that such a route of transmission had occurred.

However, Adam Friedman, MD, professor of dermatology at George Washington University, Washington, said he doubted any such transmission would occur since the virus does not infect keratinocytes, and expressed concern that the suggestion could add to the stigma experienced by dermatological patients, whose noticeable rashes can sometimes lead to social avoidance. “I don’t want to add to that,” said Dr. Friedman in an interview.

A critical aspect of dermatology is the immunosuppressive agents often used in dermatology patients. Such drugs could make them more susceptible to infections, or to worse outcomes in the event of disease. Dr. Friedman recounted sending a letter to one patient on an immunosuppressive medication, suggesting that she work remotely. “I think that’s something we have to think about in at-risk individuals. I know there’s such a focus on the elderly, but there’s a large population of individuals on medications that lower their immune system who are going to be at risk for more severe infections,” said Dr. Friedman.

To reduce patient exposure, the commentary recommended that dermatologists perform online consultation for mild and nonemergency cases.

The authors also covered hospitalized patients with primary or secondary skin conditions. A dermatologist is on site at the dermatology triage station to conduct in-depth assessments if needed. If a patient has a fever that is believed to be caused by a dermatologic condition, the on-site dermatologist assists in the consult.

Because some patients may only become symptomatic after admission to a ward, the authors recommend hospitals have a COVID-19 trained contingency group on hand to prevent and control outbreaks within the institution. The team should be in communication with respiratory intensive care and radiology departments to exclude 2019-nCoV when cases develop in-hospital, and to ensure proper care infected patients who require it.

When a hospitalized 2019-nCoV-infected patient has a skin condition requiring treatment, the authors recommend that pictures be sent to the dermatologist for evaluation, along with teleconferences to further assess the patient. If necessary, the dermatologist should go to the patient’s bedside, with as much information as possible related in advance in order to minimize bedside exposure.

There was no funding source. Dr. Tao and Dr. Friedman have no relevant financial conflicts.

Insomnia symptoms and use of sleep medications is linked to motor vehicle accidents (MVA), and young women with insomnia and reported daytime sleepiness represent a subpopulation at specific risk, according to an analysis of a 5-year population sample. The new research was published online in Sleep and led by Charles Morin, PhD, of Laval University, Quebec City.

The risks of daytime sleepiness and MVA are generally thought of in the context of obstructive sleep apnea (OSA) or men, but the results of the new work suggest that insomnia should not be overlooked, according to Krishna Sundar, MD, clinical professor of pulmonary, critical care, and sleep medicine, and medical director of the Sleep-Wake Center, at the University of Utah, Salt Lake City.

“The notion has been that it may keep them more hypervigilant and less prone to motor vehicle accidents because they are less able to fall asleep even if they want to during the daytime, as compared to other conditions like sleep apnea where there is a higher tendency to doze off,” Dr. Sundar said in an interview.

It should also be remembered that patients aren’t always completely reliable when it comes to self-assessment, according to Brandon M. Seay, MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. “Most people with insomnia won’t say they are sleepy in the daytime, but when you objectively look, you do see an element of daytime sleepiness even if it’s not perceived that well by insomnia patients,” said Dr. Seay.

SOURCE: Morin C et al. Sleep. 2020 Feb 29. DOI: 10.1093/sleep/zsaa032.

Insomnia symptoms and use of sleep medications is linked to motor vehicle accidents (MVA), and young women with insomnia and reported daytime sleepiness represent a subpopulation at specific risk, according to an analysis of a 5-year population sample. The new research was published online in Sleep and led by Charles Morin, PhD, of Laval University, Quebec City.

The risks of daytime sleepiness and MVA are generally thought of in the context of obstructive sleep apnea (OSA) or men, but the results of the new work suggest that insomnia should not be overlooked, according to Krishna Sundar, MD, clinical professor of pulmonary, critical care, and sleep medicine, and medical director of the Sleep-Wake Center, at the University of Utah, Salt Lake City.

“The notion has been that it may keep them more hypervigilant and less prone to motor vehicle accidents because they are less able to fall asleep even if they want to during the daytime, as compared to other conditions like sleep apnea where there is a higher tendency to doze off,” Dr. Sundar said in an interview.

It should also be remembered that patients aren’t always completely reliable when it comes to self-assessment, according to Brandon M. Seay, MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. “Most people with insomnia won’t say they are sleepy in the daytime, but when you objectively look, you do see an element of daytime sleepiness even if it’s not perceived that well by insomnia patients,” said Dr. Seay.

SOURCE: Morin C et al. Sleep. 2020 Feb 29. DOI: 10.1093/sleep/zsaa032.

Insomnia symptoms and use of sleep medications is linked to motor vehicle accidents (MVA), and young women with insomnia and reported daytime sleepiness represent a subpopulation at specific risk, according to an analysis of a 5-year population sample. The new research was published online in Sleep and led by Charles Morin, PhD, of Laval University, Quebec City.

The risks of daytime sleepiness and MVA are generally thought of in the context of obstructive sleep apnea (OSA) or men, but the results of the new work suggest that insomnia should not be overlooked, according to Krishna Sundar, MD, clinical professor of pulmonary, critical care, and sleep medicine, and medical director of the Sleep-Wake Center, at the University of Utah, Salt Lake City.

“The notion has been that it may keep them more hypervigilant and less prone to motor vehicle accidents because they are less able to fall asleep even if they want to during the daytime, as compared to other conditions like sleep apnea where there is a higher tendency to doze off,” Dr. Sundar said in an interview.

It should also be remembered that patients aren’t always completely reliable when it comes to self-assessment, according to Brandon M. Seay, MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. “Most people with insomnia won’t say they are sleepy in the daytime, but when you objectively look, you do see an element of daytime sleepiness even if it’s not perceived that well by insomnia patients,” said Dr. Seay.

SOURCE: Morin C et al. Sleep. 2020 Feb 29. DOI: 10.1093/sleep/zsaa032.

Treatment with the antifungal agent terbinafine during pregnancy does not appear to increase the risk of major malformations or spontaneous abortions, according to results from a large registry study in Denmark.

digitalskillet/Thinkstock

Physicians have been reluctant to prescribe the drug during pregnancy because of the limited safety data. The drug has not been associated with any signs of fetal toxicity in animal studies, but only one study – in 54 pregnancies – has examined the issue in humans and did not identify an increased fetal risk, according to Niklas Worm Andersson, MD, of the department of clinical pharmacology, Copenhagen University Hospital at Bispebjerg and Frederiksberg, and coauthors.

The retrospective, nationwide cohort study analyzed exposure to oral and tropical terbinafine in a large pregnancy registry and found no increase in the risk of major malformations or spontaneous abortions in exposed versus unexposed pregnancies. The study was published in JAMA Dermatology.

Still, these results fell short of certainty, the authors noted. “Although our results may provide reassurance for pregnancies exposed to oral terbinafine by reporting no overall increased risk of major malformations, we cannot exclude a potential increased risk of a specific malformation,” they wrote.

“To our knowledge, this is by far the largest, most statistically rigorous study in the literature regarding this topic,” Jenny E. Murase, MD, of the department of dermatology at the University of California, San Francisco, and Mary Kathryn Abel, a medical student at UCSF, wrote in an accompanying editorial. They described the study as “a substantial contribution to the nearly absent literature regarding the use of terbinafine during pregnancy. Among the antifungal medications, it is possible that terbinafine is the safest one currently available for use in pregnancy, particularly of the oral formulations.”

However, since asymptomatic onychomycosis “is typically a cosmetic, rather than medical, concern, waiting until after pregnancy to initiate therapy is reasonable. ... It is important to acknowledge the uncertainty in this field and question the appropriateness of treating non–life-threatening diseases during pregnancy and lactation,” they wrote.

The Danish researchers drew from a registry of 1,650,649 pregnancies between 1997 and 2016, which included 891 pregnancies exposed to oral terbinafine, and 3,174 exposed to topical terbinafine. Matched outcome analyses compared the exposed pregnancies with up to 40,650 controls unexposed during pregnancy.

Propensity-matched comparisons showed no increased risk of major malformations for oral terbinafine exposure versus no exposure (odds ratio, 1.01; 95% confidence interval, 0.63-1.62) or topical exposure versus no exposure (OR, 1.08; 95% CI, 0.81-1.44). There was also no difference in oral versus topical exposure (OR, 1.18; 95% CI, 0.61-2.29).

iStock

With respect to spontaneous abortions, there was no significant association with oral terbinafine (hazard ratio, 1.06; 95% CI, 0.86-1.32) or topical terbinafine (HR, 1.04; 95% CI, 0.88-1.21), compared with unexposed pregnancies, or oral over topical terbinafine-exposed pregnancies (HR, 1.19; 95% CI, 0.84-1.70).

The study is limited by the fact that it was conducted in a Danish population, and the data relied on filled prescriptions for determining exposure, which did not account for adherence. Residual confounding is possible because of the retrospective nature of the study, the authors pointed out.

No source of funding was disclosed. One of the authors has received grants and personal fees from Novartis. Dr. Murase has received fees from Sanofi Genzyme, Dermira, UCB, Regeneron, Ferndale, and UpToDate.
 

SOURCES: Andersson NW et al. JAMA Dermatol. 2020 Mar 4. doi: 10.1001/jamadermatol.2020.0142; Murase JE, Abel MK. JAMA Dermatol. 2020 Mar 4. doi: 10.1001/jamadermatol.2019.5036.

Treatment with the antifungal agent terbinafine during pregnancy does not appear to increase the risk of major malformations or spontaneous abortions, according to results from a large registry study in Denmark.

digitalskillet/Thinkstock

Physicians have been reluctant to prescribe the drug during pregnancy because of the limited safety data. The drug has not been associated with any signs of fetal toxicity in animal studies, but only one study – in 54 pregnancies – has examined the issue in humans and did not identify an increased fetal risk, according to Niklas Worm Andersson, MD, of the department of clinical pharmacology, Copenhagen University Hospital at Bispebjerg and Frederiksberg, and coauthors.

The retrospective, nationwide cohort study analyzed exposure to oral and tropical terbinafine in a large pregnancy registry and found no increase in the risk of major malformations or spontaneous abortions in exposed versus unexposed pregnancies. The study was published in JAMA Dermatology.

Still, these results fell short of certainty, the authors noted. “Although our results may provide reassurance for pregnancies exposed to oral terbinafine by reporting no overall increased risk of major malformations, we cannot exclude a potential increased risk of a specific malformation,” they wrote.

“To our knowledge, this is by far the largest, most statistically rigorous study in the literature regarding this topic,” Jenny E. Murase, MD, of the department of dermatology at the University of California, San Francisco, and Mary Kathryn Abel, a medical student at UCSF, wrote in an accompanying editorial. They described the study as “a substantial contribution to the nearly absent literature regarding the use of terbinafine during pregnancy. Among the antifungal medications, it is possible that terbinafine is the safest one currently available for use in pregnancy, particularly of the oral formulations.”

However, since asymptomatic onychomycosis “is typically a cosmetic, rather than medical, concern, waiting until after pregnancy to initiate therapy is reasonable. ... It is important to acknowledge the uncertainty in this field and question the appropriateness of treating non–life-threatening diseases during pregnancy and lactation,” they wrote.

The Danish researchers drew from a registry of 1,650,649 pregnancies between 1997 and 2016, which included 891 pregnancies exposed to oral terbinafine, and 3,174 exposed to topical terbinafine. Matched outcome analyses compared the exposed pregnancies with up to 40,650 controls unexposed during pregnancy.

Propensity-matched comparisons showed no increased risk of major malformations for oral terbinafine exposure versus no exposure (odds ratio, 1.01; 95% confidence interval, 0.63-1.62) or topical exposure versus no exposure (OR, 1.08; 95% CI, 0.81-1.44). There was also no difference in oral versus topical exposure (OR, 1.18; 95% CI, 0.61-2.29).

iStock

With respect to spontaneous abortions, there was no significant association with oral terbinafine (hazard ratio, 1.06; 95% CI, 0.86-1.32) or topical terbinafine (HR, 1.04; 95% CI, 0.88-1.21), compared with unexposed pregnancies, or oral over topical terbinafine-exposed pregnancies (HR, 1.19; 95% CI, 0.84-1.70).

The study is limited by the fact that it was conducted in a Danish population, and the data relied on filled prescriptions for determining exposure, which did not account for adherence. Residual confounding is possible because of the retrospective nature of the study, the authors pointed out.

No source of funding was disclosed. One of the authors has received grants and personal fees from Novartis. Dr. Murase has received fees from Sanofi Genzyme, Dermira, UCB, Regeneron, Ferndale, and UpToDate.
 

SOURCES: Andersson NW et al. JAMA Dermatol. 2020 Mar 4. doi: 10.1001/jamadermatol.2020.0142; Murase JE, Abel MK. JAMA Dermatol. 2020 Mar 4. doi: 10.1001/jamadermatol.2019.5036.

Treatment with the antifungal agent terbinafine during pregnancy does not appear to increase the risk of major malformations or spontaneous abortions, according to results from a large registry study in Denmark.

digitalskillet/Thinkstock

Physicians have been reluctant to prescribe the drug during pregnancy because of the limited safety data. The drug has not been associated with any signs of fetal toxicity in animal studies, but only one study – in 54 pregnancies – has examined the issue in humans and did not identify an increased fetal risk, according to Niklas Worm Andersson, MD, of the department of clinical pharmacology, Copenhagen University Hospital at Bispebjerg and Frederiksberg, and coauthors.

The retrospective, nationwide cohort study analyzed exposure to oral and tropical terbinafine in a large pregnancy registry and found no increase in the risk of major malformations or spontaneous abortions in exposed versus unexposed pregnancies. The study was published in JAMA Dermatology.

Still, these results fell short of certainty, the authors noted. “Although our results may provide reassurance for pregnancies exposed to oral terbinafine by reporting no overall increased risk of major malformations, we cannot exclude a potential increased risk of a specific malformation,” they wrote.

“To our knowledge, this is by far the largest, most statistically rigorous study in the literature regarding this topic,” Jenny E. Murase, MD, of the department of dermatology at the University of California, San Francisco, and Mary Kathryn Abel, a medical student at UCSF, wrote in an accompanying editorial. They described the study as “a substantial contribution to the nearly absent literature regarding the use of terbinafine during pregnancy. Among the antifungal medications, it is possible that terbinafine is the safest one currently available for use in pregnancy, particularly of the oral formulations.”

However, since asymptomatic onychomycosis “is typically a cosmetic, rather than medical, concern, waiting until after pregnancy to initiate therapy is reasonable. ... It is important to acknowledge the uncertainty in this field and question the appropriateness of treating non–life-threatening diseases during pregnancy and lactation,” they wrote.

The Danish researchers drew from a registry of 1,650,649 pregnancies between 1997 and 2016, which included 891 pregnancies exposed to oral terbinafine, and 3,174 exposed to topical terbinafine. Matched outcome analyses compared the exposed pregnancies with up to 40,650 controls unexposed during pregnancy.

Propensity-matched comparisons showed no increased risk of major malformations for oral terbinafine exposure versus no exposure (odds ratio, 1.01; 95% confidence interval, 0.63-1.62) or topical exposure versus no exposure (OR, 1.08; 95% CI, 0.81-1.44). There was also no difference in oral versus topical exposure (OR, 1.18; 95% CI, 0.61-2.29).

iStock

With respect to spontaneous abortions, there was no significant association with oral terbinafine (hazard ratio, 1.06; 95% CI, 0.86-1.32) or topical terbinafine (HR, 1.04; 95% CI, 0.88-1.21), compared with unexposed pregnancies, or oral over topical terbinafine-exposed pregnancies (HR, 1.19; 95% CI, 0.84-1.70).

The study is limited by the fact that it was conducted in a Danish population, and the data relied on filled prescriptions for determining exposure, which did not account for adherence. Residual confounding is possible because of the retrospective nature of the study, the authors pointed out.

No source of funding was disclosed. One of the authors has received grants and personal fees from Novartis. Dr. Murase has received fees from Sanofi Genzyme, Dermira, UCB, Regeneron, Ferndale, and UpToDate.
 

SOURCES: Andersson NW et al. JAMA Dermatol. 2020 Mar 4. doi: 10.1001/jamadermatol.2020.0142; Murase JE, Abel MK. JAMA Dermatol. 2020 Mar 4. doi: 10.1001/jamadermatol.2019.5036.

The use of skin emollients early in infancy and early introduction of certain foods failed to prevent atopic dermatitis (AD) in infants, including those at high risk, in two new clinical trials.

The BEEP (Barrier Enhancement for Eczema Prevention) study compared the rates of AD among infants identified as at risk of AD because of family history who had daily applications of emollients (Diprobase cream or Doublebase gel) for the first year of life, compared with a standard skin care group. PreventADALL (Preventing Atopic Dermatitis and Allergies in Children) is a randomized, primary-prevention study conducted in Norway and Sweden that randomized infants into one of four groups: controls whose parents followed regular skin care advice and nutrition guidelines; those who received skin emollients (the addition of emulsified oil to their bath and application of facial cream on at least 4 days a week from age 2 weeks to 8 months); those who received early complementary feeding of peanut, cow’s milk, wheat, and egg introduced between aged 12 and 16 weeks; and a group that combined both the emollient and diet interventions.

Neither of the studies, published in the Lancet, found statistically significant differences in AD rates between the intervention and control groups.

The results put a damper on hopes raised by previous studies that included two small pilot studies, which found that daily use of leave-on emollients in infants considered at high risk of AD prevented the development of AD (J Allergy Clin Immunol 2014 Oct;134:824-30.e6; J Allergy Clin Immunol Oct 2014;134:818-23).

“It was maybe a little bit overly hopeful to think that we could just moisturize and prevent such a complex disorder,” Robert Sidbury, MD, chief of dermatology at Seattle Children’s Hospital, said in an interview. He emphasized that the studies only addressed emollients as a preventative, and that “there’s no question that emollients are still critical for the therapy of eczema.”

Bruce Brod, MD, clinical professor of dermatology at the University of Pennsylvania, Philadelphia, suggested that homogeneous patient populations or insufficient numbers might explain the negative findings. PreventADALL drew patients from Norway and Sweden, while BEEP recruited from the United Kingdom. “They’re important studies, but I think they still lend themselves to further studies with different patient populations and larger groups of patients,” Dr. Brod said in an interview.

BEEP was headed by Joanne Chalmers, PhD, and Hywel Williams, DSc, of the Centre of Evidence-Based Dermatology at the University of Nottingham (England). Håvard Ove Skjerven, PhD, and Karin C Lødrup Carlsen, PhD, of Oslo University Hospital led the PreventADALL study.

The BEEP study randomized 1,394 newborns at 16 sites in the United Kingdom to daily emollient treatment with standard skin care, or standard skin care alone. At one year, compliance was 74% in the intervention group. At age 2, 23% of the intervention group had AD, compared with 25% of controls (hazard ratio, 0.95; P =.61). Skin infections were also higher in the treatment arm (mean, 0.23 per year vs. 0.15 per year; adjusted incidence ratio, 1.55; 95% confidence interval, 1.15-2.09).

“Our study does not support the use of emollients for preventing eczema in high-risk infants, a finding supported by PreventADALL, another large trial using a skin barrier enhancing intervention,” they concluded. Their data “relate only to prevention of eczema and do not directly challenge the practice of using emollients as first-line treatment for eczema.”

In the PreventADALL study, 2,397 newborn infants born between 2015 and 2017 were randomized to one of the four groups. Use of facial cream and emollients during bathing began at 2 weeks, and early complementary feeding of peanut, cow’s milk, wheat, and egg at 3-4 months. The frequency of AD at aged 12 months in the control group was 8%, compared with 11% in the skin-intervention group, 9% in the food-intervention group, and 5% in the combined-intervention group.

These differences were not statistically significant, and “the primary hypothesis that either skin intervention or food intervention reduced atopic dermatitis were not confirmed,” the authors wrote. Parental atopy did not influence the effects of the interventions. Their results were in line with the BEEP results, and the authors “cannot recommend these interventions as primary prevention strategies.”

The researchers will continue to follow children until age 3 years to evaluate the food allergy rates, if the combined-treatment group experiences a long-term benefit. Adherence to the protocol was poor, with 44% compliance with the facial cream application and 27% compliance with bathing emollients; 32% fully adhered to the diet protocols.

The studies were funded by the National Institute for Health Research Health Technology Assessment (BEEP); and a range of public and private funders (PreventADALL). One author of the PreventADALL study disclosed receiving honoraria for presentations from several pharmaceutical companies, and one author received honoraria for presentations from Thermo Fisher Scientific; the rest had no disclosures. Dr. Sidbury has been an investigator for Regeneron. Dr. Brod had no relevant financial disclosures.

SOURCES: Chalmers JR et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32984-8; Skjerven HO et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32983-6.
 

The use of skin emollients early in infancy and early introduction of certain foods failed to prevent atopic dermatitis (AD) in infants, including those at high risk, in two new clinical trials.

The BEEP (Barrier Enhancement for Eczema Prevention) study compared the rates of AD among infants identified as at risk of AD because of family history who had daily applications of emollients (Diprobase cream or Doublebase gel) for the first year of life, compared with a standard skin care group. PreventADALL (Preventing Atopic Dermatitis and Allergies in Children) is a randomized, primary-prevention study conducted in Norway and Sweden that randomized infants into one of four groups: controls whose parents followed regular skin care advice and nutrition guidelines; those who received skin emollients (the addition of emulsified oil to their bath and application of facial cream on at least 4 days a week from age 2 weeks to 8 months); those who received early complementary feeding of peanut, cow’s milk, wheat, and egg introduced between aged 12 and 16 weeks; and a group that combined both the emollient and diet interventions.

Neither of the studies, published in the Lancet, found statistically significant differences in AD rates between the intervention and control groups.

The results put a damper on hopes raised by previous studies that included two small pilot studies, which found that daily use of leave-on emollients in infants considered at high risk of AD prevented the development of AD (J Allergy Clin Immunol 2014 Oct;134:824-30.e6; J Allergy Clin Immunol Oct 2014;134:818-23).

“It was maybe a little bit overly hopeful to think that we could just moisturize and prevent such a complex disorder,” Robert Sidbury, MD, chief of dermatology at Seattle Children’s Hospital, said in an interview. He emphasized that the studies only addressed emollients as a preventative, and that “there’s no question that emollients are still critical for the therapy of eczema.”

Bruce Brod, MD, clinical professor of dermatology at the University of Pennsylvania, Philadelphia, suggested that homogeneous patient populations or insufficient numbers might explain the negative findings. PreventADALL drew patients from Norway and Sweden, while BEEP recruited from the United Kingdom. “They’re important studies, but I think they still lend themselves to further studies with different patient populations and larger groups of patients,” Dr. Brod said in an interview.

BEEP was headed by Joanne Chalmers, PhD, and Hywel Williams, DSc, of the Centre of Evidence-Based Dermatology at the University of Nottingham (England). Håvard Ove Skjerven, PhD, and Karin C Lødrup Carlsen, PhD, of Oslo University Hospital led the PreventADALL study.

The BEEP study randomized 1,394 newborns at 16 sites in the United Kingdom to daily emollient treatment with standard skin care, or standard skin care alone. At one year, compliance was 74% in the intervention group. At age 2, 23% of the intervention group had AD, compared with 25% of controls (hazard ratio, 0.95; P =.61). Skin infections were also higher in the treatment arm (mean, 0.23 per year vs. 0.15 per year; adjusted incidence ratio, 1.55; 95% confidence interval, 1.15-2.09).

“Our study does not support the use of emollients for preventing eczema in high-risk infants, a finding supported by PreventADALL, another large trial using a skin barrier enhancing intervention,” they concluded. Their data “relate only to prevention of eczema and do not directly challenge the practice of using emollients as first-line treatment for eczema.”

In the PreventADALL study, 2,397 newborn infants born between 2015 and 2017 were randomized to one of the four groups. Use of facial cream and emollients during bathing began at 2 weeks, and early complementary feeding of peanut, cow’s milk, wheat, and egg at 3-4 months. The frequency of AD at aged 12 months in the control group was 8%, compared with 11% in the skin-intervention group, 9% in the food-intervention group, and 5% in the combined-intervention group.

These differences were not statistically significant, and “the primary hypothesis that either skin intervention or food intervention reduced atopic dermatitis were not confirmed,” the authors wrote. Parental atopy did not influence the effects of the interventions. Their results were in line with the BEEP results, and the authors “cannot recommend these interventions as primary prevention strategies.”

The researchers will continue to follow children until age 3 years to evaluate the food allergy rates, if the combined-treatment group experiences a long-term benefit. Adherence to the protocol was poor, with 44% compliance with the facial cream application and 27% compliance with bathing emollients; 32% fully adhered to the diet protocols.

The studies were funded by the National Institute for Health Research Health Technology Assessment (BEEP); and a range of public and private funders (PreventADALL). One author of the PreventADALL study disclosed receiving honoraria for presentations from several pharmaceutical companies, and one author received honoraria for presentations from Thermo Fisher Scientific; the rest had no disclosures. Dr. Sidbury has been an investigator for Regeneron. Dr. Brod had no relevant financial disclosures.

SOURCES: Chalmers JR et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32984-8; Skjerven HO et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32983-6.
 

The use of skin emollients early in infancy and early introduction of certain foods failed to prevent atopic dermatitis (AD) in infants, including those at high risk, in two new clinical trials.

The BEEP (Barrier Enhancement for Eczema Prevention) study compared the rates of AD among infants identified as at risk of AD because of family history who had daily applications of emollients (Diprobase cream or Doublebase gel) for the first year of life, compared with a standard skin care group. PreventADALL (Preventing Atopic Dermatitis and Allergies in Children) is a randomized, primary-prevention study conducted in Norway and Sweden that randomized infants into one of four groups: controls whose parents followed regular skin care advice and nutrition guidelines; those who received skin emollients (the addition of emulsified oil to their bath and application of facial cream on at least 4 days a week from age 2 weeks to 8 months); those who received early complementary feeding of peanut, cow’s milk, wheat, and egg introduced between aged 12 and 16 weeks; and a group that combined both the emollient and diet interventions.

Neither of the studies, published in the Lancet, found statistically significant differences in AD rates between the intervention and control groups.

The results put a damper on hopes raised by previous studies that included two small pilot studies, which found that daily use of leave-on emollients in infants considered at high risk of AD prevented the development of AD (J Allergy Clin Immunol 2014 Oct;134:824-30.e6; J Allergy Clin Immunol Oct 2014;134:818-23).

“It was maybe a little bit overly hopeful to think that we could just moisturize and prevent such a complex disorder,” Robert Sidbury, MD, chief of dermatology at Seattle Children’s Hospital, said in an interview. He emphasized that the studies only addressed emollients as a preventative, and that “there’s no question that emollients are still critical for the therapy of eczema.”

Bruce Brod, MD, clinical professor of dermatology at the University of Pennsylvania, Philadelphia, suggested that homogeneous patient populations or insufficient numbers might explain the negative findings. PreventADALL drew patients from Norway and Sweden, while BEEP recruited from the United Kingdom. “They’re important studies, but I think they still lend themselves to further studies with different patient populations and larger groups of patients,” Dr. Brod said in an interview.

BEEP was headed by Joanne Chalmers, PhD, and Hywel Williams, DSc, of the Centre of Evidence-Based Dermatology at the University of Nottingham (England). Håvard Ove Skjerven, PhD, and Karin C Lødrup Carlsen, PhD, of Oslo University Hospital led the PreventADALL study.

The BEEP study randomized 1,394 newborns at 16 sites in the United Kingdom to daily emollient treatment with standard skin care, or standard skin care alone. At one year, compliance was 74% in the intervention group. At age 2, 23% of the intervention group had AD, compared with 25% of controls (hazard ratio, 0.95; P =.61). Skin infections were also higher in the treatment arm (mean, 0.23 per year vs. 0.15 per year; adjusted incidence ratio, 1.55; 95% confidence interval, 1.15-2.09).

“Our study does not support the use of emollients for preventing eczema in high-risk infants, a finding supported by PreventADALL, another large trial using a skin barrier enhancing intervention,” they concluded. Their data “relate only to prevention of eczema and do not directly challenge the practice of using emollients as first-line treatment for eczema.”

In the PreventADALL study, 2,397 newborn infants born between 2015 and 2017 were randomized to one of the four groups. Use of facial cream and emollients during bathing began at 2 weeks, and early complementary feeding of peanut, cow’s milk, wheat, and egg at 3-4 months. The frequency of AD at aged 12 months in the control group was 8%, compared with 11% in the skin-intervention group, 9% in the food-intervention group, and 5% in the combined-intervention group.

These differences were not statistically significant, and “the primary hypothesis that either skin intervention or food intervention reduced atopic dermatitis were not confirmed,” the authors wrote. Parental atopy did not influence the effects of the interventions. Their results were in line with the BEEP results, and the authors “cannot recommend these interventions as primary prevention strategies.”

The researchers will continue to follow children until age 3 years to evaluate the food allergy rates, if the combined-treatment group experiences a long-term benefit. Adherence to the protocol was poor, with 44% compliance with the facial cream application and 27% compliance with bathing emollients; 32% fully adhered to the diet protocols.

The studies were funded by the National Institute for Health Research Health Technology Assessment (BEEP); and a range of public and private funders (PreventADALL). One author of the PreventADALL study disclosed receiving honoraria for presentations from several pharmaceutical companies, and one author received honoraria for presentations from Thermo Fisher Scientific; the rest had no disclosures. Dr. Sidbury has been an investigator for Regeneron. Dr. Brod had no relevant financial disclosures.

SOURCES: Chalmers JR et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32984-8; Skjerven HO et al. Lancet. 2020 Feb 19. doi: 10.1016/S0140-6736(19)32983-6.
 

Treatment with the sodium-glucose transporter 2 inhibitor dapagliflozin reduced the risk for cardiovascular disease or hospitalization for heart failure (CVD/HHF) in patients with diabetes, regardless of the duration of the disease, but had a greater protective benefit against major adverse cardiovascular events (MACE) and renal events in patients with longer disease duration, according to new findings from a post hoc analysis of the DECLARE-TIMI 58 trial.

The positive effect of dapagliflozin in patients with MACE – which includes myocardial infarction (MI), CVD, and ischemic stroke – may have been driven by lower rates of MI and ischemic stroke with the drug, compared with placebo, in patients with longer disease duration, wrote Harpreet S. Bajaj, MD, and colleagues. Their report is in Diabetes, Obesity and Metabolism (2020 Feb 23. doi: 10.1111/dom.14011).

It has been previously reported that the risk for complications in diabetes increases with increasing duration of the disease. Recent studies with SGLT-2 inhibitors have shown that the drugs improve cardiovascular and renal outcomes in diabetes, and they are recommended by the American Diabetes Association as second-line therapy in patients with atherosclerotic cardiovascular disease, chronic kidney disease, or heart failure. The European Society of Cardiology and the European Association for the Study of Diabetes recommend that patients with diabetes patients who have three or more risk factors, or those with a disease duration of more than 20 years, should be deemed very high risk and be considered for early treatment with SGLT2 inhibitors.

“The MACE benefit observed with dapagliflozin in this study in patients with diabetes duration of [more than] 20 years, clearly supports that notion,” the authors wrote.

In DECLARE-TIMI 58, 17,160 patients with type 2 diabetes received dapagliflozin or placebo and were followed for a median of 4.2 years. Of those patients, 22.4% had a disease duration of fewer than 5 years; 27.6%, a duration of 5-10 years; 23.0%, 10-15 years; 14.2%, 10-15 years; and 12.9%, more than 20 years. The median duration of disease was 11 years.

Patients in all the age groups had similar reductions in CVD/HHF, compared with placebo, with hazard ratios of 0.79 (disease duration of 5 or fewer years), 0.86, 0.92, 0.81, and 0.75 (duration of 20 years), respectively (interaction trend P = .760).

Treatment with dapagliflozin reduced the incidence of MACE, but the benefit was more apparent in patients with longer-term disease: HR, 1.08; 1.02; 0.94; 0.92; and 0.67, respectively (interaction trend P = .004). Similar trends were seen with MI (interaction trend P = .019) and ischemic stroke (interaction trend P = .015).

The researchers also reported improved benefits in renal-specific outcome with increasing disease duration, with HRs ranging from 0.79 in patients with diabetes duration of fewer than 5 years, to 0.42 in those with a duration of more than 20 years (interaction trend P = .084).

Limitations of the study include the fact that the information about diabetes duration relied on patient reports, and that the original trial was not powered for all subgroup interactions. This authors emphasized that this was a post hoc analysis and as such, should be considered hypothesis generating.

All but two of the authors reported relationships with Astra Zeneca, which funded the study, and other drug companies.

SOURCE: Bajaj HS et al. Diabetes Obes Metab. 2020 Feb 23. doi: 10.1111/dom.14011.

Treatment with the sodium-glucose transporter 2 inhibitor dapagliflozin reduced the risk for cardiovascular disease or hospitalization for heart failure (CVD/HHF) in patients with diabetes, regardless of the duration of the disease, but had a greater protective benefit against major adverse cardiovascular events (MACE) and renal events in patients with longer disease duration, according to new findings from a post hoc analysis of the DECLARE-TIMI 58 trial.

The positive effect of dapagliflozin in patients with MACE – which includes myocardial infarction (MI), CVD, and ischemic stroke – may have been driven by lower rates of MI and ischemic stroke with the drug, compared with placebo, in patients with longer disease duration, wrote Harpreet S. Bajaj, MD, and colleagues. Their report is in Diabetes, Obesity and Metabolism (2020 Feb 23. doi: 10.1111/dom.14011).

It has been previously reported that the risk for complications in diabetes increases with increasing duration of the disease. Recent studies with SGLT-2 inhibitors have shown that the drugs improve cardiovascular and renal outcomes in diabetes, and they are recommended by the American Diabetes Association as second-line therapy in patients with atherosclerotic cardiovascular disease, chronic kidney disease, or heart failure. The European Society of Cardiology and the European Association for the Study of Diabetes recommend that patients with diabetes patients who have three or more risk factors, or those with a disease duration of more than 20 years, should be deemed very high risk and be considered for early treatment with SGLT2 inhibitors.

“The MACE benefit observed with dapagliflozin in this study in patients with diabetes duration of [more than] 20 years, clearly supports that notion,” the authors wrote.

In DECLARE-TIMI 58, 17,160 patients with type 2 diabetes received dapagliflozin or placebo and were followed for a median of 4.2 years. Of those patients, 22.4% had a disease duration of fewer than 5 years; 27.6%, a duration of 5-10 years; 23.0%, 10-15 years; 14.2%, 10-15 years; and 12.9%, more than 20 years. The median duration of disease was 11 years.

Patients in all the age groups had similar reductions in CVD/HHF, compared with placebo, with hazard ratios of 0.79 (disease duration of 5 or fewer years), 0.86, 0.92, 0.81, and 0.75 (duration of 20 years), respectively (interaction trend P = .760).

Treatment with dapagliflozin reduced the incidence of MACE, but the benefit was more apparent in patients with longer-term disease: HR, 1.08; 1.02; 0.94; 0.92; and 0.67, respectively (interaction trend P = .004). Similar trends were seen with MI (interaction trend P = .019) and ischemic stroke (interaction trend P = .015).

The researchers also reported improved benefits in renal-specific outcome with increasing disease duration, with HRs ranging from 0.79 in patients with diabetes duration of fewer than 5 years, to 0.42 in those with a duration of more than 20 years (interaction trend P = .084).

Limitations of the study include the fact that the information about diabetes duration relied on patient reports, and that the original trial was not powered for all subgroup interactions. This authors emphasized that this was a post hoc analysis and as such, should be considered hypothesis generating.

All but two of the authors reported relationships with Astra Zeneca, which funded the study, and other drug companies.

SOURCE: Bajaj HS et al. Diabetes Obes Metab. 2020 Feb 23. doi: 10.1111/dom.14011.

Treatment with the sodium-glucose transporter 2 inhibitor dapagliflozin reduced the risk for cardiovascular disease or hospitalization for heart failure (CVD/HHF) in patients with diabetes, regardless of the duration of the disease, but had a greater protective benefit against major adverse cardiovascular events (MACE) and renal events in patients with longer disease duration, according to new findings from a post hoc analysis of the DECLARE-TIMI 58 trial.

The positive effect of dapagliflozin in patients with MACE – which includes myocardial infarction (MI), CVD, and ischemic stroke – may have been driven by lower rates of MI and ischemic stroke with the drug, compared with placebo, in patients with longer disease duration, wrote Harpreet S. Bajaj, MD, and colleagues. Their report is in Diabetes, Obesity and Metabolism (2020 Feb 23. doi: 10.1111/dom.14011).

It has been previously reported that the risk for complications in diabetes increases with increasing duration of the disease. Recent studies with SGLT-2 inhibitors have shown that the drugs improve cardiovascular and renal outcomes in diabetes, and they are recommended by the American Diabetes Association as second-line therapy in patients with atherosclerotic cardiovascular disease, chronic kidney disease, or heart failure. The European Society of Cardiology and the European Association for the Study of Diabetes recommend that patients with diabetes patients who have three or more risk factors, or those with a disease duration of more than 20 years, should be deemed very high risk and be considered for early treatment with SGLT2 inhibitors.

“The MACE benefit observed with dapagliflozin in this study in patients with diabetes duration of [more than] 20 years, clearly supports that notion,” the authors wrote.

In DECLARE-TIMI 58, 17,160 patients with type 2 diabetes received dapagliflozin or placebo and were followed for a median of 4.2 years. Of those patients, 22.4% had a disease duration of fewer than 5 years; 27.6%, a duration of 5-10 years; 23.0%, 10-15 years; 14.2%, 10-15 years; and 12.9%, more than 20 years. The median duration of disease was 11 years.

Patients in all the age groups had similar reductions in CVD/HHF, compared with placebo, with hazard ratios of 0.79 (disease duration of 5 or fewer years), 0.86, 0.92, 0.81, and 0.75 (duration of 20 years), respectively (interaction trend P = .760).

Treatment with dapagliflozin reduced the incidence of MACE, but the benefit was more apparent in patients with longer-term disease: HR, 1.08; 1.02; 0.94; 0.92; and 0.67, respectively (interaction trend P = .004). Similar trends were seen with MI (interaction trend P = .019) and ischemic stroke (interaction trend P = .015).

The researchers also reported improved benefits in renal-specific outcome with increasing disease duration, with HRs ranging from 0.79 in patients with diabetes duration of fewer than 5 years, to 0.42 in those with a duration of more than 20 years (interaction trend P = .084).

Limitations of the study include the fact that the information about diabetes duration relied on patient reports, and that the original trial was not powered for all subgroup interactions. This authors emphasized that this was a post hoc analysis and as such, should be considered hypothesis generating.

All but two of the authors reported relationships with Astra Zeneca, which funded the study, and other drug companies.

SOURCE: Bajaj HS et al. Diabetes Obes Metab. 2020 Feb 23. doi: 10.1111/dom.14011.

Glucocorticoid use is associated with greater mortality and cardiovascular risk in RA patients, and the associated risk is greater still in patients with RA and comorbid diabetes. The findings come from a new retrospective analysis derived from U.K. primary care records.

Although patients with diabetes actually had a lower relative risk for mortality than the nondiabetes cohort, they had a greater mortality difference because of a greater baseline risk. Ultimately, glucocorticoid (GC) use was associated with an additional 44.9 deaths per 1,000 person-years in the diabetes group, compared with 34.4 per 1,000 person-years in the RA-only group.

The study, led by Ruth Costello and William Dixon, MBBS, PhD of the University of Manchester (England), was published in BMC Rheumatology.

The findings aren’t particularly surprising, given that steroid use and diabetes have associated cardiovascular risks, and physicians generally try to reduce or eliminate their use. “There’s a group [of physicians] saying that we don’t need to use steroids at all in rheumatoid arthritis, except maybe for [a] short time at diagnosis to bridge to other therapies, or during flares,” Gordon Starkebaum, MD, professor emeritus of rheumatology at the University of Washington, Seattle, said in an interview. He recounted a session at last year’s annual meeting of the American College of Rheumatology that advocated for only injectable steroid use during flare-ups. “That was provocative,” Dr. Starkebaum said.

“It’s a retrospective study, so it has some limitations, but it provides good insight, and some substantiation to what we already think,” added Brett Smith, DO, a rheumatologist practicing in Knoxville, Tenn.

Dr. Smith suggested that the study further underscores the need to follow treat-to-target protocols in RA. He emphasized that lifetime exposure to steroids is likely the greatest concern, and that steady accumulating doses are a sign of trouble. “If you need that much steroids, you need to go up on your medication – your methotrexate, or sulfasalazine, or your biologic,” said Dr. Smith. “At least 50% of people will need a biologic to [achieve] disease control, and if you get them on it, they’re going to have better disease control, compliance is typically better, and they’re going to have less steroid exposure.”

Dr. Smith also noted that comorbid diabetes shouldn’t affect treat-to-target strategies. In fact, in such patients “you should probably be following it more tightly to reduce the cardiovascular outcomes,” he said.

The retrospective analysis included 9,085 patients with RA and with or without type 2 diabetes, with a mean follow-up of 5.2 years. They were recruited to the study between 1998 and 2011. Among patients with comorbid diabetes, those exposed to GC had a mortality of 67.4 per 1,000 person-years, compared with 22.5 among those not exposed to GC. Among those with RA alone, mortality was 44.6 versus 10.2 with and without GC exposure, respectively. Those with diabetes had a lower risk ratio for mortality (2.99 vs. 4.37), but a higher mortality difference (44.9 vs. 34.4 per 1,000 person-years).

“The increased absolute hazard for all-cause mortality indicates the greater public health impact of people with RA using GCs if they have [diabetes],” the researchers wrote. “Rheumatologists should consider [diabetes] status when prescribing GCs to patients with RA given this potential impact of GC therapy on glucose control and mortality.”

The study was limited by a lack of information on GC dose and cumulative exposure. Given its retrospective nature, the study could have been affected by confounding by indication, as well as unknown confounders.

The study was funded by the Centre for Epidemiology Versus Arthritis and the National Institute for Health Research Biomedical Research Centre. Dr. Starkebaum has no relevant financial disclosures. Dr. Smith is on the speaker’s bureau for AbbVie and serves on the company’s advisory board. He is also on the advisory boards of Regeneron and Sanofi Genzyme.

SOURCE: Costello R et al. BMC Rheumatol. 2020 Feb 19. doi: 10.1186/s41927-019-0105-4.

Glucocorticoid use is associated with greater mortality and cardiovascular risk in RA patients, and the associated risk is greater still in patients with RA and comorbid diabetes. The findings come from a new retrospective analysis derived from U.K. primary care records.

Although patients with diabetes actually had a lower relative risk for mortality than the nondiabetes cohort, they had a greater mortality difference because of a greater baseline risk. Ultimately, glucocorticoid (GC) use was associated with an additional 44.9 deaths per 1,000 person-years in the diabetes group, compared with 34.4 per 1,000 person-years in the RA-only group.

The study, led by Ruth Costello and William Dixon, MBBS, PhD of the University of Manchester (England), was published in BMC Rheumatology.

The findings aren’t particularly surprising, given that steroid use and diabetes have associated cardiovascular risks, and physicians generally try to reduce or eliminate their use. “There’s a group [of physicians] saying that we don’t need to use steroids at all in rheumatoid arthritis, except maybe for [a] short time at diagnosis to bridge to other therapies, or during flares,” Gordon Starkebaum, MD, professor emeritus of rheumatology at the University of Washington, Seattle, said in an interview. He recounted a session at last year’s annual meeting of the American College of Rheumatology that advocated for only injectable steroid use during flare-ups. “That was provocative,” Dr. Starkebaum said.

“It’s a retrospective study, so it has some limitations, but it provides good insight, and some substantiation to what we already think,” added Brett Smith, DO, a rheumatologist practicing in Knoxville, Tenn.

Dr. Smith suggested that the study further underscores the need to follow treat-to-target protocols in RA. He emphasized that lifetime exposure to steroids is likely the greatest concern, and that steady accumulating doses are a sign of trouble. “If you need that much steroids, you need to go up on your medication – your methotrexate, or sulfasalazine, or your biologic,” said Dr. Smith. “At least 50% of people will need a biologic to [achieve] disease control, and if you get them on it, they’re going to have better disease control, compliance is typically better, and they’re going to have less steroid exposure.”

Dr. Smith also noted that comorbid diabetes shouldn’t affect treat-to-target strategies. In fact, in such patients “you should probably be following it more tightly to reduce the cardiovascular outcomes,” he said.

The retrospective analysis included 9,085 patients with RA and with or without type 2 diabetes, with a mean follow-up of 5.2 years. They were recruited to the study between 1998 and 2011. Among patients with comorbid diabetes, those exposed to GC had a mortality of 67.4 per 1,000 person-years, compared with 22.5 among those not exposed to GC. Among those with RA alone, mortality was 44.6 versus 10.2 with and without GC exposure, respectively. Those with diabetes had a lower risk ratio for mortality (2.99 vs. 4.37), but a higher mortality difference (44.9 vs. 34.4 per 1,000 person-years).

“The increased absolute hazard for all-cause mortality indicates the greater public health impact of people with RA using GCs if they have [diabetes],” the researchers wrote. “Rheumatologists should consider [diabetes] status when prescribing GCs to patients with RA given this potential impact of GC therapy on glucose control and mortality.”

The study was limited by a lack of information on GC dose and cumulative exposure. Given its retrospective nature, the study could have been affected by confounding by indication, as well as unknown confounders.

The study was funded by the Centre for Epidemiology Versus Arthritis and the National Institute for Health Research Biomedical Research Centre. Dr. Starkebaum has no relevant financial disclosures. Dr. Smith is on the speaker’s bureau for AbbVie and serves on the company’s advisory board. He is also on the advisory boards of Regeneron and Sanofi Genzyme.

SOURCE: Costello R et al. BMC Rheumatol. 2020 Feb 19. doi: 10.1186/s41927-019-0105-4.

Glucocorticoid use is associated with greater mortality and cardiovascular risk in RA patients, and the associated risk is greater still in patients with RA and comorbid diabetes. The findings come from a new retrospective analysis derived from U.K. primary care records.

Although patients with diabetes actually had a lower relative risk for mortality than the nondiabetes cohort, they had a greater mortality difference because of a greater baseline risk. Ultimately, glucocorticoid (GC) use was associated with an additional 44.9 deaths per 1,000 person-years in the diabetes group, compared with 34.4 per 1,000 person-years in the RA-only group.

The study, led by Ruth Costello and William Dixon, MBBS, PhD of the University of Manchester (England), was published in BMC Rheumatology.

The findings aren’t particularly surprising, given that steroid use and diabetes have associated cardiovascular risks, and physicians generally try to reduce or eliminate their use. “There’s a group [of physicians] saying that we don’t need to use steroids at all in rheumatoid arthritis, except maybe for [a] short time at diagnosis to bridge to other therapies, or during flares,” Gordon Starkebaum, MD, professor emeritus of rheumatology at the University of Washington, Seattle, said in an interview. He recounted a session at last year’s annual meeting of the American College of Rheumatology that advocated for only injectable steroid use during flare-ups. “That was provocative,” Dr. Starkebaum said.

“It’s a retrospective study, so it has some limitations, but it provides good insight, and some substantiation to what we already think,” added Brett Smith, DO, a rheumatologist practicing in Knoxville, Tenn.

Dr. Smith suggested that the study further underscores the need to follow treat-to-target protocols in RA. He emphasized that lifetime exposure to steroids is likely the greatest concern, and that steady accumulating doses are a sign of trouble. “If you need that much steroids, you need to go up on your medication – your methotrexate, or sulfasalazine, or your biologic,” said Dr. Smith. “At least 50% of people will need a biologic to [achieve] disease control, and if you get them on it, they’re going to have better disease control, compliance is typically better, and they’re going to have less steroid exposure.”

Dr. Smith also noted that comorbid diabetes shouldn’t affect treat-to-target strategies. In fact, in such patients “you should probably be following it more tightly to reduce the cardiovascular outcomes,” he said.

The retrospective analysis included 9,085 patients with RA and with or without type 2 diabetes, with a mean follow-up of 5.2 years. They were recruited to the study between 1998 and 2011. Among patients with comorbid diabetes, those exposed to GC had a mortality of 67.4 per 1,000 person-years, compared with 22.5 among those not exposed to GC. Among those with RA alone, mortality was 44.6 versus 10.2 with and without GC exposure, respectively. Those with diabetes had a lower risk ratio for mortality (2.99 vs. 4.37), but a higher mortality difference (44.9 vs. 34.4 per 1,000 person-years).

“The increased absolute hazard for all-cause mortality indicates the greater public health impact of people with RA using GCs if they have [diabetes],” the researchers wrote. “Rheumatologists should consider [diabetes] status when prescribing GCs to patients with RA given this potential impact of GC therapy on glucose control and mortality.”

The study was limited by a lack of information on GC dose and cumulative exposure. Given its retrospective nature, the study could have been affected by confounding by indication, as well as unknown confounders.

The study was funded by the Centre for Epidemiology Versus Arthritis and the National Institute for Health Research Biomedical Research Centre. Dr. Starkebaum has no relevant financial disclosures. Dr. Smith is on the speaker’s bureau for AbbVie and serves on the company’s advisory board. He is also on the advisory boards of Regeneron and Sanofi Genzyme.

SOURCE: Costello R et al. BMC Rheumatol. 2020 Feb 19. doi: 10.1186/s41927-019-0105-4.

Thyroid dysfunction is common in patients with diabetes, with a prevalence of around 17%, according to a new analysis of an Australian population.

The results add to the debate over whether patients with diabetes should undergo clinical or biochemical screening for thyroid dysfunction. The American Diabetes Association and U.K. National Institute for Health and Care Excellence guidelines do not recommend general thyroid function monitoring in type 2 diabetes, but the authors of the new study noted concerns that thyroid dysfunction could have metabolic consequences in type 2 disease.

Although the prevalence of undiagnosed thyroid disease in participants with type 2 diabetes was similar to that found in the general Australian population, the researchers, led by Kristen E. Peters, PhD, MedSc, and Timothy M.E. Davis, BMedSc MB, DPhil, of the University of Western Australia, Perth, noted in an article in Clinical Endocrinology that thyroid disease may worsen cardiometabolic risk factors, potentially giving it more significance in this population.

For their study, the researchers analyzed longitudinal data from 1,617 participants in the Fremantle Diabetes Study Phase II, of whom 8.0% had type 1 diabetes, 87.1% had type 2 diabetes, and 4.9% had latent autoimmune diabetes of adults (LADA).

All of the participants filled out questionnaires and underwent baseline fasting biochemical tests and were invited to return for biennial clinical and biochemical measures and to complete biennial questionnaires that were mailed to them. The participants were followed from 2008-2011 (baseline/recruitment period) to 2016. At baseline, 11.7% of the sample (189 of 1,617) had known thyroid disease, based on previous hospitalization of self-reported thyroid medication. Thyroid disease was more prevalent in women than in men (20.4% vs. 3.8%; P less than .001), and there was a nonsignificant trend for a higher prevalence of thyroid disease in participants with type 1 disease, compared with LADA and type 2 (16.9%, 11.4%, and 11.2%, respectively).

Among the 1,428 participants with no documented thyroid disease, 93 (6.5%) were found to have an abnormal thyroid-stimulating hormone (TSH) at baseline testing. Of those 93 participants, 79 had type 2 diabetes, 9 had type 1, and 5 had LADA; across all diabetes types, 5.1% of the participants had subclinical hypothyroidism, 1.1% had overt hypothyroidism, 0.1% had subclinical hyperthyroidism, and 0.2% had overt hyperthyroidism.

Overall, the baseline prevalence of any thyroid disease, known or previously undiagnosed, was 17.4% – 282 of 1,617 participants, of whom 23.8% had type 1 diabetes, 17.7% had LADA, and 16.8% had type 2.

At the end of year 4, serum concentrations were available for 844 participants who had no history of thyroid disease and normal baseline TSH. Over the course of the follow-up period (5,694 patient-years), 25 participants (3%) with normal baseline TSH levels had a first hospitalization for thyroid disease or started thyroid medication, including 2.8% of those with type 1 diabetes and 3.1% of those with type 2. Of the remaining 819 participants who did not have baseline thyroid disease, 3.4% developed subclinical hypothyroidism, 0.2% developed overt hypothyroidism, and 0.5% developed subclinical hyperthyroidism. In each case, there was no statistically significant difference in risk of developing thyroid dysfunction by diabetes type.

“The incidence of any new thyroid disease, including those [participants] with an abnormal follow-up TSH and those with known incident thyroid disease, was 59/844 (7.0%) during [4 years] of follow-up,” the authors noted. “The total incidence of new overt disease was 3.2% (27/844), with 7.4% (2/27) of these patients unaware of the condition. All of the patients with LADA remained euthyroid during follow-up.”

Among the limitations of the study, the authors noted, were that the identification of participants with thyroid disease depended on the available documentation in the databases the researchers used, they were not able to establish pretreatment of thyroid function in most participants with incident thyroid dysfunction, and they did not record free T3.

“Thyroid dysfunction, whether diagnosed or detected on biochemical screening, is common in diabetes regardless of type,” the authors wrote. “Subclinical hypothyroidism is the commonest form [of thyroid dysfunction], and it has a variable course. This latter observation alone makes an argument for periodic biochemical screening in all people with diabetes (not just type 1) as part of routine management.”

However, in an interview, Robert Eckel, MD, professor of medicine at University of Colorado at Denver, Aurora, said that the authors’ suggestion for routine thyroid function testing of patients with any type of diabetes may be premature. He noted that the study lacked a control group, making it difficult to justify a change in practice.

“My take-home message is that the current guidelines are probably not modified by [these findings], but the idea that 17% [of individuals with diabetes] have thyroid disease is worth noting. However, the absence of a control group limits changing recommendations based on this particular study,” said Dr. Eckel, who is also current president, medicine and science, of the ADA.

The study was supported by the National Health and Medical Research Council of Australia and the Spinnaker Health Research Foundation. The study authors did not disclose an financial conflicts.

SOURCE: Peters KE et al. Clin Endocrinol. 2020 Jan 27. doi: 10.1111/cen.14164.

Thyroid dysfunction is common in patients with diabetes, with a prevalence of around 17%, according to a new analysis of an Australian population.

The results add to the debate over whether patients with diabetes should undergo clinical or biochemical screening for thyroid dysfunction. The American Diabetes Association and U.K. National Institute for Health and Care Excellence guidelines do not recommend general thyroid function monitoring in type 2 diabetes, but the authors of the new study noted concerns that thyroid dysfunction could have metabolic consequences in type 2 disease.

Although the prevalence of undiagnosed thyroid disease in participants with type 2 diabetes was similar to that found in the general Australian population, the researchers, led by Kristen E. Peters, PhD, MedSc, and Timothy M.E. Davis, BMedSc MB, DPhil, of the University of Western Australia, Perth, noted in an article in Clinical Endocrinology that thyroid disease may worsen cardiometabolic risk factors, potentially giving it more significance in this population.

For their study, the researchers analyzed longitudinal data from 1,617 participants in the Fremantle Diabetes Study Phase II, of whom 8.0% had type 1 diabetes, 87.1% had type 2 diabetes, and 4.9% had latent autoimmune diabetes of adults (LADA).

All of the participants filled out questionnaires and underwent baseline fasting biochemical tests and were invited to return for biennial clinical and biochemical measures and to complete biennial questionnaires that were mailed to them. The participants were followed from 2008-2011 (baseline/recruitment period) to 2016. At baseline, 11.7% of the sample (189 of 1,617) had known thyroid disease, based on previous hospitalization of self-reported thyroid medication. Thyroid disease was more prevalent in women than in men (20.4% vs. 3.8%; P less than .001), and there was a nonsignificant trend for a higher prevalence of thyroid disease in participants with type 1 disease, compared with LADA and type 2 (16.9%, 11.4%, and 11.2%, respectively).

Among the 1,428 participants with no documented thyroid disease, 93 (6.5%) were found to have an abnormal thyroid-stimulating hormone (TSH) at baseline testing. Of those 93 participants, 79 had type 2 diabetes, 9 had type 1, and 5 had LADA; across all diabetes types, 5.1% of the participants had subclinical hypothyroidism, 1.1% had overt hypothyroidism, 0.1% had subclinical hyperthyroidism, and 0.2% had overt hyperthyroidism.

Overall, the baseline prevalence of any thyroid disease, known or previously undiagnosed, was 17.4% – 282 of 1,617 participants, of whom 23.8% had type 1 diabetes, 17.7% had LADA, and 16.8% had type 2.

At the end of year 4, serum concentrations were available for 844 participants who had no history of thyroid disease and normal baseline TSH. Over the course of the follow-up period (5,694 patient-years), 25 participants (3%) with normal baseline TSH levels had a first hospitalization for thyroid disease or started thyroid medication, including 2.8% of those with type 1 diabetes and 3.1% of those with type 2. Of the remaining 819 participants who did not have baseline thyroid disease, 3.4% developed subclinical hypothyroidism, 0.2% developed overt hypothyroidism, and 0.5% developed subclinical hyperthyroidism. In each case, there was no statistically significant difference in risk of developing thyroid dysfunction by diabetes type.

“The incidence of any new thyroid disease, including those [participants] with an abnormal follow-up TSH and those with known incident thyroid disease, was 59/844 (7.0%) during [4 years] of follow-up,” the authors noted. “The total incidence of new overt disease was 3.2% (27/844), with 7.4% (2/27) of these patients unaware of the condition. All of the patients with LADA remained euthyroid during follow-up.”

Among the limitations of the study, the authors noted, were that the identification of participants with thyroid disease depended on the available documentation in the databases the researchers used, they were not able to establish pretreatment of thyroid function in most participants with incident thyroid dysfunction, and they did not record free T3.

“Thyroid dysfunction, whether diagnosed or detected on biochemical screening, is common in diabetes regardless of type,” the authors wrote. “Subclinical hypothyroidism is the commonest form [of thyroid dysfunction], and it has a variable course. This latter observation alone makes an argument for periodic biochemical screening in all people with diabetes (not just type 1) as part of routine management.”

However, in an interview, Robert Eckel, MD, professor of medicine at University of Colorado at Denver, Aurora, said that the authors’ suggestion for routine thyroid function testing of patients with any type of diabetes may be premature. He noted that the study lacked a control group, making it difficult to justify a change in practice.

“My take-home message is that the current guidelines are probably not modified by [these findings], but the idea that 17% [of individuals with diabetes] have thyroid disease is worth noting. However, the absence of a control group limits changing recommendations based on this particular study,” said Dr. Eckel, who is also current president, medicine and science, of the ADA.

The study was supported by the National Health and Medical Research Council of Australia and the Spinnaker Health Research Foundation. The study authors did not disclose an financial conflicts.

SOURCE: Peters KE et al. Clin Endocrinol. 2020 Jan 27. doi: 10.1111/cen.14164.

Thyroid dysfunction is common in patients with diabetes, with a prevalence of around 17%, according to a new analysis of an Australian population.

The results add to the debate over whether patients with diabetes should undergo clinical or biochemical screening for thyroid dysfunction. The American Diabetes Association and U.K. National Institute for Health and Care Excellence guidelines do not recommend general thyroid function monitoring in type 2 diabetes, but the authors of the new study noted concerns that thyroid dysfunction could have metabolic consequences in type 2 disease.

Although the prevalence of undiagnosed thyroid disease in participants with type 2 diabetes was similar to that found in the general Australian population, the researchers, led by Kristen E. Peters, PhD, MedSc, and Timothy M.E. Davis, BMedSc MB, DPhil, of the University of Western Australia, Perth, noted in an article in Clinical Endocrinology that thyroid disease may worsen cardiometabolic risk factors, potentially giving it more significance in this population.

For their study, the researchers analyzed longitudinal data from 1,617 participants in the Fremantle Diabetes Study Phase II, of whom 8.0% had type 1 diabetes, 87.1% had type 2 diabetes, and 4.9% had latent autoimmune diabetes of adults (LADA).

All of the participants filled out questionnaires and underwent baseline fasting biochemical tests and were invited to return for biennial clinical and biochemical measures and to complete biennial questionnaires that were mailed to them. The participants were followed from 2008-2011 (baseline/recruitment period) to 2016. At baseline, 11.7% of the sample (189 of 1,617) had known thyroid disease, based on previous hospitalization of self-reported thyroid medication. Thyroid disease was more prevalent in women than in men (20.4% vs. 3.8%; P less than .001), and there was a nonsignificant trend for a higher prevalence of thyroid disease in participants with type 1 disease, compared with LADA and type 2 (16.9%, 11.4%, and 11.2%, respectively).

Among the 1,428 participants with no documented thyroid disease, 93 (6.5%) were found to have an abnormal thyroid-stimulating hormone (TSH) at baseline testing. Of those 93 participants, 79 had type 2 diabetes, 9 had type 1, and 5 had LADA; across all diabetes types, 5.1% of the participants had subclinical hypothyroidism, 1.1% had overt hypothyroidism, 0.1% had subclinical hyperthyroidism, and 0.2% had overt hyperthyroidism.

Overall, the baseline prevalence of any thyroid disease, known or previously undiagnosed, was 17.4% – 282 of 1,617 participants, of whom 23.8% had type 1 diabetes, 17.7% had LADA, and 16.8% had type 2.

At the end of year 4, serum concentrations were available for 844 participants who had no history of thyroid disease and normal baseline TSH. Over the course of the follow-up period (5,694 patient-years), 25 participants (3%) with normal baseline TSH levels had a first hospitalization for thyroid disease or started thyroid medication, including 2.8% of those with type 1 diabetes and 3.1% of those with type 2. Of the remaining 819 participants who did not have baseline thyroid disease, 3.4% developed subclinical hypothyroidism, 0.2% developed overt hypothyroidism, and 0.5% developed subclinical hyperthyroidism. In each case, there was no statistically significant difference in risk of developing thyroid dysfunction by diabetes type.

“The incidence of any new thyroid disease, including those [participants] with an abnormal follow-up TSH and those with known incident thyroid disease, was 59/844 (7.0%) during [4 years] of follow-up,” the authors noted. “The total incidence of new overt disease was 3.2% (27/844), with 7.4% (2/27) of these patients unaware of the condition. All of the patients with LADA remained euthyroid during follow-up.”

Among the limitations of the study, the authors noted, were that the identification of participants with thyroid disease depended on the available documentation in the databases the researchers used, they were not able to establish pretreatment of thyroid function in most participants with incident thyroid dysfunction, and they did not record free T3.

“Thyroid dysfunction, whether diagnosed or detected on biochemical screening, is common in diabetes regardless of type,” the authors wrote. “Subclinical hypothyroidism is the commonest form [of thyroid dysfunction], and it has a variable course. This latter observation alone makes an argument for periodic biochemical screening in all people with diabetes (not just type 1) as part of routine management.”

However, in an interview, Robert Eckel, MD, professor of medicine at University of Colorado at Denver, Aurora, said that the authors’ suggestion for routine thyroid function testing of patients with any type of diabetes may be premature. He noted that the study lacked a control group, making it difficult to justify a change in practice.

“My take-home message is that the current guidelines are probably not modified by [these findings], but the idea that 17% [of individuals with diabetes] have thyroid disease is worth noting. However, the absence of a control group limits changing recommendations based on this particular study,” said Dr. Eckel, who is also current president, medicine and science, of the ADA.

The study was supported by the National Health and Medical Research Council of Australia and the Spinnaker Health Research Foundation. The study authors did not disclose an financial conflicts.

SOURCE: Peters KE et al. Clin Endocrinol. 2020 Jan 27. doi: 10.1111/cen.14164.