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M. Alexander Otto began his reporting career early in 1999 covering the pharmaceutical industry for a national pharmacists' magazine and freelancing for the Washington Post and other newspapers. He then joined BNA, now part of Bloomberg News, covering health law and the protection of people and animals in medical research. Alex next worked for the McClatchy Company. Based on his work, Alex won a year-long Knight Science Journalism Fellowship to MIT in 2008-2009. He joined the company shortly thereafter. Alex has a newspaper journalism degree from Syracuse (N.Y.) University and a master's degree in medical science -- a physician assistant degree -- from George Washington University. Alex is based in Seattle.
USPSTF: Insufficient evidence for ABI screening in asymptomatic adults
in asymptomatic adults without known cardiovascular or chronic kidney disease, according to the U.S. Preventive Services Task Force.
“A substantial number of asymptomatic persons with low ABI may never develop clinical signs or symptoms of CVD or PAD but would still be subjected to the harms of testing,” including false positives, exposure to gadolinium or contrast dye with subsequent imaging, and others, the Task Force wrote in JAMA.
In short, it found “inadequate evidence to assess whether screening for and treatment of PAD in asymptomatic patients leads to clinically important benefits in either preventing the progression of PAD or preventing CVD events. ... The current evidence is insufficient to assess the balance of benefits and harms of screening for PAD and CVD risk with the ABI in asymptomatic adults.”
The group made no recommendation, and issued an I statement, for insufficient evidence, July 10. The new work replaces the Task Force’s last visitation in 2013, which was also an “I statement.”
ABI is systolic blood pressure at the ankle divided by the systolic blood pressure in the arm while the patient is lying down. A ratio below 1 is considered abnormal.
ABI is low in perhaps about 6% of adults over 40 years old but “the natural history of screen-detected PAD, including the development of morbidity and mortality directly related to atherosclerosis in the lower limbs, is not well known. ... Large, population-based, randomized trials of screening [versus] no screening are needed to determine whether screening for PAD with the ABI improves clinical outcomes,” the task force said.
Among the many studies it reviewed were two large trials of asymptomatic women with low ABI treated with aspirin 100 mg/d for several years. Neither study showed any significant difference in CVD events, mortality, or development of intermittent claudication.
Even in high-risk people – diabetes, high blood pressure, high cholesterol, current tobacco use – there was “no compelling evidence” to support routine screening, so long as they have no symptoms.
The new review is broader than the group’s 2013 effort, and includes a broader population and range of interventions. Even so, “the recommendation remains an I statement,” it said.
The USPSTF is supported by the U.S. Agency for Healthcare Research and Quality.
SOURCE: JAMA. 2018 Jul 10;320(2):177-83
The USPSTF’s conclusion that current evidence is insufficient to recommend screening for PAD and cardiovascular risk with the ABI in asymptomatic adults should not be misconstrued as a determination that PAD is not common, clinically important, or associated with significant adverse outcomes.
The recommendation does not apply to people with ischemic symptoms during walking activity, who should be tested for PAD with the ABI. The ABI is important for diagnosing nonspecific leg symptoms, common in older people at risk for PAD who frequently have comorbidities such as spinal stenosis, arthritis, and neuropathy that contribute to leg symptoms. The USPSTF recommendation does not apply to these people.
Because most people with PAD do not have classic symptoms of intermittent claudication, the ABI is an important clinical tool for diagnosing PAD and identifying people at increased risk of cardiovascular events and functional decline.
Mary McDermott, MD , is a professor of internal medicine, geriatrics, and preventive medicine at Northwestern University, Chicago, and a JAMA senior editor. Michael Criqui, MD , is a professor of family medicine and public health at the University of California, San Diego. They made their comments in an editorial. Dr. McDermott disclosed research funding from Novartis and Regeneron ( JAMA. 2018 Jul 10;320[2]:143-5 ).
The USPSTF’s conclusion that current evidence is insufficient to recommend screening for PAD and cardiovascular risk with the ABI in asymptomatic adults should not be misconstrued as a determination that PAD is not common, clinically important, or associated with significant adverse outcomes.
The recommendation does not apply to people with ischemic symptoms during walking activity, who should be tested for PAD with the ABI. The ABI is important for diagnosing nonspecific leg symptoms, common in older people at risk for PAD who frequently have comorbidities such as spinal stenosis, arthritis, and neuropathy that contribute to leg symptoms. The USPSTF recommendation does not apply to these people.
Because most people with PAD do not have classic symptoms of intermittent claudication, the ABI is an important clinical tool for diagnosing PAD and identifying people at increased risk of cardiovascular events and functional decline.
Mary McDermott, MD , is a professor of internal medicine, geriatrics, and preventive medicine at Northwestern University, Chicago, and a JAMA senior editor. Michael Criqui, MD , is a professor of family medicine and public health at the University of California, San Diego. They made their comments in an editorial. Dr. McDermott disclosed research funding from Novartis and Regeneron ( JAMA. 2018 Jul 10;320[2]:143-5 ).
The USPSTF’s conclusion that current evidence is insufficient to recommend screening for PAD and cardiovascular risk with the ABI in asymptomatic adults should not be misconstrued as a determination that PAD is not common, clinically important, or associated with significant adverse outcomes.
The recommendation does not apply to people with ischemic symptoms during walking activity, who should be tested for PAD with the ABI. The ABI is important for diagnosing nonspecific leg symptoms, common in older people at risk for PAD who frequently have comorbidities such as spinal stenosis, arthritis, and neuropathy that contribute to leg symptoms. The USPSTF recommendation does not apply to these people.
Because most people with PAD do not have classic symptoms of intermittent claudication, the ABI is an important clinical tool for diagnosing PAD and identifying people at increased risk of cardiovascular events and functional decline.
Mary McDermott, MD , is a professor of internal medicine, geriatrics, and preventive medicine at Northwestern University, Chicago, and a JAMA senior editor. Michael Criqui, MD , is a professor of family medicine and public health at the University of California, San Diego. They made their comments in an editorial. Dr. McDermott disclosed research funding from Novartis and Regeneron ( JAMA. 2018 Jul 10;320[2]:143-5 ).
in asymptomatic adults without known cardiovascular or chronic kidney disease, according to the U.S. Preventive Services Task Force.
“A substantial number of asymptomatic persons with low ABI may never develop clinical signs or symptoms of CVD or PAD but would still be subjected to the harms of testing,” including false positives, exposure to gadolinium or contrast dye with subsequent imaging, and others, the Task Force wrote in JAMA.
In short, it found “inadequate evidence to assess whether screening for and treatment of PAD in asymptomatic patients leads to clinically important benefits in either preventing the progression of PAD or preventing CVD events. ... The current evidence is insufficient to assess the balance of benefits and harms of screening for PAD and CVD risk with the ABI in asymptomatic adults.”
The group made no recommendation, and issued an I statement, for insufficient evidence, July 10. The new work replaces the Task Force’s last visitation in 2013, which was also an “I statement.”
ABI is systolic blood pressure at the ankle divided by the systolic blood pressure in the arm while the patient is lying down. A ratio below 1 is considered abnormal.
ABI is low in perhaps about 6% of adults over 40 years old but “the natural history of screen-detected PAD, including the development of morbidity and mortality directly related to atherosclerosis in the lower limbs, is not well known. ... Large, population-based, randomized trials of screening [versus] no screening are needed to determine whether screening for PAD with the ABI improves clinical outcomes,” the task force said.
Among the many studies it reviewed were two large trials of asymptomatic women with low ABI treated with aspirin 100 mg/d for several years. Neither study showed any significant difference in CVD events, mortality, or development of intermittent claudication.
Even in high-risk people – diabetes, high blood pressure, high cholesterol, current tobacco use – there was “no compelling evidence” to support routine screening, so long as they have no symptoms.
The new review is broader than the group’s 2013 effort, and includes a broader population and range of interventions. Even so, “the recommendation remains an I statement,” it said.
The USPSTF is supported by the U.S. Agency for Healthcare Research and Quality.
SOURCE: JAMA. 2018 Jul 10;320(2):177-83
in asymptomatic adults without known cardiovascular or chronic kidney disease, according to the U.S. Preventive Services Task Force.
“A substantial number of asymptomatic persons with low ABI may never develop clinical signs or symptoms of CVD or PAD but would still be subjected to the harms of testing,” including false positives, exposure to gadolinium or contrast dye with subsequent imaging, and others, the Task Force wrote in JAMA.
In short, it found “inadequate evidence to assess whether screening for and treatment of PAD in asymptomatic patients leads to clinically important benefits in either preventing the progression of PAD or preventing CVD events. ... The current evidence is insufficient to assess the balance of benefits and harms of screening for PAD and CVD risk with the ABI in asymptomatic adults.”
The group made no recommendation, and issued an I statement, for insufficient evidence, July 10. The new work replaces the Task Force’s last visitation in 2013, which was also an “I statement.”
ABI is systolic blood pressure at the ankle divided by the systolic blood pressure in the arm while the patient is lying down. A ratio below 1 is considered abnormal.
ABI is low in perhaps about 6% of adults over 40 years old but “the natural history of screen-detected PAD, including the development of morbidity and mortality directly related to atherosclerosis in the lower limbs, is not well known. ... Large, population-based, randomized trials of screening [versus] no screening are needed to determine whether screening for PAD with the ABI improves clinical outcomes,” the task force said.
Among the many studies it reviewed were two large trials of asymptomatic women with low ABI treated with aspirin 100 mg/d for several years. Neither study showed any significant difference in CVD events, mortality, or development of intermittent claudication.
Even in high-risk people – diabetes, high blood pressure, high cholesterol, current tobacco use – there was “no compelling evidence” to support routine screening, so long as they have no symptoms.
The new review is broader than the group’s 2013 effort, and includes a broader population and range of interventions. Even so, “the recommendation remains an I statement,” it said.
The USPSTF is supported by the U.S. Agency for Healthcare Research and Quality.
SOURCE: JAMA. 2018 Jul 10;320(2):177-83
FROM JAMA
USPSTF: Nontraditional CVD risk factors not ready for prime time
Current evidence is insufficient to assess the balance harms and benefits of adding ankle-brachial index, high-sensitivity C-reactive protein, or coronary artery calcium burden to traditional cardiovascular disease risk scores for asymptomatic adults, according to the United States Preventive Services Task Force.
USPSTF did note that many of the comments to its draft document “provided evidence that risk assessment with CAC [coronary artery calcium] was strong enough to warrant a separate, more positive recommendation” and “is useful for patients whose risk stratification is unclear or for those who fall into intermediate-risk groups.” However, evidence is inadequate that this would translate into improved health outcomes in asymptomatic patients.
Meanwhile, treatment decisions guided by the markers have not been shown to reduce cardiovascular events or mortality. There are no trials evaluating the additional benefit of adding the ankle-brachial index (ABI), high-sensitivity C-reactive level (hsCRP), or CAC score to traditional risk assessment models.
The USPSTF recommended “that clinicians use the Pooled Cohort Equations to assess CVD risk and to guide treatment decisions until further evidence is available,” noting that these equations, introduced in 2013, were developed using more contemporary and diverse cohort data than were the older Framingham Risk Score. Traditional CVD risk factors include age, sex, high blood pressure, current smoking, abnormal cholesterol levels, diabetes, obesity, and physical inactivity.
The work replaces the group’s 2009 statement on nontraditional risk factors, which also was considered an I statement, for inadequate evidence. Unlike that document, the new work focused on ABI, hsCRP level, and CAC because these offer the most promising evidence base and are independently associated with CVD events.
The group noted that testing for hsCRP level and ABI is noninvasive, with little direct harm. Harms of testing for CAC score include exposure to radiation and incidental findings on CT of the chest, such as pulmonary nodules, that may lead to further invasive testing and procedures, among other problems.
The ABI is the ratio of the systolic blood pressure at the ankle to the systolic blood pressure in the arm while the patient is lying down; a value less than 1 is abnormal. High-sensitivity CRP is a serum protein involved in inflammatory and immune responses. Coronary artery calcium score is a measure of calcium content in the coronary arteries.
Good-quality studies that compare traditional risk assessment with ABI, hsCRP level, or CAC scores “are needed to measure the effect of adding nontraditional risk factors on clinical decision thresholds and patient outcomes, especially in more diverse populations (women, racial/ethnic minorities, persons of lower socioeconomic status), in whom assessment of nontraditional risk factors may help address the shortcomings of traditional risk models,” USPSTF said.
The group is funded by the Agency for Healthcare Research and Quality.
These conclusions are understandable from the policy perspective but do not fully address the issues faced by individual patients and clinicians in decisions about the relative merits of primary preventive therapies.
In middle-aged and older U.S. adults whose estimated absolute risks of developing CVD events are near a treatment threshold (e.g., 7.5%), the presence of CAC scores greater than 100, or higher than the 75th percentile for a given age, accurately reclassifies individuals to a higher category of risk. Even individuals with low estimated 10-year risks and high CAC scores (more than 100 Agatston units) have substantially greater observed risks than do those with CAC scores of 0. Thus, the presence of CAC in these patients effectively identifies those at higher risk who may benefit from statin therapy. Avoidance of statin therapy in the majority of intermediate-risk patients who have a CAC score of 0 also is desirable.
Meanwhile, a low ABI represents an advanced form of atherosclerosis. Clinicians should be aware of PAD and, if it is present, should strongly consider statin therapy. Use of the ABI in routine clinical practice to screen for PAD in at-risk patients is reasonable, but its routine use in estimation of CVD risk is limited. Measurement of subclinical inflammation with hsCRP has been shown to reclassify some individuals at intermediate levels of risk. However, the utility of hsCRP measurement in routine assessment of CVD risk for primary prevention is limited.
John Wilkins, MD, is an assistant professor of cardiology and preventive medicine and Donald Lloyd-Jones, MD, is the chair of the Department of Preventive Medicine at Northwestern University, Chicago. They had no disclosures, and made their comments in an editorial (JAMA. 2018 Jul 10. doi: 10.1001/jama.2018.9346 ).
These conclusions are understandable from the policy perspective but do not fully address the issues faced by individual patients and clinicians in decisions about the relative merits of primary preventive therapies.
In middle-aged and older U.S. adults whose estimated absolute risks of developing CVD events are near a treatment threshold (e.g., 7.5%), the presence of CAC scores greater than 100, or higher than the 75th percentile for a given age, accurately reclassifies individuals to a higher category of risk. Even individuals with low estimated 10-year risks and high CAC scores (more than 100 Agatston units) have substantially greater observed risks than do those with CAC scores of 0. Thus, the presence of CAC in these patients effectively identifies those at higher risk who may benefit from statin therapy. Avoidance of statin therapy in the majority of intermediate-risk patients who have a CAC score of 0 also is desirable.
Meanwhile, a low ABI represents an advanced form of atherosclerosis. Clinicians should be aware of PAD and, if it is present, should strongly consider statin therapy. Use of the ABI in routine clinical practice to screen for PAD in at-risk patients is reasonable, but its routine use in estimation of CVD risk is limited. Measurement of subclinical inflammation with hsCRP has been shown to reclassify some individuals at intermediate levels of risk. However, the utility of hsCRP measurement in routine assessment of CVD risk for primary prevention is limited.
John Wilkins, MD, is an assistant professor of cardiology and preventive medicine and Donald Lloyd-Jones, MD, is the chair of the Department of Preventive Medicine at Northwestern University, Chicago. They had no disclosures, and made their comments in an editorial (JAMA. 2018 Jul 10. doi: 10.1001/jama.2018.9346 ).
These conclusions are understandable from the policy perspective but do not fully address the issues faced by individual patients and clinicians in decisions about the relative merits of primary preventive therapies.
In middle-aged and older U.S. adults whose estimated absolute risks of developing CVD events are near a treatment threshold (e.g., 7.5%), the presence of CAC scores greater than 100, or higher than the 75th percentile for a given age, accurately reclassifies individuals to a higher category of risk. Even individuals with low estimated 10-year risks and high CAC scores (more than 100 Agatston units) have substantially greater observed risks than do those with CAC scores of 0. Thus, the presence of CAC in these patients effectively identifies those at higher risk who may benefit from statin therapy. Avoidance of statin therapy in the majority of intermediate-risk patients who have a CAC score of 0 also is desirable.
Meanwhile, a low ABI represents an advanced form of atherosclerosis. Clinicians should be aware of PAD and, if it is present, should strongly consider statin therapy. Use of the ABI in routine clinical practice to screen for PAD in at-risk patients is reasonable, but its routine use in estimation of CVD risk is limited. Measurement of subclinical inflammation with hsCRP has been shown to reclassify some individuals at intermediate levels of risk. However, the utility of hsCRP measurement in routine assessment of CVD risk for primary prevention is limited.
John Wilkins, MD, is an assistant professor of cardiology and preventive medicine and Donald Lloyd-Jones, MD, is the chair of the Department of Preventive Medicine at Northwestern University, Chicago. They had no disclosures, and made their comments in an editorial (JAMA. 2018 Jul 10. doi: 10.1001/jama.2018.9346 ).
Current evidence is insufficient to assess the balance harms and benefits of adding ankle-brachial index, high-sensitivity C-reactive protein, or coronary artery calcium burden to traditional cardiovascular disease risk scores for asymptomatic adults, according to the United States Preventive Services Task Force.
USPSTF did note that many of the comments to its draft document “provided evidence that risk assessment with CAC [coronary artery calcium] was strong enough to warrant a separate, more positive recommendation” and “is useful for patients whose risk stratification is unclear or for those who fall into intermediate-risk groups.” However, evidence is inadequate that this would translate into improved health outcomes in asymptomatic patients.
Meanwhile, treatment decisions guided by the markers have not been shown to reduce cardiovascular events or mortality. There are no trials evaluating the additional benefit of adding the ankle-brachial index (ABI), high-sensitivity C-reactive level (hsCRP), or CAC score to traditional risk assessment models.
The USPSTF recommended “that clinicians use the Pooled Cohort Equations to assess CVD risk and to guide treatment decisions until further evidence is available,” noting that these equations, introduced in 2013, were developed using more contemporary and diverse cohort data than were the older Framingham Risk Score. Traditional CVD risk factors include age, sex, high blood pressure, current smoking, abnormal cholesterol levels, diabetes, obesity, and physical inactivity.
The work replaces the group’s 2009 statement on nontraditional risk factors, which also was considered an I statement, for inadequate evidence. Unlike that document, the new work focused on ABI, hsCRP level, and CAC because these offer the most promising evidence base and are independently associated with CVD events.
The group noted that testing for hsCRP level and ABI is noninvasive, with little direct harm. Harms of testing for CAC score include exposure to radiation and incidental findings on CT of the chest, such as pulmonary nodules, that may lead to further invasive testing and procedures, among other problems.
The ABI is the ratio of the systolic blood pressure at the ankle to the systolic blood pressure in the arm while the patient is lying down; a value less than 1 is abnormal. High-sensitivity CRP is a serum protein involved in inflammatory and immune responses. Coronary artery calcium score is a measure of calcium content in the coronary arteries.
Good-quality studies that compare traditional risk assessment with ABI, hsCRP level, or CAC scores “are needed to measure the effect of adding nontraditional risk factors on clinical decision thresholds and patient outcomes, especially in more diverse populations (women, racial/ethnic minorities, persons of lower socioeconomic status), in whom assessment of nontraditional risk factors may help address the shortcomings of traditional risk models,” USPSTF said.
The group is funded by the Agency for Healthcare Research and Quality.
Current evidence is insufficient to assess the balance harms and benefits of adding ankle-brachial index, high-sensitivity C-reactive protein, or coronary artery calcium burden to traditional cardiovascular disease risk scores for asymptomatic adults, according to the United States Preventive Services Task Force.
USPSTF did note that many of the comments to its draft document “provided evidence that risk assessment with CAC [coronary artery calcium] was strong enough to warrant a separate, more positive recommendation” and “is useful for patients whose risk stratification is unclear or for those who fall into intermediate-risk groups.” However, evidence is inadequate that this would translate into improved health outcomes in asymptomatic patients.
Meanwhile, treatment decisions guided by the markers have not been shown to reduce cardiovascular events or mortality. There are no trials evaluating the additional benefit of adding the ankle-brachial index (ABI), high-sensitivity C-reactive level (hsCRP), or CAC score to traditional risk assessment models.
The USPSTF recommended “that clinicians use the Pooled Cohort Equations to assess CVD risk and to guide treatment decisions until further evidence is available,” noting that these equations, introduced in 2013, were developed using more contemporary and diverse cohort data than were the older Framingham Risk Score. Traditional CVD risk factors include age, sex, high blood pressure, current smoking, abnormal cholesterol levels, diabetes, obesity, and physical inactivity.
The work replaces the group’s 2009 statement on nontraditional risk factors, which also was considered an I statement, for inadequate evidence. Unlike that document, the new work focused on ABI, hsCRP level, and CAC because these offer the most promising evidence base and are independently associated with CVD events.
The group noted that testing for hsCRP level and ABI is noninvasive, with little direct harm. Harms of testing for CAC score include exposure to radiation and incidental findings on CT of the chest, such as pulmonary nodules, that may lead to further invasive testing and procedures, among other problems.
The ABI is the ratio of the systolic blood pressure at the ankle to the systolic blood pressure in the arm while the patient is lying down; a value less than 1 is abnormal. High-sensitivity CRP is a serum protein involved in inflammatory and immune responses. Coronary artery calcium score is a measure of calcium content in the coronary arteries.
Good-quality studies that compare traditional risk assessment with ABI, hsCRP level, or CAC scores “are needed to measure the effect of adding nontraditional risk factors on clinical decision thresholds and patient outcomes, especially in more diverse populations (women, racial/ethnic minorities, persons of lower socioeconomic status), in whom assessment of nontraditional risk factors may help address the shortcomings of traditional risk models,” USPSTF said.
The group is funded by the Agency for Healthcare Research and Quality.
FROM JAMA
Uric acid tied to pediatric diabetic kidney disease
ORLANDO – , according to a 7-year investigation of 539 children.
Every 1-mg/dL climb in baseline serum uric acid increased the risk of subsequent elevated urine albumin excretion 1.23 fold, after adjustment for potential confounders (P = .02).
The finding adds to growing evidence that serum uric acid (SUA) isn’t just a marker of diabetic kidney disease, but a contributor to it. “There is definitely” cross-talk between gout and diabetes, said lead investigator Petter Bjornstad, MD, assistant professor of pediatric endocrinology at the University of Colorado, Aurora.
Elevated SUA is common in both conditions and a risk factor for kidney disease. Newer studies have linked higher levels to nephron number decline and other pathologies, perhaps through renal inflammation. Allopurinol, the traditional uric acid lowering agent in gout, is already under investigation to prevent kidney decline in adults with type 1 diabetes mellitus. There’s also evidence that the potent uric acid lowering agent, febuxostat (Uloric), attenuates hypofiltration in early diabetic kidney disease.
The 539 children, all part of the Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) trial, were assessed annually over a mean of 5.7 years. At baseline, they were 13.9 years old and had T2DM for 7.9 months, on average. The mean body mass index was 34.6 kg/m2, mean hemoglobin A1c was 6%.
Almost 20% of the children were hypertensive at baseline (130/80 mm Hg or higher); 26% were hyperuricemic (6.8 mg/dL or higher); and 6.1% had elevated urine albumin excretion (urine albumin creatinine ratio of at least 30 mg/g), a marker of renal pathology. At the end of follow-up, 18% had elevated albumin excretion and 37.4% were hypertensive.
“Hyperuricemia was common in youth with type 2 diabetes,” just as it’s been shown in adults with the disease. “Higher baseline SUA independently increase[s] risk for onset of hypertension and elevated urine albumin excretion,” Dr. Bjornstad said.
However, the association between SUA and elevated albumin excretion was statistically significant only in boys – 36% of the study population – and non-Hispanic whites, 20% of the subjects, after adjustment for BMI, hemoglobin A1c, estimated glomerular filtration rate, and use of ACE inhibitors and angiotensin II receptor blockers.
The National Institutes of Health funded the work. Dr. Bjornstad is a consultant for Boehringer Ingelheim.
SOURCE: Bjornstad P et al. ADA 2018, abstract 339-OR.
ORLANDO – , according to a 7-year investigation of 539 children.
Every 1-mg/dL climb in baseline serum uric acid increased the risk of subsequent elevated urine albumin excretion 1.23 fold, after adjustment for potential confounders (P = .02).
The finding adds to growing evidence that serum uric acid (SUA) isn’t just a marker of diabetic kidney disease, but a contributor to it. “There is definitely” cross-talk between gout and diabetes, said lead investigator Petter Bjornstad, MD, assistant professor of pediatric endocrinology at the University of Colorado, Aurora.
Elevated SUA is common in both conditions and a risk factor for kidney disease. Newer studies have linked higher levels to nephron number decline and other pathologies, perhaps through renal inflammation. Allopurinol, the traditional uric acid lowering agent in gout, is already under investigation to prevent kidney decline in adults with type 1 diabetes mellitus. There’s also evidence that the potent uric acid lowering agent, febuxostat (Uloric), attenuates hypofiltration in early diabetic kidney disease.
The 539 children, all part of the Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) trial, were assessed annually over a mean of 5.7 years. At baseline, they were 13.9 years old and had T2DM for 7.9 months, on average. The mean body mass index was 34.6 kg/m2, mean hemoglobin A1c was 6%.
Almost 20% of the children were hypertensive at baseline (130/80 mm Hg or higher); 26% were hyperuricemic (6.8 mg/dL or higher); and 6.1% had elevated urine albumin excretion (urine albumin creatinine ratio of at least 30 mg/g), a marker of renal pathology. At the end of follow-up, 18% had elevated albumin excretion and 37.4% were hypertensive.
“Hyperuricemia was common in youth with type 2 diabetes,” just as it’s been shown in adults with the disease. “Higher baseline SUA independently increase[s] risk for onset of hypertension and elevated urine albumin excretion,” Dr. Bjornstad said.
However, the association between SUA and elevated albumin excretion was statistically significant only in boys – 36% of the study population – and non-Hispanic whites, 20% of the subjects, after adjustment for BMI, hemoglobin A1c, estimated glomerular filtration rate, and use of ACE inhibitors and angiotensin II receptor blockers.
The National Institutes of Health funded the work. Dr. Bjornstad is a consultant for Boehringer Ingelheim.
SOURCE: Bjornstad P et al. ADA 2018, abstract 339-OR.
ORLANDO – , according to a 7-year investigation of 539 children.
Every 1-mg/dL climb in baseline serum uric acid increased the risk of subsequent elevated urine albumin excretion 1.23 fold, after adjustment for potential confounders (P = .02).
The finding adds to growing evidence that serum uric acid (SUA) isn’t just a marker of diabetic kidney disease, but a contributor to it. “There is definitely” cross-talk between gout and diabetes, said lead investigator Petter Bjornstad, MD, assistant professor of pediatric endocrinology at the University of Colorado, Aurora.
Elevated SUA is common in both conditions and a risk factor for kidney disease. Newer studies have linked higher levels to nephron number decline and other pathologies, perhaps through renal inflammation. Allopurinol, the traditional uric acid lowering agent in gout, is already under investigation to prevent kidney decline in adults with type 1 diabetes mellitus. There’s also evidence that the potent uric acid lowering agent, febuxostat (Uloric), attenuates hypofiltration in early diabetic kidney disease.
The 539 children, all part of the Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) trial, were assessed annually over a mean of 5.7 years. At baseline, they were 13.9 years old and had T2DM for 7.9 months, on average. The mean body mass index was 34.6 kg/m2, mean hemoglobin A1c was 6%.
Almost 20% of the children were hypertensive at baseline (130/80 mm Hg or higher); 26% were hyperuricemic (6.8 mg/dL or higher); and 6.1% had elevated urine albumin excretion (urine albumin creatinine ratio of at least 30 mg/g), a marker of renal pathology. At the end of follow-up, 18% had elevated albumin excretion and 37.4% were hypertensive.
“Hyperuricemia was common in youth with type 2 diabetes,” just as it’s been shown in adults with the disease. “Higher baseline SUA independently increase[s] risk for onset of hypertension and elevated urine albumin excretion,” Dr. Bjornstad said.
However, the association between SUA and elevated albumin excretion was statistically significant only in boys – 36% of the study population – and non-Hispanic whites, 20% of the subjects, after adjustment for BMI, hemoglobin A1c, estimated glomerular filtration rate, and use of ACE inhibitors and angiotensin II receptor blockers.
The National Institutes of Health funded the work. Dr. Bjornstad is a consultant for Boehringer Ingelheim.
SOURCE: Bjornstad P et al. ADA 2018, abstract 339-OR.
REPORTING FROM ADA 2018
Key clinical point: Serum uric acid lowering might help prevent kidney disease in children with T2DM.
Major finding: Every1-mg/dL climb in baseline serum uric acid increased the risk of subsequent elevated urine albumin excretion 1.23 fold, after adjustment for potential confounders (P = .02)
Study details: Seven-year investigation of 539 children with new-onset T2DM.
Disclosures: The National Institutes of Health funded the work. The study lead is a consultant for Boehringer Ingelheim.
Source: Bjornstad P et al. ADA 2018 Abstract 339-OR.
Study questions canagliflozin amputation risk, but concerns remain
ORLANDO – but clinicians should still favor other options in patients at risk for amputations, according to investigator John Buse, MD, PhD, chief of the division of endocrinology at the University of North Carolina at Chapel Hill.
Canagliflozin is the only sodium-glucose transporter 2 (SGLT2) inhibitor that carries a black box warning of “lower limb amputations, most frequently of the toe and midfoot” but also the leg. The drug doubled the risk versus placebo in its approval trials, particularly in patients with baseline histories of prior amputations, peripheral vascular disease, neuropathy, or diabetic foot ulcers.
One trial, for instance, reported 7.5 amputations per 1,000 patient years versus 4.2 with placebo, according to labeling.
The new, observational study, which was funded by canagliflozin’s maker Johnson & Johnson and, with the exception of Dr. Buse, conducted by its employees, found no such connection. Investigators reviewed claims data from 142,800 new users of canagliflozin, 110,897 new users of the competing SGLT2 inhibitors empagliflozin (Jardiance) and dapagliflozin (Farxiga), and 460,885 new users of other diabetes drugs except for metformin, Dr. Buse said when he presented the results at the annual scientific sessions of the American Diabetes Association.
The hazard ratio for below-knee amputations with canagliflozin versus non-SGLT2 inhibitors was 0.75 (95% confidence interval, 0.40-1.41; P = 0.30). The ratio versus other SGLT2 inhibitors was 1.14 (95% CI, 0.67-1.93; P = 0.53). Overall, there were 1-5 amputations per 1,000 patient years with the drug.
However, the median follow-up was a few months, far shorter than the median follow-up of over 2 years in the randomized trials. “Therefore, the current study had limited statistical power to detect differences in the 6-12 month time period, the time at which amputation risk began to emerge” in the trials, the study report noted. Also, the investigators didn’t parse out results according to baseline amputation risk. Overall, “none of the analyses were sufficiently powered to rule out the possibility of a modest effect” on amputation rates (Diabetes Obes Metab. 2018 Jun 25. doi: 10.1111/dom.13424).
When moderator Robert H. Eckel, MD, a professor in the division of endocrinology, metabolism, and diabetes at the University of Colorado at Denver, Aurora, asked the 150 or so people who heard the presentation if they use SGLT2 inhibitors in their practices, only a small number raised their hands. Few, if any, raised their hands when he asked if the new results would make them more comfortable prescribing canagliflozin.
“I find [the study] somewhat informative,” Dr. Eckel said in an interview afterwards, “but I think the issue is that the prescribing label still demands that patients be informed of the black box warning. I think we are going to have to wait for the longer term outcomes to determine if [amputation] is a molecule effect or a class effect.”
Dr. Buse later said that “I think for the general population of patients with diabetes, they are at low risk for an amputation,” but “if you are at high risk for having an amputation, we really have to take this risk very seriously. [Canagliflozin] may increase your risk for amputation.
“If I have a patient who has had an amputation and I want to use an SGLT2 inhibitor, I wouldn’t use canagliflozin because of the label. I would use empagliflozin because [amputation] is not in the label, and there was no evidence” of it in trials, he added.
The new study, meanwhile, confirmed the cardiac benefits of SGLT2 inhibitors in type 2 patients. Canagliflozin, for instance, reduced the risk of hospitalization for heart failure by about 60%, compared with non-SGLT2 inhibitors in patients with cardiovascular disease, but it offered no statistically significant heart benefit over other members of its class.
Dr. Buse is an investigator for Johnson and Johnson.
ORLANDO – but clinicians should still favor other options in patients at risk for amputations, according to investigator John Buse, MD, PhD, chief of the division of endocrinology at the University of North Carolina at Chapel Hill.
Canagliflozin is the only sodium-glucose transporter 2 (SGLT2) inhibitor that carries a black box warning of “lower limb amputations, most frequently of the toe and midfoot” but also the leg. The drug doubled the risk versus placebo in its approval trials, particularly in patients with baseline histories of prior amputations, peripheral vascular disease, neuropathy, or diabetic foot ulcers.
One trial, for instance, reported 7.5 amputations per 1,000 patient years versus 4.2 with placebo, according to labeling.
The new, observational study, which was funded by canagliflozin’s maker Johnson & Johnson and, with the exception of Dr. Buse, conducted by its employees, found no such connection. Investigators reviewed claims data from 142,800 new users of canagliflozin, 110,897 new users of the competing SGLT2 inhibitors empagliflozin (Jardiance) and dapagliflozin (Farxiga), and 460,885 new users of other diabetes drugs except for metformin, Dr. Buse said when he presented the results at the annual scientific sessions of the American Diabetes Association.
The hazard ratio for below-knee amputations with canagliflozin versus non-SGLT2 inhibitors was 0.75 (95% confidence interval, 0.40-1.41; P = 0.30). The ratio versus other SGLT2 inhibitors was 1.14 (95% CI, 0.67-1.93; P = 0.53). Overall, there were 1-5 amputations per 1,000 patient years with the drug.
However, the median follow-up was a few months, far shorter than the median follow-up of over 2 years in the randomized trials. “Therefore, the current study had limited statistical power to detect differences in the 6-12 month time period, the time at which amputation risk began to emerge” in the trials, the study report noted. Also, the investigators didn’t parse out results according to baseline amputation risk. Overall, “none of the analyses were sufficiently powered to rule out the possibility of a modest effect” on amputation rates (Diabetes Obes Metab. 2018 Jun 25. doi: 10.1111/dom.13424).
When moderator Robert H. Eckel, MD, a professor in the division of endocrinology, metabolism, and diabetes at the University of Colorado at Denver, Aurora, asked the 150 or so people who heard the presentation if they use SGLT2 inhibitors in their practices, only a small number raised their hands. Few, if any, raised their hands when he asked if the new results would make them more comfortable prescribing canagliflozin.
“I find [the study] somewhat informative,” Dr. Eckel said in an interview afterwards, “but I think the issue is that the prescribing label still demands that patients be informed of the black box warning. I think we are going to have to wait for the longer term outcomes to determine if [amputation] is a molecule effect or a class effect.”
Dr. Buse later said that “I think for the general population of patients with diabetes, they are at low risk for an amputation,” but “if you are at high risk for having an amputation, we really have to take this risk very seriously. [Canagliflozin] may increase your risk for amputation.
“If I have a patient who has had an amputation and I want to use an SGLT2 inhibitor, I wouldn’t use canagliflozin because of the label. I would use empagliflozin because [amputation] is not in the label, and there was no evidence” of it in trials, he added.
The new study, meanwhile, confirmed the cardiac benefits of SGLT2 inhibitors in type 2 patients. Canagliflozin, for instance, reduced the risk of hospitalization for heart failure by about 60%, compared with non-SGLT2 inhibitors in patients with cardiovascular disease, but it offered no statistically significant heart benefit over other members of its class.
Dr. Buse is an investigator for Johnson and Johnson.
ORLANDO – but clinicians should still favor other options in patients at risk for amputations, according to investigator John Buse, MD, PhD, chief of the division of endocrinology at the University of North Carolina at Chapel Hill.
Canagliflozin is the only sodium-glucose transporter 2 (SGLT2) inhibitor that carries a black box warning of “lower limb amputations, most frequently of the toe and midfoot” but also the leg. The drug doubled the risk versus placebo in its approval trials, particularly in patients with baseline histories of prior amputations, peripheral vascular disease, neuropathy, or diabetic foot ulcers.
One trial, for instance, reported 7.5 amputations per 1,000 patient years versus 4.2 with placebo, according to labeling.
The new, observational study, which was funded by canagliflozin’s maker Johnson & Johnson and, with the exception of Dr. Buse, conducted by its employees, found no such connection. Investigators reviewed claims data from 142,800 new users of canagliflozin, 110,897 new users of the competing SGLT2 inhibitors empagliflozin (Jardiance) and dapagliflozin (Farxiga), and 460,885 new users of other diabetes drugs except for metformin, Dr. Buse said when he presented the results at the annual scientific sessions of the American Diabetes Association.
The hazard ratio for below-knee amputations with canagliflozin versus non-SGLT2 inhibitors was 0.75 (95% confidence interval, 0.40-1.41; P = 0.30). The ratio versus other SGLT2 inhibitors was 1.14 (95% CI, 0.67-1.93; P = 0.53). Overall, there were 1-5 amputations per 1,000 patient years with the drug.
However, the median follow-up was a few months, far shorter than the median follow-up of over 2 years in the randomized trials. “Therefore, the current study had limited statistical power to detect differences in the 6-12 month time period, the time at which amputation risk began to emerge” in the trials, the study report noted. Also, the investigators didn’t parse out results according to baseline amputation risk. Overall, “none of the analyses were sufficiently powered to rule out the possibility of a modest effect” on amputation rates (Diabetes Obes Metab. 2018 Jun 25. doi: 10.1111/dom.13424).
When moderator Robert H. Eckel, MD, a professor in the division of endocrinology, metabolism, and diabetes at the University of Colorado at Denver, Aurora, asked the 150 or so people who heard the presentation if they use SGLT2 inhibitors in their practices, only a small number raised their hands. Few, if any, raised their hands when he asked if the new results would make them more comfortable prescribing canagliflozin.
“I find [the study] somewhat informative,” Dr. Eckel said in an interview afterwards, “but I think the issue is that the prescribing label still demands that patients be informed of the black box warning. I think we are going to have to wait for the longer term outcomes to determine if [amputation] is a molecule effect or a class effect.”
Dr. Buse later said that “I think for the general population of patients with diabetes, they are at low risk for an amputation,” but “if you are at high risk for having an amputation, we really have to take this risk very seriously. [Canagliflozin] may increase your risk for amputation.
“If I have a patient who has had an amputation and I want to use an SGLT2 inhibitor, I wouldn’t use canagliflozin because of the label. I would use empagliflozin because [amputation] is not in the label, and there was no evidence” of it in trials, he added.
The new study, meanwhile, confirmed the cardiac benefits of SGLT2 inhibitors in type 2 patients. Canagliflozin, for instance, reduced the risk of hospitalization for heart failure by about 60%, compared with non-SGLT2 inhibitors in patients with cardiovascular disease, but it offered no statistically significant heart benefit over other members of its class.
Dr. Buse is an investigator for Johnson and Johnson.
REPORTING FROM ADA 2018
Key clinical point: A large, observational study found no increased risk of below-the-knee amputations with canagliflozin for type 2 diabetes, but clinicians should still favor other options in patients at risk for amputations.
Major finding: The hazard ratio for below-knee amputations with canagliflozin versus non-SGLT2 inhibitors was 0.75 (95% confidence interval, 0.40-1.41; P = 0.30).
Study details: An observational study of over 700,000 patients with type 2 diabetes.
Disclosures: The work was funded by canagliflozin’s maker Johnson & Johnson and, with the exception of the presenter, conducted by its employees.
Adalimumab strikes out for aortic inflammation in psoriasis
ORLANDO – Adalimumab (Humira) did not reduce aortic inflammation in a year-long, randomized trial that pitted the tumor necrosis factor (TNF) blocker against phototherapy and placebo in 97 psoriasis patients.
a risk factor for cardiovascular events, said senior investigator Joel M. Gelfand, MD, a dermatology professor at the University of Pennsylvania, Philadelphia.
The other trial, from Canada, also found no effect in the ascending aorta after 52 weeks of treatment, but it did find a modest increase in carotid inflammation (J Invest Dermatol. 2017 Aug;137[8]:1638-45).
Both studies used positron emission tomography/computed tomography to assess vascular inflammation.
“We know patients with psoriasis are at increased risk for cardiovascular disease. We think the same kind of inflammation that occurs in atherosclerosis occurs in psoriasis, but we are still teasing out the impact of therapy and which one is most likely to lower the risk of heart attacks, strokes, and things of that nature,” Dr. Gelfand said at the International Investigative Dermatology meeting. The study was published when he gave his presentation (Circ Cardiovasc Imaging. 2018 Jun. doi: 10.1161/CIRCIMAGING.117.007394).
Although it didn’t reduce aortic inflammation, adalimumab had a positive effect on glycoprotein acetylation, a marker of inflammation and subclinical cardiovascular disease in psoriasis. Observational studies have also reported a drop in cardiovascular events with adalimumab. Taken together, the mixed findings “give us pause for thought,” Dr. Gelfand said.
In a previous trial, he and his colleagues had found that the interleukin blocker ustekinumab (Stelara) reduced aortic inflammation in psoriasis by about 19%, but Dr. Gelfand said at the meeting that it’s too early to opt for ustekinumab over adalimumab for cardiovascular protection: “I don’t think we are quite there yet; we are still not certain.”
Following washout of psoriasis treatments, the 97 subjects were randomized to either adalimumab for 12 months or ultraviolet B phototherapy or placebo for 12 weeks, followed by adalimumab for 12 months.
Aortic inflammation was used as a proxy for cardiovascular events because trials to assess actual event rates would require thousands of patients treated for several years. “They’re not likely to be done in psoriasis any time soon,” Dr. Gelfand said.
At both 12 and 52 weeks, adalimumab patients had no change in aortic inflammation, compared with placebo and baseline. Phototherapy patients had a 4% drop from baseline at 12 weeks, but it was not statistically significant when compared with placebo.
Both adalimumab and phototherapy decreased systemic inflammation as gauged by serum C-reactive protein and interleukin-6 levels, but only adalimumab reduced TNF levels and glycoprotein acetylation at 12 and 52 weeks. Neither treatment affected insulin, adiponectin, or leptin levels. Adalimumab dropped HDL cholesterol a bit, a known side effect, while phototherapy increased it.
About half of the patients in both treatment arms had a 75% reduction in the Psoriasis Area and Severity Index at 12 weeks, compared with 7% of those on placebo. Subjects were aged 43 years, on average, and more than two-thirds were men. They had a mean psoriasis duration of 17 years and a baseline PASI score of 19.
The work was funded by the National Institutes of Health and AbbVie, adalimumab’s maker. Among many industry ties, Dr. Gelfand is a consultant for Janssen, maker of ustekinumab, and receives research grants from Janssen and AbbVie.
SOURCE: Gelfand JM et al. IID 2018, Abstract 393.
ORLANDO – Adalimumab (Humira) did not reduce aortic inflammation in a year-long, randomized trial that pitted the tumor necrosis factor (TNF) blocker against phototherapy and placebo in 97 psoriasis patients.
a risk factor for cardiovascular events, said senior investigator Joel M. Gelfand, MD, a dermatology professor at the University of Pennsylvania, Philadelphia.
The other trial, from Canada, also found no effect in the ascending aorta after 52 weeks of treatment, but it did find a modest increase in carotid inflammation (J Invest Dermatol. 2017 Aug;137[8]:1638-45).
Both studies used positron emission tomography/computed tomography to assess vascular inflammation.
“We know patients with psoriasis are at increased risk for cardiovascular disease. We think the same kind of inflammation that occurs in atherosclerosis occurs in psoriasis, but we are still teasing out the impact of therapy and which one is most likely to lower the risk of heart attacks, strokes, and things of that nature,” Dr. Gelfand said at the International Investigative Dermatology meeting. The study was published when he gave his presentation (Circ Cardiovasc Imaging. 2018 Jun. doi: 10.1161/CIRCIMAGING.117.007394).
Although it didn’t reduce aortic inflammation, adalimumab had a positive effect on glycoprotein acetylation, a marker of inflammation and subclinical cardiovascular disease in psoriasis. Observational studies have also reported a drop in cardiovascular events with adalimumab. Taken together, the mixed findings “give us pause for thought,” Dr. Gelfand said.
In a previous trial, he and his colleagues had found that the interleukin blocker ustekinumab (Stelara) reduced aortic inflammation in psoriasis by about 19%, but Dr. Gelfand said at the meeting that it’s too early to opt for ustekinumab over adalimumab for cardiovascular protection: “I don’t think we are quite there yet; we are still not certain.”
Following washout of psoriasis treatments, the 97 subjects were randomized to either adalimumab for 12 months or ultraviolet B phototherapy or placebo for 12 weeks, followed by adalimumab for 12 months.
Aortic inflammation was used as a proxy for cardiovascular events because trials to assess actual event rates would require thousands of patients treated for several years. “They’re not likely to be done in psoriasis any time soon,” Dr. Gelfand said.
At both 12 and 52 weeks, adalimumab patients had no change in aortic inflammation, compared with placebo and baseline. Phototherapy patients had a 4% drop from baseline at 12 weeks, but it was not statistically significant when compared with placebo.
Both adalimumab and phototherapy decreased systemic inflammation as gauged by serum C-reactive protein and interleukin-6 levels, but only adalimumab reduced TNF levels and glycoprotein acetylation at 12 and 52 weeks. Neither treatment affected insulin, adiponectin, or leptin levels. Adalimumab dropped HDL cholesterol a bit, a known side effect, while phototherapy increased it.
About half of the patients in both treatment arms had a 75% reduction in the Psoriasis Area and Severity Index at 12 weeks, compared with 7% of those on placebo. Subjects were aged 43 years, on average, and more than two-thirds were men. They had a mean psoriasis duration of 17 years and a baseline PASI score of 19.
The work was funded by the National Institutes of Health and AbbVie, adalimumab’s maker. Among many industry ties, Dr. Gelfand is a consultant for Janssen, maker of ustekinumab, and receives research grants from Janssen and AbbVie.
SOURCE: Gelfand JM et al. IID 2018, Abstract 393.
ORLANDO – Adalimumab (Humira) did not reduce aortic inflammation in a year-long, randomized trial that pitted the tumor necrosis factor (TNF) blocker against phototherapy and placebo in 97 psoriasis patients.
a risk factor for cardiovascular events, said senior investigator Joel M. Gelfand, MD, a dermatology professor at the University of Pennsylvania, Philadelphia.
The other trial, from Canada, also found no effect in the ascending aorta after 52 weeks of treatment, but it did find a modest increase in carotid inflammation (J Invest Dermatol. 2017 Aug;137[8]:1638-45).
Both studies used positron emission tomography/computed tomography to assess vascular inflammation.
“We know patients with psoriasis are at increased risk for cardiovascular disease. We think the same kind of inflammation that occurs in atherosclerosis occurs in psoriasis, but we are still teasing out the impact of therapy and which one is most likely to lower the risk of heart attacks, strokes, and things of that nature,” Dr. Gelfand said at the International Investigative Dermatology meeting. The study was published when he gave his presentation (Circ Cardiovasc Imaging. 2018 Jun. doi: 10.1161/CIRCIMAGING.117.007394).
Although it didn’t reduce aortic inflammation, adalimumab had a positive effect on glycoprotein acetylation, a marker of inflammation and subclinical cardiovascular disease in psoriasis. Observational studies have also reported a drop in cardiovascular events with adalimumab. Taken together, the mixed findings “give us pause for thought,” Dr. Gelfand said.
In a previous trial, he and his colleagues had found that the interleukin blocker ustekinumab (Stelara) reduced aortic inflammation in psoriasis by about 19%, but Dr. Gelfand said at the meeting that it’s too early to opt for ustekinumab over adalimumab for cardiovascular protection: “I don’t think we are quite there yet; we are still not certain.”
Following washout of psoriasis treatments, the 97 subjects were randomized to either adalimumab for 12 months or ultraviolet B phototherapy or placebo for 12 weeks, followed by adalimumab for 12 months.
Aortic inflammation was used as a proxy for cardiovascular events because trials to assess actual event rates would require thousands of patients treated for several years. “They’re not likely to be done in psoriasis any time soon,” Dr. Gelfand said.
At both 12 and 52 weeks, adalimumab patients had no change in aortic inflammation, compared with placebo and baseline. Phototherapy patients had a 4% drop from baseline at 12 weeks, but it was not statistically significant when compared with placebo.
Both adalimumab and phototherapy decreased systemic inflammation as gauged by serum C-reactive protein and interleukin-6 levels, but only adalimumab reduced TNF levels and glycoprotein acetylation at 12 and 52 weeks. Neither treatment affected insulin, adiponectin, or leptin levels. Adalimumab dropped HDL cholesterol a bit, a known side effect, while phototherapy increased it.
About half of the patients in both treatment arms had a 75% reduction in the Psoriasis Area and Severity Index at 12 weeks, compared with 7% of those on placebo. Subjects were aged 43 years, on average, and more than two-thirds were men. They had a mean psoriasis duration of 17 years and a baseline PASI score of 19.
The work was funded by the National Institutes of Health and AbbVie, adalimumab’s maker. Among many industry ties, Dr. Gelfand is a consultant for Janssen, maker of ustekinumab, and receives research grants from Janssen and AbbVie.
SOURCE: Gelfand JM et al. IID 2018, Abstract 393.
REPORTING FROM IID 2018
Key clinical point: Adalimumab does not appear to reduce aortic inflammation in psoriasis, a risk factor for cardiovascular events.
Major finding: After a year of treatment, patients had no change in aortic inflammation, compared with placebo and baseline.
Study details: Randomized, controlled trial of 97 patients
Disclosures: The National Institutes of Health and AbbVie, adalimumab’s maker, funded the work. Among many industry ties, Dr. Gelfand is a consultant for Janssen, maker of ustekinumab, and receives research grants from Janssen and AbbVie.
Source: Gelfand JM et al. IID 2018, abstract 393
Diabetes patients pushed into high-deductible plans
ORLANDO – The proportion of diabetes patients enrolled in high-deductible health plans jumped from 10% in 2005 to about 50% in 2014, according to a review of insurance data for 63 million Americans under age 65 years.
Diabetes patients often don’t have a choice. To cut costs, high-deductible plans are increasingly the only ones employers offer.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
While that may be adequate for healthy people, it’s quite another issue for people with chronic conditions, especially ones with low income. Out-of-pocket expenses can be thousands of dollars more than with traditional health plans, and the extra costs aren’t always offset by lower premiums.
The trend is concerning, said senior investigator J. Frank Wharam, MB, MPH, an associate professor of population medicine at Harvard Medical School, Boston. He explained the problem, and what’s being done about it, in an interview at the annual scientific sessions of the American Diabetes Association.
SOURCE: Garabedian LF et al. ADA 2018. Abstract 175-OR.
ORLANDO – The proportion of diabetes patients enrolled in high-deductible health plans jumped from 10% in 2005 to about 50% in 2014, according to a review of insurance data for 63 million Americans under age 65 years.
Diabetes patients often don’t have a choice. To cut costs, high-deductible plans are increasingly the only ones employers offer.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
While that may be adequate for healthy people, it’s quite another issue for people with chronic conditions, especially ones with low income. Out-of-pocket expenses can be thousands of dollars more than with traditional health plans, and the extra costs aren’t always offset by lower premiums.
The trend is concerning, said senior investigator J. Frank Wharam, MB, MPH, an associate professor of population medicine at Harvard Medical School, Boston. He explained the problem, and what’s being done about it, in an interview at the annual scientific sessions of the American Diabetes Association.
SOURCE: Garabedian LF et al. ADA 2018. Abstract 175-OR.
ORLANDO – The proportion of diabetes patients enrolled in high-deductible health plans jumped from 10% in 2005 to about 50% in 2014, according to a review of insurance data for 63 million Americans under age 65 years.
Diabetes patients often don’t have a choice. To cut costs, high-deductible plans are increasingly the only ones employers offer.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
While that may be adequate for healthy people, it’s quite another issue for people with chronic conditions, especially ones with low income. Out-of-pocket expenses can be thousands of dollars more than with traditional health plans, and the extra costs aren’t always offset by lower premiums.
The trend is concerning, said senior investigator J. Frank Wharam, MB, MPH, an associate professor of population medicine at Harvard Medical School, Boston. He explained the problem, and what’s being done about it, in an interview at the annual scientific sessions of the American Diabetes Association.
SOURCE: Garabedian LF et al. ADA 2018. Abstract 175-OR.
REPORTING FROM ADA 2018
Switch back to human insulin a viable money saver
ORLANDO – It’s safe to switch many Medicare beneficiaries with type 2 diabetes to human insulins to save money on analogues, according to a review of 14,635 members of CareMore, a Medicare Advantage company based in Cerritos, Calif.
The company noticed that it’s spending on analogue insulins had ballooned to over $3 million a month by the end of 2014, in the wake of a more than 300% price increase in analogue insulins in recent years, while copays on analogues rose from nothing to $37.50. In 2015, it launched a program to switch type 2 patients to less costly human insulins. Physicians were counseled to stop secretagogues and move patients to premixed insulins at 80% of their former total daily analogue dose, two-thirds at breakfast, and one-third a dinner, with appropriate follow-up.
Analogue insulins fell from 90% of all insulins dispensed to 30%, with a corresponding rise in human insulin prescriptions. Total plan spending on analogues fell to about a half million dollars a month by the end of 2016. Spending on human insulins rose to just under a million dollars. The risk of patients falling into the Medicare Part D coverage gap – where they assume a greater proportion of their drug costs – was reduced by 55% (P less than .001).
“A lot of money was saved as a result of this intervention,” said lead investigator Jin Luo, MD, an internist and health services researcher at Brigham and Women’s Hospital, Boston.
Mean hemoglobin A1c rose 0.14 % from a baseline of 8.46% in 2014 (P less than 0.01), “but we do not believe that this is clinically important because this value falls within the biological within-subject variation of most modern HbA1c assays,” he said at the annual scientific sessions of the American Diabetes Association.
Meanwhile, there was no statistically significant change in the rate of hospitalizations or emergency department visits for hypoglycemia or hyperglycemia.
“Patients with type 2 diabetes and their clinical providers should strongly consider human insulin as a clinically viable and cost effective option,” Dr. Luo said.
“My personal clinical opinion is that if I have a patient who is really hard to control, and after four or five different regimens, we finally settle on an analogue regimen that [keeps] them under control” and out of the hospital, “I’m not going to switch them just because a health plan tells me I should. They are just too brittle, and I’m not comfortable doing that. Whereas if I have a patient who’d be fine with either option, and I’m not really worried about hypoglycemia, I’ll switch them,” he said.
There was no industry funding. Dr. Luo is a consultant for Alosa Health and Health Action International.
SOURCE: Luo J et al. 2018 American Diabetes Association scientific session abstract 4-OR
ORLANDO – It’s safe to switch many Medicare beneficiaries with type 2 diabetes to human insulins to save money on analogues, according to a review of 14,635 members of CareMore, a Medicare Advantage company based in Cerritos, Calif.
The company noticed that it’s spending on analogue insulins had ballooned to over $3 million a month by the end of 2014, in the wake of a more than 300% price increase in analogue insulins in recent years, while copays on analogues rose from nothing to $37.50. In 2015, it launched a program to switch type 2 patients to less costly human insulins. Physicians were counseled to stop secretagogues and move patients to premixed insulins at 80% of their former total daily analogue dose, two-thirds at breakfast, and one-third a dinner, with appropriate follow-up.
Analogue insulins fell from 90% of all insulins dispensed to 30%, with a corresponding rise in human insulin prescriptions. Total plan spending on analogues fell to about a half million dollars a month by the end of 2016. Spending on human insulins rose to just under a million dollars. The risk of patients falling into the Medicare Part D coverage gap – where they assume a greater proportion of their drug costs – was reduced by 55% (P less than .001).
“A lot of money was saved as a result of this intervention,” said lead investigator Jin Luo, MD, an internist and health services researcher at Brigham and Women’s Hospital, Boston.
Mean hemoglobin A1c rose 0.14 % from a baseline of 8.46% in 2014 (P less than 0.01), “but we do not believe that this is clinically important because this value falls within the biological within-subject variation of most modern HbA1c assays,” he said at the annual scientific sessions of the American Diabetes Association.
Meanwhile, there was no statistically significant change in the rate of hospitalizations or emergency department visits for hypoglycemia or hyperglycemia.
“Patients with type 2 diabetes and their clinical providers should strongly consider human insulin as a clinically viable and cost effective option,” Dr. Luo said.
“My personal clinical opinion is that if I have a patient who is really hard to control, and after four or five different regimens, we finally settle on an analogue regimen that [keeps] them under control” and out of the hospital, “I’m not going to switch them just because a health plan tells me I should. They are just too brittle, and I’m not comfortable doing that. Whereas if I have a patient who’d be fine with either option, and I’m not really worried about hypoglycemia, I’ll switch them,” he said.
There was no industry funding. Dr. Luo is a consultant for Alosa Health and Health Action International.
SOURCE: Luo J et al. 2018 American Diabetes Association scientific session abstract 4-OR
ORLANDO – It’s safe to switch many Medicare beneficiaries with type 2 diabetes to human insulins to save money on analogues, according to a review of 14,635 members of CareMore, a Medicare Advantage company based in Cerritos, Calif.
The company noticed that it’s spending on analogue insulins had ballooned to over $3 million a month by the end of 2014, in the wake of a more than 300% price increase in analogue insulins in recent years, while copays on analogues rose from nothing to $37.50. In 2015, it launched a program to switch type 2 patients to less costly human insulins. Physicians were counseled to stop secretagogues and move patients to premixed insulins at 80% of their former total daily analogue dose, two-thirds at breakfast, and one-third a dinner, with appropriate follow-up.
Analogue insulins fell from 90% of all insulins dispensed to 30%, with a corresponding rise in human insulin prescriptions. Total plan spending on analogues fell to about a half million dollars a month by the end of 2016. Spending on human insulins rose to just under a million dollars. The risk of patients falling into the Medicare Part D coverage gap – where they assume a greater proportion of their drug costs – was reduced by 55% (P less than .001).
“A lot of money was saved as a result of this intervention,” said lead investigator Jin Luo, MD, an internist and health services researcher at Brigham and Women’s Hospital, Boston.
Mean hemoglobin A1c rose 0.14 % from a baseline of 8.46% in 2014 (P less than 0.01), “but we do not believe that this is clinically important because this value falls within the biological within-subject variation of most modern HbA1c assays,” he said at the annual scientific sessions of the American Diabetes Association.
Meanwhile, there was no statistically significant change in the rate of hospitalizations or emergency department visits for hypoglycemia or hyperglycemia.
“Patients with type 2 diabetes and their clinical providers should strongly consider human insulin as a clinically viable and cost effective option,” Dr. Luo said.
“My personal clinical opinion is that if I have a patient who is really hard to control, and after four or five different regimens, we finally settle on an analogue regimen that [keeps] them under control” and out of the hospital, “I’m not going to switch them just because a health plan tells me I should. They are just too brittle, and I’m not comfortable doing that. Whereas if I have a patient who’d be fine with either option, and I’m not really worried about hypoglycemia, I’ll switch them,” he said.
There was no industry funding. Dr. Luo is a consultant for Alosa Health and Health Action International.
SOURCE: Luo J et al. 2018 American Diabetes Association scientific session abstract 4-OR
REPORTING FROM ADA 2018
Key clinical point:
Major finding: Mean HbA1c rose just 0.14% from a baseline of 8.46% (P less than 0.01).
Study details: A review of 14,635 members Medicare patients with type 2 diabetes.
Disclosures: There was no industry funding. The lead investigator is a consultant for Alosa Health and Health Action International.
Source: Luo J et al. ADA 2018, Abstract 4-OR
Patients going without as insulin prices skyrocket
ORLANDO – About a quarter of diabetes patients use less insulin than prescribed because they can’t afford it, and they have worse glycemic control because of it, according to a survey of patients at the Yale Diabetes Center in New Haven, Conn.
The soaring cost of insulin – especially analogues – has been in the news following a more than 300% increase from 2004-2018. The cash price for a 10 mL vial of insulin lispro (Humalog), for example, has climbed from $59 to $320. The American Diabetes Association recently released a white paper on the issue, citing a “lack of transparency throughout the insulin supply chain” that obscures the reasons for the surge. It’s working with other groups to ensure affordable access.
Six questions were key: In the past 12 months, did you, because of cost, use less insulin than prescribed; try to stretch out your insulin; take smaller doses of insulin than prescribed; stop insulin; not fill an insulin prescription; or not start insulin?
Fifty-one patients answered “yes” to at least one of those questions, signaling to investigators that they were using less insulin than prescribed because they couldn’t afford it. Compared with other patients, they were three times more likely to have HbA1c levels above 9%, controlling for age, sex, diabetes duration, and income (P = 0.03).
“One in four patients were using less of an essential medication because it costs too much for them to take the prescribed amount,” said investigator Darby Herkert, who participated in the study as an undergraduate at Yale. “It’s having a tangible health effect.”
The problem was greatest among people making less than $100,000 dollars a year, and was not associated with race or the type of diabetes they had. Employer health coverage was not protective, and patients who were covered by a mix of government and employer insurance were at greater risk of underuse, as were those who were unable to work.
The situation is probably common in the United States, Ms. Herkert noted at the American Diabetes Association scientific sessions meeting. “New Haven is a demographic microcosm of the U.S.”
“These results highlight an urgent need to address high insulin prices,” she said. This may be done through greater transparency in pricing, advocacy for patients who can’t afford their prescription, use of alternative insulin options for some patients, and assistance programs,” she said.
The work was funded in part by the National Institutes of Health. The investigators had no disclosures.
SOURCE: Herkert D et al. ADA 2018 abstract 2-OR
ORLANDO – About a quarter of diabetes patients use less insulin than prescribed because they can’t afford it, and they have worse glycemic control because of it, according to a survey of patients at the Yale Diabetes Center in New Haven, Conn.
The soaring cost of insulin – especially analogues – has been in the news following a more than 300% increase from 2004-2018. The cash price for a 10 mL vial of insulin lispro (Humalog), for example, has climbed from $59 to $320. The American Diabetes Association recently released a white paper on the issue, citing a “lack of transparency throughout the insulin supply chain” that obscures the reasons for the surge. It’s working with other groups to ensure affordable access.
Six questions were key: In the past 12 months, did you, because of cost, use less insulin than prescribed; try to stretch out your insulin; take smaller doses of insulin than prescribed; stop insulin; not fill an insulin prescription; or not start insulin?
Fifty-one patients answered “yes” to at least one of those questions, signaling to investigators that they were using less insulin than prescribed because they couldn’t afford it. Compared with other patients, they were three times more likely to have HbA1c levels above 9%, controlling for age, sex, diabetes duration, and income (P = 0.03).
“One in four patients were using less of an essential medication because it costs too much for them to take the prescribed amount,” said investigator Darby Herkert, who participated in the study as an undergraduate at Yale. “It’s having a tangible health effect.”
The problem was greatest among people making less than $100,000 dollars a year, and was not associated with race or the type of diabetes they had. Employer health coverage was not protective, and patients who were covered by a mix of government and employer insurance were at greater risk of underuse, as were those who were unable to work.
The situation is probably common in the United States, Ms. Herkert noted at the American Diabetes Association scientific sessions meeting. “New Haven is a demographic microcosm of the U.S.”
“These results highlight an urgent need to address high insulin prices,” she said. This may be done through greater transparency in pricing, advocacy for patients who can’t afford their prescription, use of alternative insulin options for some patients, and assistance programs,” she said.
The work was funded in part by the National Institutes of Health. The investigators had no disclosures.
SOURCE: Herkert D et al. ADA 2018 abstract 2-OR
ORLANDO – About a quarter of diabetes patients use less insulin than prescribed because they can’t afford it, and they have worse glycemic control because of it, according to a survey of patients at the Yale Diabetes Center in New Haven, Conn.
The soaring cost of insulin – especially analogues – has been in the news following a more than 300% increase from 2004-2018. The cash price for a 10 mL vial of insulin lispro (Humalog), for example, has climbed from $59 to $320. The American Diabetes Association recently released a white paper on the issue, citing a “lack of transparency throughout the insulin supply chain” that obscures the reasons for the surge. It’s working with other groups to ensure affordable access.
Six questions were key: In the past 12 months, did you, because of cost, use less insulin than prescribed; try to stretch out your insulin; take smaller doses of insulin than prescribed; stop insulin; not fill an insulin prescription; or not start insulin?
Fifty-one patients answered “yes” to at least one of those questions, signaling to investigators that they were using less insulin than prescribed because they couldn’t afford it. Compared with other patients, they were three times more likely to have HbA1c levels above 9%, controlling for age, sex, diabetes duration, and income (P = 0.03).
“One in four patients were using less of an essential medication because it costs too much for them to take the prescribed amount,” said investigator Darby Herkert, who participated in the study as an undergraduate at Yale. “It’s having a tangible health effect.”
The problem was greatest among people making less than $100,000 dollars a year, and was not associated with race or the type of diabetes they had. Employer health coverage was not protective, and patients who were covered by a mix of government and employer insurance were at greater risk of underuse, as were those who were unable to work.
The situation is probably common in the United States, Ms. Herkert noted at the American Diabetes Association scientific sessions meeting. “New Haven is a demographic microcosm of the U.S.”
“These results highlight an urgent need to address high insulin prices,” she said. This may be done through greater transparency in pricing, advocacy for patients who can’t afford their prescription, use of alternative insulin options for some patients, and assistance programs,” she said.
The work was funded in part by the National Institutes of Health. The investigators had no disclosures.
SOURCE: Herkert D et al. ADA 2018 abstract 2-OR
REPORTING FROM ADA 2018
Key clinical point: because of it.
Major finding: Compared with other patients, they were three times more likely to have hemoglobin A1c levels above 9%, controlling for age, sex, diabetes duration, and income (P = 0.03).
Study details: A single-center survey of 199 patients with type 1 or type 2 diabetes.
Disclosures: The work was funded in part by the National Institutes of Health. The investigators had no disclosures.
Source: Herkert D et al. ADA 2018, Abstract 2-OR
JAK inhibitor therapy promising for refractory dermatomyositis
ORLANDO – The according to Ruth Ann Vleugels, MD, director of the autoimmune skin diseases program at Brigham and Women’s Hospital, Boston.
“We will have patients who essentially fail all of our typical therapies and are still coming to us for help. This is a huge challenge,” said Dr. Vleugels, who, several years ago, started to use tofacitinib to treat these patients. “Similar to my colleagues who use tofacitinib to treat alopecia areata, we often have to push” beyond the dose used to treat rheumatoid arthritis, to 10 mg twice a day, she said at the International Conference on Cutaneous Lupus Erythematosus. Tofacitinib helps counter the overexpression of interferon in DM.
Getting insurance coverage for this off-label indication can be tough, however, but Dr. Vleugels said she’s had success when she tells insurers that tofacitinib will likely reduce the need for IVIg.
It’s safe to keep patients on methotrexate if there are concerns about muscle involvement while their skin is brought under control with tofacitinib. In terms of side effects, “we see increased shingles,” so recommending the shingles vaccine for these patients is a good idea, she added.
It’s also important to counsel DM patients that they are at particular risk for skin reactions with antimalarials, which can be serious, so that, “if there is a drug reaction that develops, it’s noticed right away” and the drug can be stopped, she said. “If you have a patient who has very severe disease, I might skip over an antimalarial altogether,” she commented.
Methotrexate is the next option, especially if there are work ups for cancer or the patients have cancer, but Dr. Femia, director of inpatient dermatology at NYU, said she leans towards mycophenolate if there’s concern about lung involvement.
The next step, if necessary, is IVIg, which she said is “particularly helpful” for recalcitrant skin disease and can help some patients discontinue other immunosuppressives. To counter headache, a common side effect, she will space dosing out over 3 days, instead of the usual 2, and have a bag of saline administered before and after the infusion to keep patients hydrated; this counters the headache-inducing viscosity of IVIg.
Patients often see a result after the first infusion, but if there’s no benefit by the third cycle, “it’s probably time to move on,” she said. “If you have a refractory muscle disease patient and skin isn’t the main issue, rituximab is reasonable to try,” she added, noting that the benefit of tumor necrosis factor blockers, “at best, is very mixed in the DM population. They are very low down in the treatment algorithm.”
Dr. Vleugels and Dr. Femia are both Pfizer investigators.
ORLANDO – The according to Ruth Ann Vleugels, MD, director of the autoimmune skin diseases program at Brigham and Women’s Hospital, Boston.
“We will have patients who essentially fail all of our typical therapies and are still coming to us for help. This is a huge challenge,” said Dr. Vleugels, who, several years ago, started to use tofacitinib to treat these patients. “Similar to my colleagues who use tofacitinib to treat alopecia areata, we often have to push” beyond the dose used to treat rheumatoid arthritis, to 10 mg twice a day, she said at the International Conference on Cutaneous Lupus Erythematosus. Tofacitinib helps counter the overexpression of interferon in DM.
Getting insurance coverage for this off-label indication can be tough, however, but Dr. Vleugels said she’s had success when she tells insurers that tofacitinib will likely reduce the need for IVIg.
It’s safe to keep patients on methotrexate if there are concerns about muscle involvement while their skin is brought under control with tofacitinib. In terms of side effects, “we see increased shingles,” so recommending the shingles vaccine for these patients is a good idea, she added.
It’s also important to counsel DM patients that they are at particular risk for skin reactions with antimalarials, which can be serious, so that, “if there is a drug reaction that develops, it’s noticed right away” and the drug can be stopped, she said. “If you have a patient who has very severe disease, I might skip over an antimalarial altogether,” she commented.
Methotrexate is the next option, especially if there are work ups for cancer or the patients have cancer, but Dr. Femia, director of inpatient dermatology at NYU, said she leans towards mycophenolate if there’s concern about lung involvement.
The next step, if necessary, is IVIg, which she said is “particularly helpful” for recalcitrant skin disease and can help some patients discontinue other immunosuppressives. To counter headache, a common side effect, she will space dosing out over 3 days, instead of the usual 2, and have a bag of saline administered before and after the infusion to keep patients hydrated; this counters the headache-inducing viscosity of IVIg.
Patients often see a result after the first infusion, but if there’s no benefit by the third cycle, “it’s probably time to move on,” she said. “If you have a refractory muscle disease patient and skin isn’t the main issue, rituximab is reasonable to try,” she added, noting that the benefit of tumor necrosis factor blockers, “at best, is very mixed in the DM population. They are very low down in the treatment algorithm.”
Dr. Vleugels and Dr. Femia are both Pfizer investigators.
ORLANDO – The according to Ruth Ann Vleugels, MD, director of the autoimmune skin diseases program at Brigham and Women’s Hospital, Boston.
“We will have patients who essentially fail all of our typical therapies and are still coming to us for help. This is a huge challenge,” said Dr. Vleugels, who, several years ago, started to use tofacitinib to treat these patients. “Similar to my colleagues who use tofacitinib to treat alopecia areata, we often have to push” beyond the dose used to treat rheumatoid arthritis, to 10 mg twice a day, she said at the International Conference on Cutaneous Lupus Erythematosus. Tofacitinib helps counter the overexpression of interferon in DM.
Getting insurance coverage for this off-label indication can be tough, however, but Dr. Vleugels said she’s had success when she tells insurers that tofacitinib will likely reduce the need for IVIg.
It’s safe to keep patients on methotrexate if there are concerns about muscle involvement while their skin is brought under control with tofacitinib. In terms of side effects, “we see increased shingles,” so recommending the shingles vaccine for these patients is a good idea, she added.
It’s also important to counsel DM patients that they are at particular risk for skin reactions with antimalarials, which can be serious, so that, “if there is a drug reaction that develops, it’s noticed right away” and the drug can be stopped, she said. “If you have a patient who has very severe disease, I might skip over an antimalarial altogether,” she commented.
Methotrexate is the next option, especially if there are work ups for cancer or the patients have cancer, but Dr. Femia, director of inpatient dermatology at NYU, said she leans towards mycophenolate if there’s concern about lung involvement.
The next step, if necessary, is IVIg, which she said is “particularly helpful” for recalcitrant skin disease and can help some patients discontinue other immunosuppressives. To counter headache, a common side effect, she will space dosing out over 3 days, instead of the usual 2, and have a bag of saline administered before and after the infusion to keep patients hydrated; this counters the headache-inducing viscosity of IVIg.
Patients often see a result after the first infusion, but if there’s no benefit by the third cycle, “it’s probably time to move on,” she said. “If you have a refractory muscle disease patient and skin isn’t the main issue, rituximab is reasonable to try,” she added, noting that the benefit of tumor necrosis factor blockers, “at best, is very mixed in the DM population. They are very low down in the treatment algorithm.”
Dr. Vleugels and Dr. Femia are both Pfizer investigators.
EXPERT ANALYSIS FROM ICCLE 2018
Midlife retinopathy predicts ischemic stroke
LOS ANGELES – The more severe retinopathy is at midlife, the greater the risk of ischemic stroke – particularly lacunar stroke – later on, according to investigators from Johns Hopkins University, Baltimore.
Retinopathy has been associated with strokes before, but the investigators wanted to see whether it could predict stroke type. The idea is that microvascular changes in the retina could mirror microvascular changes in the brain that could lead to stroke.
The positive findings mean that “retinal microvasculature may serve as a biomarker for cerebrovascular health. Retinal imaging may enable further risk stratification of cerebrovascular and neurodegenerative diseases for early, intensive preventive interventions,” said lead investigator Michelle Lin, MD, a stroke fellow at Johns Hopkins.
A full evaluation is beyond the scope of a quick ophthalmoscope check up in the office. The advent of smartphone fundoscopic cameras and optical coherence tomography – which provides images of retinal vasculature at micrometer-level resolution – will likely help retinal imaging reach its full potential in the clinic, she said at the annual meeting of the American Academy of Neurology.
Dr. Lin and her team reviewed 10,468 participants in the Atherosclerosis Risk in Communities Study database. They had baseline retinal photographs from 1993-1995 when they were 45-65 years old. The photos were checked for four types of retinopathy: arteriovenous nicking, focal arteriolar narrowing, retinal microaneurysms, and retinal hemorrhage. The presence of each one was given a score of 1, yielding a retinopathy severity score of 0-4, with 4 meaning subjects had all four types.
Over a median follow-up period of 18.8 years, 578 participants had an ischemic stroke, including 114 lacunar strokes, 292 nonlacunar strokes, and 172 cardioembolic strokes. Hemorrhagic strokes occurred in 95 subjects.
The incidence of ischemic stroke increased with the severity of baseline retinopathy, from 2.7 strokes per 1,000 participant-years among those with no retinopathy to 10.2 among those with a severity score of 3 or higher (P less than .001). The 15-year cumulative risk of ischemic stroke with any retinopathy was 3.4% versus 1.6% with no retinopathy (P less than .001).
After adjustment for age, sex, race, comorbidities, and other confounders, retinal microvasculopathy associated positively with ischemic stroke, especially lacunar stroke (adjusted hazard ratio, 1.84; 95% confidence interval, 1.23-2.74; P = .005).
Trends linking retinopathy severity to the incidence of nonlacunar, cardioembolic, and hemorrhagic strokes were not statistically significant. Factors associated with higher retinopathy grade included older age, black race, hypertension, and diabetes, among others.
There were slightly more women than men in the review. The average age at baseline was 59 years. Patients with stroke histories at baseline were excluded.
The work was funded by the National Institutes of Health. The investigators had no disclosures.
SOURCE: Lin MP et al. Neurology. 2018 Apr;90(15 Suppl.):CCI.001.
The findings are really not surprising. Retinal microvascular changes are a sign of end-organ damage. Small-vessel disease in the eye, small-vessel disease in the brain. This makes a lot of sense.
The question is: Which magic wand do we need to be able to measure and calculate these changes? These are not changes you are going to be able to detect easily when looking at the ocular fundus with your ophthalmoscope. These are very subtle changes we are taking about.
There’s new technology, like optical coherence tomography, and this is what will save us. People are working to provide us tools to automatically calculate retinal microvascular changes from fundus photographs. I have no doubt that within the next 2-3 years we will be able to use this technology. We are almost there; we are in the hands of engineers.
Valerie Biousse, MD , is a professor of neuro-ophthalmology at Emory University, Atlanta. She had no relevant disclosures.
The findings are really not surprising. Retinal microvascular changes are a sign of end-organ damage. Small-vessel disease in the eye, small-vessel disease in the brain. This makes a lot of sense.
The question is: Which magic wand do we need to be able to measure and calculate these changes? These are not changes you are going to be able to detect easily when looking at the ocular fundus with your ophthalmoscope. These are very subtle changes we are taking about.
There’s new technology, like optical coherence tomography, and this is what will save us. People are working to provide us tools to automatically calculate retinal microvascular changes from fundus photographs. I have no doubt that within the next 2-3 years we will be able to use this technology. We are almost there; we are in the hands of engineers.
Valerie Biousse, MD , is a professor of neuro-ophthalmology at Emory University, Atlanta. She had no relevant disclosures.
The findings are really not surprising. Retinal microvascular changes are a sign of end-organ damage. Small-vessel disease in the eye, small-vessel disease in the brain. This makes a lot of sense.
The question is: Which magic wand do we need to be able to measure and calculate these changes? These are not changes you are going to be able to detect easily when looking at the ocular fundus with your ophthalmoscope. These are very subtle changes we are taking about.
There’s new technology, like optical coherence tomography, and this is what will save us. People are working to provide us tools to automatically calculate retinal microvascular changes from fundus photographs. I have no doubt that within the next 2-3 years we will be able to use this technology. We are almost there; we are in the hands of engineers.
Valerie Biousse, MD , is a professor of neuro-ophthalmology at Emory University, Atlanta. She had no relevant disclosures.
LOS ANGELES – The more severe retinopathy is at midlife, the greater the risk of ischemic stroke – particularly lacunar stroke – later on, according to investigators from Johns Hopkins University, Baltimore.
Retinopathy has been associated with strokes before, but the investigators wanted to see whether it could predict stroke type. The idea is that microvascular changes in the retina could mirror microvascular changes in the brain that could lead to stroke.
The positive findings mean that “retinal microvasculature may serve as a biomarker for cerebrovascular health. Retinal imaging may enable further risk stratification of cerebrovascular and neurodegenerative diseases for early, intensive preventive interventions,” said lead investigator Michelle Lin, MD, a stroke fellow at Johns Hopkins.
A full evaluation is beyond the scope of a quick ophthalmoscope check up in the office. The advent of smartphone fundoscopic cameras and optical coherence tomography – which provides images of retinal vasculature at micrometer-level resolution – will likely help retinal imaging reach its full potential in the clinic, she said at the annual meeting of the American Academy of Neurology.
Dr. Lin and her team reviewed 10,468 participants in the Atherosclerosis Risk in Communities Study database. They had baseline retinal photographs from 1993-1995 when they were 45-65 years old. The photos were checked for four types of retinopathy: arteriovenous nicking, focal arteriolar narrowing, retinal microaneurysms, and retinal hemorrhage. The presence of each one was given a score of 1, yielding a retinopathy severity score of 0-4, with 4 meaning subjects had all four types.
Over a median follow-up period of 18.8 years, 578 participants had an ischemic stroke, including 114 lacunar strokes, 292 nonlacunar strokes, and 172 cardioembolic strokes. Hemorrhagic strokes occurred in 95 subjects.
The incidence of ischemic stroke increased with the severity of baseline retinopathy, from 2.7 strokes per 1,000 participant-years among those with no retinopathy to 10.2 among those with a severity score of 3 or higher (P less than .001). The 15-year cumulative risk of ischemic stroke with any retinopathy was 3.4% versus 1.6% with no retinopathy (P less than .001).
After adjustment for age, sex, race, comorbidities, and other confounders, retinal microvasculopathy associated positively with ischemic stroke, especially lacunar stroke (adjusted hazard ratio, 1.84; 95% confidence interval, 1.23-2.74; P = .005).
Trends linking retinopathy severity to the incidence of nonlacunar, cardioembolic, and hemorrhagic strokes were not statistically significant. Factors associated with higher retinopathy grade included older age, black race, hypertension, and diabetes, among others.
There were slightly more women than men in the review. The average age at baseline was 59 years. Patients with stroke histories at baseline were excluded.
The work was funded by the National Institutes of Health. The investigators had no disclosures.
SOURCE: Lin MP et al. Neurology. 2018 Apr;90(15 Suppl.):CCI.001.
LOS ANGELES – The more severe retinopathy is at midlife, the greater the risk of ischemic stroke – particularly lacunar stroke – later on, according to investigators from Johns Hopkins University, Baltimore.
Retinopathy has been associated with strokes before, but the investigators wanted to see whether it could predict stroke type. The idea is that microvascular changes in the retina could mirror microvascular changes in the brain that could lead to stroke.
The positive findings mean that “retinal microvasculature may serve as a biomarker for cerebrovascular health. Retinal imaging may enable further risk stratification of cerebrovascular and neurodegenerative diseases for early, intensive preventive interventions,” said lead investigator Michelle Lin, MD, a stroke fellow at Johns Hopkins.
A full evaluation is beyond the scope of a quick ophthalmoscope check up in the office. The advent of smartphone fundoscopic cameras and optical coherence tomography – which provides images of retinal vasculature at micrometer-level resolution – will likely help retinal imaging reach its full potential in the clinic, she said at the annual meeting of the American Academy of Neurology.
Dr. Lin and her team reviewed 10,468 participants in the Atherosclerosis Risk in Communities Study database. They had baseline retinal photographs from 1993-1995 when they were 45-65 years old. The photos were checked for four types of retinopathy: arteriovenous nicking, focal arteriolar narrowing, retinal microaneurysms, and retinal hemorrhage. The presence of each one was given a score of 1, yielding a retinopathy severity score of 0-4, with 4 meaning subjects had all four types.
Over a median follow-up period of 18.8 years, 578 participants had an ischemic stroke, including 114 lacunar strokes, 292 nonlacunar strokes, and 172 cardioembolic strokes. Hemorrhagic strokes occurred in 95 subjects.
The incidence of ischemic stroke increased with the severity of baseline retinopathy, from 2.7 strokes per 1,000 participant-years among those with no retinopathy to 10.2 among those with a severity score of 3 or higher (P less than .001). The 15-year cumulative risk of ischemic stroke with any retinopathy was 3.4% versus 1.6% with no retinopathy (P less than .001).
After adjustment for age, sex, race, comorbidities, and other confounders, retinal microvasculopathy associated positively with ischemic stroke, especially lacunar stroke (adjusted hazard ratio, 1.84; 95% confidence interval, 1.23-2.74; P = .005).
Trends linking retinopathy severity to the incidence of nonlacunar, cardioembolic, and hemorrhagic strokes were not statistically significant. Factors associated with higher retinopathy grade included older age, black race, hypertension, and diabetes, among others.
There were slightly more women than men in the review. The average age at baseline was 59 years. Patients with stroke histories at baseline were excluded.
The work was funded by the National Institutes of Health. The investigators had no disclosures.
SOURCE: Lin MP et al. Neurology. 2018 Apr;90(15 Suppl.):CCI.001.
REPORTING FROM AAN 2018
Key clinical point:
Major finding: The incidence of ischemic stroke increased with the severity of baseline retinopathy, from 2.7 strokes per 1,000 participant-years with no retinopathy to 10.2 with a severity score of 3 or higher (P less than .001).
Study details: Review of 10,468 subjects in a population-based cohort study.
Disclosures: The work was funded by the National Institutes of Health. The investigators had no disclosures.
Source: Lin MP et al. Neurology. 2018 Apr;90(15 Suppl.):CCI.001.