Carol Bernstein: Physician burnout

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In this edition, Carol A. Bernstein, MD, joins Lorenzo Norris, MD, to discuss physician burnout and mental health.

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In this edition, Carol A. Bernstein, MD, joins Lorenzo Norris, MD, to discuss physician burnout and mental health.

In this edition, Carol A. Bernstein, MD, joins Lorenzo Norris, MD, to discuss physician burnout and mental health.

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HCV, HBV, and HIV associated with autoimmune kidney diseases

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Chronic viral infection can be associated with a variety of autoimmune kidney diseases, according to a review published in Rheumatic Disease Clinics.

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In particular, hepatitis C virus (HCV) infection can cause several kidney disorders. These include cryoglobulinemic glomerulonephritis, membranous nephropathy, fibrillary glomerulopathy, immunotactoid glomerulopathy, and IgA nephropathy, wrote Joshua D. Long and his colleagues at Massachusetts General Hospital, Boston.

Similarly, hepatitis B virus (HBV) infection was found to be associated with both membranous nephropathy and polyarteritis nodosa, and human immunodeficiency virus (HIV) infection can cause HIV-associated nephropathy and HIV-associated immune complex diseases, which affect the kidneys.

In their detailed review, the authors discussed the various causal mechanisms and clinical presentations of each of these various autoimmune kidney diseases caused by HCV, HBV, and HIV, along with current treatment modalities.

“Control of the kidney disease relies primarily on treatment of viremia with antiviral agents; however, immunosuppression also may be needed in severe cases,” said the reviewers. However, “more clinical trials are needed to determine first-line therapies for patients who develop autoimmune kidney diseases in the context of chronic viral infections and to define when adjunctive immunosuppressive therapy is warranted,” they concluded.

One of the authors reported grant support and acting as a consultant for various pharmaceutical companies.

mlesney@mdedge.com

SOURCE: Long JD et al. Rheum Dis Clin N Am 2018;44:675-98.

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Chronic viral infection can be associated with a variety of autoimmune kidney diseases, according to a review published in Rheumatic Disease Clinics.

London_England/Thinkstock

In particular, hepatitis C virus (HCV) infection can cause several kidney disorders. These include cryoglobulinemic glomerulonephritis, membranous nephropathy, fibrillary glomerulopathy, immunotactoid glomerulopathy, and IgA nephropathy, wrote Joshua D. Long and his colleagues at Massachusetts General Hospital, Boston.

Similarly, hepatitis B virus (HBV) infection was found to be associated with both membranous nephropathy and polyarteritis nodosa, and human immunodeficiency virus (HIV) infection can cause HIV-associated nephropathy and HIV-associated immune complex diseases, which affect the kidneys.

In their detailed review, the authors discussed the various causal mechanisms and clinical presentations of each of these various autoimmune kidney diseases caused by HCV, HBV, and HIV, along with current treatment modalities.

“Control of the kidney disease relies primarily on treatment of viremia with antiviral agents; however, immunosuppression also may be needed in severe cases,” said the reviewers. However, “more clinical trials are needed to determine first-line therapies for patients who develop autoimmune kidney diseases in the context of chronic viral infections and to define when adjunctive immunosuppressive therapy is warranted,” they concluded.

One of the authors reported grant support and acting as a consultant for various pharmaceutical companies.

mlesney@mdedge.com

SOURCE: Long JD et al. Rheum Dis Clin N Am 2018;44:675-98.

Chronic viral infection can be associated with a variety of autoimmune kidney diseases, according to a review published in Rheumatic Disease Clinics.

London_England/Thinkstock

In particular, hepatitis C virus (HCV) infection can cause several kidney disorders. These include cryoglobulinemic glomerulonephritis, membranous nephropathy, fibrillary glomerulopathy, immunotactoid glomerulopathy, and IgA nephropathy, wrote Joshua D. Long and his colleagues at Massachusetts General Hospital, Boston.

Similarly, hepatitis B virus (HBV) infection was found to be associated with both membranous nephropathy and polyarteritis nodosa, and human immunodeficiency virus (HIV) infection can cause HIV-associated nephropathy and HIV-associated immune complex diseases, which affect the kidneys.

In their detailed review, the authors discussed the various causal mechanisms and clinical presentations of each of these various autoimmune kidney diseases caused by HCV, HBV, and HIV, along with current treatment modalities.

“Control of the kidney disease relies primarily on treatment of viremia with antiviral agents; however, immunosuppression also may be needed in severe cases,” said the reviewers. However, “more clinical trials are needed to determine first-line therapies for patients who develop autoimmune kidney diseases in the context of chronic viral infections and to define when adjunctive immunosuppressive therapy is warranted,” they concluded.

One of the authors reported grant support and acting as a consultant for various pharmaceutical companies.

mlesney@mdedge.com

SOURCE: Long JD et al. Rheum Dis Clin N Am 2018;44:675-98.

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FROM RHEUMATIC DISEASE CLINICS

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Cardiomyopathy could be under recognized in lupus

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Cardiomyopathy induced by antimalarial treatment for systemic lupus erythematosus may not be as rare as previously thought. Also today, low bone mineral density and spinal syndesmophytes predict radiographic progression in axial spondyloarthritis, sensory feedback modalities tackle gait and balance problems in Parkinson’s disease, and clinically meaningful change is determined for RAPID-3 in active RA.
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Cardiomyopathy induced by antimalarial treatment for systemic lupus erythematosus may not be as rare as previously thought. Also today, low bone mineral density and spinal syndesmophytes predict radiographic progression in axial spondyloarthritis, sensory feedback modalities tackle gait and balance problems in Parkinson’s disease, and clinically meaningful change is determined for RAPID-3 in active RA.
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Cardiomyopathy induced by antimalarial treatment for systemic lupus erythematosus may not be as rare as previously thought. Also today, low bone mineral density and spinal syndesmophytes predict radiographic progression in axial spondyloarthritis, sensory feedback modalities tackle gait and balance problems in Parkinson’s disease, and clinically meaningful change is determined for RAPID-3 in active RA.
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A new smartphone device detects post-stroke AF

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A smartphone-based method beat post-discharge Holter monitoring for the detection of atrial fibrillation. Also today, extended release naltrexone beats oral medication for opioid use disorder, it’s important to pay attention to kidney disease risk in people living with HIV, and physician organizations call out the details of CMS site-neutral payment proposal.

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A smartphone-based method beat post-discharge Holter monitoring for the detection of atrial fibrillation. Also today, extended release naltrexone beats oral medication for opioid use disorder, it’s important to pay attention to kidney disease risk in people living with HIV, and physician organizations call out the details of CMS site-neutral payment proposal.

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A smartphone-based method beat post-discharge Holter monitoring for the detection of atrial fibrillation. Also today, extended release naltrexone beats oral medication for opioid use disorder, it’s important to pay attention to kidney disease risk in people living with HIV, and physician organizations call out the details of CMS site-neutral payment proposal.

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Phantom Odor: Don’t You Smell That?

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Researchers find smelling phantom odors could be signs of medical trouble.

“Phantom odor”—an unexplained and nonexistent smell, such as burning hair—is a fact of life for 1 in 15 American adults aged > 40 years, according to a study at the National Institute on Deafness and Other Communication Disorders. And it can complicate daily life: The sense of smell has an impact on appetite, food preferences, and the ability to detect dangerous smells, such as gas leaks and spoiled food. People with the disorder may even have trouble maintaining a healthy weight. 

The researchers analyzed data from 7,417 participants in the 2011-2014 National Health and Nutrition Examination Survey. The survey included the question “Do you sometimes smell an unpleasant, bad, or burning odor when nothing is there?”  

Adults aged 40 to 60 years had the highest prevalence of phantom odor perception. Women were twice as likely as men to report phantom odors—female predominance was “particularly striking” for those aged < 60 years, the researchers say. Interestingly, phantom odor perception is not related to the individual’s ability to correctly identify odors.

What causes the problem is poorly understood. It might be related to overactive odor-sensing cells in the nasal cavity or perhaps a malfunction in the part of the brain that understands odor signals, said Kathleen Bainbridge, PhD, study leader.

Risk factors for smelling phantom odors include head injury, dry mouth, and poor health. Low socioeconomic status also is a factor: Poor people may be exposed to more environmental pollutants and toxins. Other possibilities include effects of medicines.

To find out the cause—and ultimately develop treatments—a “good first step,” says Bainbridge, “is a clear description of the phenomenon.”

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Researchers find smelling phantom odors could be signs of medical trouble.
Researchers find smelling phantom odors could be signs of medical trouble.

“Phantom odor”—an unexplained and nonexistent smell, such as burning hair—is a fact of life for 1 in 15 American adults aged > 40 years, according to a study at the National Institute on Deafness and Other Communication Disorders. And it can complicate daily life: The sense of smell has an impact on appetite, food preferences, and the ability to detect dangerous smells, such as gas leaks and spoiled food. People with the disorder may even have trouble maintaining a healthy weight. 

The researchers analyzed data from 7,417 participants in the 2011-2014 National Health and Nutrition Examination Survey. The survey included the question “Do you sometimes smell an unpleasant, bad, or burning odor when nothing is there?”  

Adults aged 40 to 60 years had the highest prevalence of phantom odor perception. Women were twice as likely as men to report phantom odors—female predominance was “particularly striking” for those aged < 60 years, the researchers say. Interestingly, phantom odor perception is not related to the individual’s ability to correctly identify odors.

What causes the problem is poorly understood. It might be related to overactive odor-sensing cells in the nasal cavity or perhaps a malfunction in the part of the brain that understands odor signals, said Kathleen Bainbridge, PhD, study leader.

Risk factors for smelling phantom odors include head injury, dry mouth, and poor health. Low socioeconomic status also is a factor: Poor people may be exposed to more environmental pollutants and toxins. Other possibilities include effects of medicines.

To find out the cause—and ultimately develop treatments—a “good first step,” says Bainbridge, “is a clear description of the phenomenon.”

“Phantom odor”—an unexplained and nonexistent smell, such as burning hair—is a fact of life for 1 in 15 American adults aged > 40 years, according to a study at the National Institute on Deafness and Other Communication Disorders. And it can complicate daily life: The sense of smell has an impact on appetite, food preferences, and the ability to detect dangerous smells, such as gas leaks and spoiled food. People with the disorder may even have trouble maintaining a healthy weight. 

The researchers analyzed data from 7,417 participants in the 2011-2014 National Health and Nutrition Examination Survey. The survey included the question “Do you sometimes smell an unpleasant, bad, or burning odor when nothing is there?”  

Adults aged 40 to 60 years had the highest prevalence of phantom odor perception. Women were twice as likely as men to report phantom odors—female predominance was “particularly striking” for those aged < 60 years, the researchers say. Interestingly, phantom odor perception is not related to the individual’s ability to correctly identify odors.

What causes the problem is poorly understood. It might be related to overactive odor-sensing cells in the nasal cavity or perhaps a malfunction in the part of the brain that understands odor signals, said Kathleen Bainbridge, PhD, study leader.

Risk factors for smelling phantom odors include head injury, dry mouth, and poor health. Low socioeconomic status also is a factor: Poor people may be exposed to more environmental pollutants and toxins. Other possibilities include effects of medicines.

To find out the cause—and ultimately develop treatments—a “good first step,” says Bainbridge, “is a clear description of the phenomenon.”

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Antimalarial-induced cardiomyopathy in lupus may be underrecognized

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Cardiomyopathy induced by antimalarial treatment for systematic lupus erythematosus may not be as rare as previously thought, according to the authors of a case series published Oct. 15 in The Journal of Rheumatology.

The paper describes eight patients attending a lupus clinic, who were diagnosed with definite or possible antimalarial-induced cardiomyopathy over the course of 2 years.

Konstantinos Tselios, MD, PhD, a clinical research fellow at the University of Toronto Lupus Clinic, and his coauthors wrote that antimalarial-induced cardiomyopathy was thought to be relatively rare, with only 47 previous isolated reports, but they suggested the complication may be significantly underrecognized.

“Hypertrophic cardiomyopathy and heart failure, the most common clinical features of AM-induced cardiomyopathy (AMIC), may be falsely attributed to other causes, such as arterial hypertension or ischemic cardiomyopathy,” the authors wrote. “Consequently, nonspecific therapeutic approaches with diuretics and/or antihypertensives will exert minimum or even deleterious effects on such patients.”

All eight patients in this series were female, with a median age of 62.5 years, median disease duration of 35 years, and median antimalarial use of 22 years. They presented with conditions such as heart failure, exertional dyspnea, and pedal edema. Several patients were asymptomatic but had been found to have elevated heart biomarker levels that prompted further investigation.


All patients showed abnormal cardiac troponin I and brain natriuretic peptide levels, and seven of the eight also had chronically elevated creatine phosphokinase.

In three patients, endomyocardial biopsy showed cardiomyocyte vacuolation, intracytoplasmic myelinoid inclusions, and curvilinear bodies.

Four patients were diagnosed based on cardiac MRI, which showed features suggestive of antimalarial-induced cardiomyopathy, including ventricular hypertrophy with or without atrial enlargement and late gadolinium enhancement in a nonvascular pattern.

All patients had left ventricular hypertrophy, and four also had right ventricular hypertrophy. Only one patient showed impaired systolic function, compared with around half of patients in the literature with antimalarial-induced cardiomyopathy, but seven patients showed a restrictive filling pattern of the left ventricle.

“It seems possible that AMIC is a chronic process and systolic dysfunction will become apparent only in late stages,” the authors suggested.

One patient showed complete atrioventricular block, left ventricular and septal hypertrophy, and concomitant ocular toxicity.

After patients stopped antimalarials, the hypertrophy regressed and heart biomarkers decreased in seven patients, but one patient died from refractory heart failure.

Based on their findings, the authors proposed that heart-specific biomarkers be used as a regular screening tool for detecting myocardial injury, followed by more thorough investigations, such as cardiac MRI, in patients with positive biomarker findings.

“However, drug cessation should be prompt and probably upon suspicion of AMIC, because complete investigation may be delayed significantly.”

One author was supported by the Geoff Carr Fellowship from Lupus Ontario. The University of Toronto Lupus Research Program is supported by the University Health Network, Lou and Marissa Rocca, and the Lupus Foundation of Ontario.

SOURCE: Tselios K et al. J Rheumatol, 2018 Oct 15. doi: 10.3899/jrheum.180124.

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Cardiomyopathy induced by antimalarial treatment for systematic lupus erythematosus may not be as rare as previously thought, according to the authors of a case series published Oct. 15 in The Journal of Rheumatology.

The paper describes eight patients attending a lupus clinic, who were diagnosed with definite or possible antimalarial-induced cardiomyopathy over the course of 2 years.

Konstantinos Tselios, MD, PhD, a clinical research fellow at the University of Toronto Lupus Clinic, and his coauthors wrote that antimalarial-induced cardiomyopathy was thought to be relatively rare, with only 47 previous isolated reports, but they suggested the complication may be significantly underrecognized.

“Hypertrophic cardiomyopathy and heart failure, the most common clinical features of AM-induced cardiomyopathy (AMIC), may be falsely attributed to other causes, such as arterial hypertension or ischemic cardiomyopathy,” the authors wrote. “Consequently, nonspecific therapeutic approaches with diuretics and/or antihypertensives will exert minimum or even deleterious effects on such patients.”

All eight patients in this series were female, with a median age of 62.5 years, median disease duration of 35 years, and median antimalarial use of 22 years. They presented with conditions such as heart failure, exertional dyspnea, and pedal edema. Several patients were asymptomatic but had been found to have elevated heart biomarker levels that prompted further investigation.


All patients showed abnormal cardiac troponin I and brain natriuretic peptide levels, and seven of the eight also had chronically elevated creatine phosphokinase.

In three patients, endomyocardial biopsy showed cardiomyocyte vacuolation, intracytoplasmic myelinoid inclusions, and curvilinear bodies.

Four patients were diagnosed based on cardiac MRI, which showed features suggestive of antimalarial-induced cardiomyopathy, including ventricular hypertrophy with or without atrial enlargement and late gadolinium enhancement in a nonvascular pattern.

All patients had left ventricular hypertrophy, and four also had right ventricular hypertrophy. Only one patient showed impaired systolic function, compared with around half of patients in the literature with antimalarial-induced cardiomyopathy, but seven patients showed a restrictive filling pattern of the left ventricle.

“It seems possible that AMIC is a chronic process and systolic dysfunction will become apparent only in late stages,” the authors suggested.

One patient showed complete atrioventricular block, left ventricular and septal hypertrophy, and concomitant ocular toxicity.

After patients stopped antimalarials, the hypertrophy regressed and heart biomarkers decreased in seven patients, but one patient died from refractory heart failure.

Based on their findings, the authors proposed that heart-specific biomarkers be used as a regular screening tool for detecting myocardial injury, followed by more thorough investigations, such as cardiac MRI, in patients with positive biomarker findings.

“However, drug cessation should be prompt and probably upon suspicion of AMIC, because complete investigation may be delayed significantly.”

One author was supported by the Geoff Carr Fellowship from Lupus Ontario. The University of Toronto Lupus Research Program is supported by the University Health Network, Lou and Marissa Rocca, and the Lupus Foundation of Ontario.

SOURCE: Tselios K et al. J Rheumatol, 2018 Oct 15. doi: 10.3899/jrheum.180124.

Cardiomyopathy induced by antimalarial treatment for systematic lupus erythematosus may not be as rare as previously thought, according to the authors of a case series published Oct. 15 in The Journal of Rheumatology.

The paper describes eight patients attending a lupus clinic, who were diagnosed with definite or possible antimalarial-induced cardiomyopathy over the course of 2 years.

Konstantinos Tselios, MD, PhD, a clinical research fellow at the University of Toronto Lupus Clinic, and his coauthors wrote that antimalarial-induced cardiomyopathy was thought to be relatively rare, with only 47 previous isolated reports, but they suggested the complication may be significantly underrecognized.

“Hypertrophic cardiomyopathy and heart failure, the most common clinical features of AM-induced cardiomyopathy (AMIC), may be falsely attributed to other causes, such as arterial hypertension or ischemic cardiomyopathy,” the authors wrote. “Consequently, nonspecific therapeutic approaches with diuretics and/or antihypertensives will exert minimum or even deleterious effects on such patients.”

All eight patients in this series were female, with a median age of 62.5 years, median disease duration of 35 years, and median antimalarial use of 22 years. They presented with conditions such as heart failure, exertional dyspnea, and pedal edema. Several patients were asymptomatic but had been found to have elevated heart biomarker levels that prompted further investigation.


All patients showed abnormal cardiac troponin I and brain natriuretic peptide levels, and seven of the eight also had chronically elevated creatine phosphokinase.

In three patients, endomyocardial biopsy showed cardiomyocyte vacuolation, intracytoplasmic myelinoid inclusions, and curvilinear bodies.

Four patients were diagnosed based on cardiac MRI, which showed features suggestive of antimalarial-induced cardiomyopathy, including ventricular hypertrophy with or without atrial enlargement and late gadolinium enhancement in a nonvascular pattern.

All patients had left ventricular hypertrophy, and four also had right ventricular hypertrophy. Only one patient showed impaired systolic function, compared with around half of patients in the literature with antimalarial-induced cardiomyopathy, but seven patients showed a restrictive filling pattern of the left ventricle.

“It seems possible that AMIC is a chronic process and systolic dysfunction will become apparent only in late stages,” the authors suggested.

One patient showed complete atrioventricular block, left ventricular and septal hypertrophy, and concomitant ocular toxicity.

After patients stopped antimalarials, the hypertrophy regressed and heart biomarkers decreased in seven patients, but one patient died from refractory heart failure.

Based on their findings, the authors proposed that heart-specific biomarkers be used as a regular screening tool for detecting myocardial injury, followed by more thorough investigations, such as cardiac MRI, in patients with positive biomarker findings.

“However, drug cessation should be prompt and probably upon suspicion of AMIC, because complete investigation may be delayed significantly.”

One author was supported by the Geoff Carr Fellowship from Lupus Ontario. The University of Toronto Lupus Research Program is supported by the University Health Network, Lou and Marissa Rocca, and the Lupus Foundation of Ontario.

SOURCE: Tselios K et al. J Rheumatol, 2018 Oct 15. doi: 10.3899/jrheum.180124.

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FROM THE JOURNAL OF RHEUMATOLOGY

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Key clinical point: Antimalarial-induced cardiomyopathy in SLE may not be as rare as previously thought.

Major finding: Elevated cardiac troponin I and brain natriuretic peptide, and abnormal cardiac MRI may indicate antimalarial-induced cardiomyopathy.

Study details: Case series of eight patients with antimalarial-induced cardiomyopathy.

Disclosures: One author was supported by the Geoff Carr Fellowship from Lupus Ontario. The University of Toronto Lupus Research Program is supported by the University Health Network, Lou and Marissa Rocca, and the Lupus Foundation of Ontario.

Source: Tselios K et al. J Rheumatol. 2018 Oct 15. doi: 10.3899/jrheum.180124.

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Jaya Aysola: Gender inclusivity

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Jaya Aysola, MD, MPH, joins Nick to talk about workplace inclusivity among genders. Dr. Aysola is an assistant professor of medicine and pediatrics at the Perelman School of Medicine. Her primary appointment in the Divisions of General Internal Medicine.

In early August 2018, Dr. Aysola and her colleagues published a qualitative narrative analysis regarding the perceptions of the factors associated with inclusive workplaces in healthcare.



 

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Jaya Aysola, MD, MPH, joins Nick to talk about workplace inclusivity among genders. Dr. Aysola is an assistant professor of medicine and pediatrics at the Perelman School of Medicine. Her primary appointment in the Divisions of General Internal Medicine.

In early August 2018, Dr. Aysola and her colleagues published a qualitative narrative analysis regarding the perceptions of the factors associated with inclusive workplaces in healthcare.



 

 

Jaya Aysola, MD, MPH, joins Nick to talk about workplace inclusivity among genders. Dr. Aysola is an assistant professor of medicine and pediatrics at the Perelman School of Medicine. Her primary appointment in the Divisions of General Internal Medicine.

In early August 2018, Dr. Aysola and her colleagues published a qualitative narrative analysis regarding the perceptions of the factors associated with inclusive workplaces in healthcare.



 

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Ultrasound screening improves ovarian cancer survival?

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Annual ultrasound screening for asymptomatic women at risk of epithelial ovarian cancer can lead to lower staging and improved survival. Also today, fat attenuation index boosts coronary CT prognostication, peripheral arterial disease diagnostic tests vary wildly in patients with diabetes, and big drinkers face a new massive health burden.

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Annual ultrasound screening for asymptomatic women at risk of epithelial ovarian cancer can lead to lower staging and improved survival. Also today, fat attenuation index boosts coronary CT prognostication, peripheral arterial disease diagnostic tests vary wildly in patients with diabetes, and big drinkers face a new massive health burden.

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Annual ultrasound screening for asymptomatic women at risk of epithelial ovarian cancer can lead to lower staging and improved survival. Also today, fat attenuation index boosts coronary CT prognostication, peripheral arterial disease diagnostic tests vary wildly in patients with diabetes, and big drinkers face a new massive health burden.

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Glucocorticoids plus tofacitinib may boost herpes zoster risk

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Concomitant use of glucocorticoids with tofacitinib in rheumatoid arthritis may double the risk of herpes zoster, but methotrexate does not appear to increase the risk, outcomes from a cohort study of 8,030 rheumatoid arthritis patients – including 222 cases of herpes zoster – suggest.

Courtesy UAB Photo
Dr. Jeffrey R. Curtis

Using information from Medicare and MarketScan, researchers found that dual therapy with tofacitinib and glucocorticoids was associated with a 96% increase in the risk of herpes zoster, compared with monotherapy with the Janus kinase inhibitor tofacitinib (95% confidence interval, 33%-188%). The crude incidence rate in those taking concomitant tofacitinib and glucocorticoids was 6 cases per 100 patient-years, compared with an incidence rate of 3.4 cases per 100 patient-years with tofacitinib monotherapy.

However, the addition of methotrexate therapy to tofacitinib was not associated with an increased risk of herpes zoster, and the incidence rate in patients on this dual therapy was 3.7 cases per 100 patient-years, Jeffrey R. Curtis, MD, MS, MPH, of the University of Alabama at Birmingham and his coauthors reported in Arthritis Care & Research.

Women – who constituted 80% of the study population – showed a significantly increased risk of herpes zoster, as did older patients.

The study also found that individuals who had received the live herpes zoster vaccine showed a trend toward a decrease in risk.

“We saw a strong trend for decreased risk related to vaccination with the live agent (Zostavax); the concern with this form of vaccination is that any live vaccination is potentially dangerous in patients receiving potent immunosuppression,” Dr. Curtis and his associates wrote.

“The risks for disease flare, and potentially problematic tolerability related to a relatively high incidence of grade 3 (severe) systemic reactogenicity, may limit enthusiasm until specific data in an RA population is available,” they wrote. However, they noted that a randomized, controlled trial of the live virus vaccine was underway in patients with rheumatoid arthritis who were being treated with tumor necrosis factor inhibitors and suggested that vaccination should be considered in at-risk patients who didn’t have contraindications.

The authors noted that the effect of glucocorticoid exposure on herpes zoster risk in patients taking tofacitinib was similar to that seen in rheumatoid arthritis patients receiving conventional synthetic disease-modifying antirheumatic drugs or biologic therapies.

The study was partly funded by the Patient-Centered Outcomes Research Institute. Two authors declared research grants and other funding from the pharmaceutical industry, but no other conflicts of interest were declared.

SOURCE: Curtis J et al. Arthritis Care Res. 2018 Oct 8. doi: 10.1002/acr.23769.

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Concomitant use of glucocorticoids with tofacitinib in rheumatoid arthritis may double the risk of herpes zoster, but methotrexate does not appear to increase the risk, outcomes from a cohort study of 8,030 rheumatoid arthritis patients – including 222 cases of herpes zoster – suggest.

Courtesy UAB Photo
Dr. Jeffrey R. Curtis

Using information from Medicare and MarketScan, researchers found that dual therapy with tofacitinib and glucocorticoids was associated with a 96% increase in the risk of herpes zoster, compared with monotherapy with the Janus kinase inhibitor tofacitinib (95% confidence interval, 33%-188%). The crude incidence rate in those taking concomitant tofacitinib and glucocorticoids was 6 cases per 100 patient-years, compared with an incidence rate of 3.4 cases per 100 patient-years with tofacitinib monotherapy.

However, the addition of methotrexate therapy to tofacitinib was not associated with an increased risk of herpes zoster, and the incidence rate in patients on this dual therapy was 3.7 cases per 100 patient-years, Jeffrey R. Curtis, MD, MS, MPH, of the University of Alabama at Birmingham and his coauthors reported in Arthritis Care & Research.

Women – who constituted 80% of the study population – showed a significantly increased risk of herpes zoster, as did older patients.

The study also found that individuals who had received the live herpes zoster vaccine showed a trend toward a decrease in risk.

“We saw a strong trend for decreased risk related to vaccination with the live agent (Zostavax); the concern with this form of vaccination is that any live vaccination is potentially dangerous in patients receiving potent immunosuppression,” Dr. Curtis and his associates wrote.

“The risks for disease flare, and potentially problematic tolerability related to a relatively high incidence of grade 3 (severe) systemic reactogenicity, may limit enthusiasm until specific data in an RA population is available,” they wrote. However, they noted that a randomized, controlled trial of the live virus vaccine was underway in patients with rheumatoid arthritis who were being treated with tumor necrosis factor inhibitors and suggested that vaccination should be considered in at-risk patients who didn’t have contraindications.

The authors noted that the effect of glucocorticoid exposure on herpes zoster risk in patients taking tofacitinib was similar to that seen in rheumatoid arthritis patients receiving conventional synthetic disease-modifying antirheumatic drugs or biologic therapies.

The study was partly funded by the Patient-Centered Outcomes Research Institute. Two authors declared research grants and other funding from the pharmaceutical industry, but no other conflicts of interest were declared.

SOURCE: Curtis J et al. Arthritis Care Res. 2018 Oct 8. doi: 10.1002/acr.23769.

 

Concomitant use of glucocorticoids with tofacitinib in rheumatoid arthritis may double the risk of herpes zoster, but methotrexate does not appear to increase the risk, outcomes from a cohort study of 8,030 rheumatoid arthritis patients – including 222 cases of herpes zoster – suggest.

Courtesy UAB Photo
Dr. Jeffrey R. Curtis

Using information from Medicare and MarketScan, researchers found that dual therapy with tofacitinib and glucocorticoids was associated with a 96% increase in the risk of herpes zoster, compared with monotherapy with the Janus kinase inhibitor tofacitinib (95% confidence interval, 33%-188%). The crude incidence rate in those taking concomitant tofacitinib and glucocorticoids was 6 cases per 100 patient-years, compared with an incidence rate of 3.4 cases per 100 patient-years with tofacitinib monotherapy.

However, the addition of methotrexate therapy to tofacitinib was not associated with an increased risk of herpes zoster, and the incidence rate in patients on this dual therapy was 3.7 cases per 100 patient-years, Jeffrey R. Curtis, MD, MS, MPH, of the University of Alabama at Birmingham and his coauthors reported in Arthritis Care & Research.

Women – who constituted 80% of the study population – showed a significantly increased risk of herpes zoster, as did older patients.

The study also found that individuals who had received the live herpes zoster vaccine showed a trend toward a decrease in risk.

“We saw a strong trend for decreased risk related to vaccination with the live agent (Zostavax); the concern with this form of vaccination is that any live vaccination is potentially dangerous in patients receiving potent immunosuppression,” Dr. Curtis and his associates wrote.

“The risks for disease flare, and potentially problematic tolerability related to a relatively high incidence of grade 3 (severe) systemic reactogenicity, may limit enthusiasm until specific data in an RA population is available,” they wrote. However, they noted that a randomized, controlled trial of the live virus vaccine was underway in patients with rheumatoid arthritis who were being treated with tumor necrosis factor inhibitors and suggested that vaccination should be considered in at-risk patients who didn’t have contraindications.

The authors noted that the effect of glucocorticoid exposure on herpes zoster risk in patients taking tofacitinib was similar to that seen in rheumatoid arthritis patients receiving conventional synthetic disease-modifying antirheumatic drugs or biologic therapies.

The study was partly funded by the Patient-Centered Outcomes Research Institute. Two authors declared research grants and other funding from the pharmaceutical industry, but no other conflicts of interest were declared.

SOURCE: Curtis J et al. Arthritis Care Res. 2018 Oct 8. doi: 10.1002/acr.23769.

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Key clinical point: Patients treated with concomitant glucocorticoids and tofacitinib showed increased risk of herpes zoster.

Major finding: Concomitant use of glucocorticoids and tofacitinib is associated with nearly twofold increase in the risk of herpes zoster.

Study details: Cohort study using data from 8,030 rheumatoid arthritis patients.

Disclosures: The study was partly funded by the Patient-Centered Outcomes Research Institute. Two authors declared research grants and other funding from the pharmaceutical industry, but no other conflicts of interest were declared.

Source: Curtis J et al. Arthritis Care Res. 2018 Oct 8. doi: 10.1002/acr.23769.

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This week, a revelation that coronary artery bypass grafting instead of percutaneous is safer as time goes by, a new index stretches the prognostic power of cardiac CT, a weight-loss drug cuts new-onset diabetes, and a controversial diet score is validated.

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This week, a revelation that coronary artery bypass grafting instead of percutaneous is safer as time goes by, a new index stretches the prognostic power of cardiac CT, a weight-loss drug cuts new-onset diabetes, and a controversial diet score is validated.

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This week, a revelation that coronary artery bypass grafting instead of percutaneous is safer as time goes by, a new index stretches the prognostic power of cardiac CT, a weight-loss drug cuts new-onset diabetes, and a controversial diet score is validated.

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