Rheumatoid Arthritis

TOPLINE:

A substantial proportion of older adults with early rheumatoid arthritis (RA) initiate glucocorticoids before receiving care from a rheumatologist. The early initiation of glucocorticoids in this group is associated with prolonged use.

METHODOLOGY:

• Researchers analyzed data from Medicare claims and Rheumatology Informatics System for Effectiveness registry of the American College of Rheumatology from 2016 to 2018 to assess the relationship between the timing of glucocorticoid initiation and the subsequent duration of glucocorticoid use in older adults with early RA in the United States.
• They included 1733 patients aged ≥ 65 years (mean age, 76 years; 67% women) with early RA.
• Glucocorticoid initiation was defined as the first use between 3 months before and 6 months after entrance into rheumatology care.
• The continuous administration of glucocorticoid therapy was monitored for all individuals who initiated glucocorticoid treatment for up to 12 months after entering rheumatology care.
• The primary outcome was the duration of continuous glucocorticoid use after entering rheumatology care.

TAKEAWAY:

• Glucocorticoids were initiated in 41% of patients, with 65% starting them before the initial RA diagnosis by a rheumatologist. The median duration of glucocorticoid use was 157 days.
• Patients with early RA who initiated glucocorticoids before entering rheumatology care showed a significantly longer duration of glucocorticoid use than those who initiated it later (median, 186 vs 97 days; P < .0001).
• Patients who initiated glucocorticoids before entering rheumatology care were 39% less likely to stop its use within 1 year (hazard ratio, 0.61; 95% CI, 0.51-0.74).
• The mean daily dose of glucocorticoids was < 5 mg/d for patients who received them for at least 3 months, indicating a trend toward low-dose, long-term use.

IN PRACTICE:

“Initiatives to reduce GC [glucocorticoid] exposure among patients with eRA [early RA] will likely require attention to rheumatology workforce shortages and close collaboration between rheumatologists and primary care clinicians to expedite referrals to rheumatology care,” the authors wrote.

SOURCE:

This study was led by Andriko Palmowski, MD, Department of Rheumatology and Clinical Immunology, Charité – Universitätsmedizin Berlin in Germany, and was published online in Seminars in Arthritis and Rheumatism.

LIMITATIONS:

The observational nature of this study limited the ability to establish causality between early glucocorticoid initiation and the prolonged use of glucocorticoids. Moreover, the study population was limited to older adults, which affected the generalizability of the findings to younger populations. It also did not account for the fact that patients with more severe early RA were more likely to start glucocorticoid therapy early and continue it for longer durations.

DISCLOSURES:

The study was supported by research grants from the Deutsche Autoimmun-Stiftung and other sources. Some authors declared receiving grant support, consultancy fees, honoraria, and travel expenses and had other ties with various pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A substantial proportion of older adults with early rheumatoid arthritis (RA) initiate glucocorticoids before receiving care from a rheumatologist. The early initiation of glucocorticoids in this group is associated with prolonged use.

METHODOLOGY:

• Researchers analyzed data from Medicare claims and Rheumatology Informatics System for Effectiveness registry of the American College of Rheumatology from 2016 to 2018 to assess the relationship between the timing of glucocorticoid initiation and the subsequent duration of glucocorticoid use in older adults with early RA in the United States.
• They included 1733 patients aged ≥ 65 years (mean age, 76 years; 67% women) with early RA.
• Glucocorticoid initiation was defined as the first use between 3 months before and 6 months after entrance into rheumatology care.
• The continuous administration of glucocorticoid therapy was monitored for all individuals who initiated glucocorticoid treatment for up to 12 months after entering rheumatology care.
• The primary outcome was the duration of continuous glucocorticoid use after entering rheumatology care.

TAKEAWAY:

• Glucocorticoids were initiated in 41% of patients, with 65% starting them before the initial RA diagnosis by a rheumatologist. The median duration of glucocorticoid use was 157 days.
• Patients with early RA who initiated glucocorticoids before entering rheumatology care showed a significantly longer duration of glucocorticoid use than those who initiated it later (median, 186 vs 97 days; P < .0001).
• Patients who initiated glucocorticoids before entering rheumatology care were 39% less likely to stop its use within 1 year (hazard ratio, 0.61; 95% CI, 0.51-0.74).
• The mean daily dose of glucocorticoids was < 5 mg/d for patients who received them for at least 3 months, indicating a trend toward low-dose, long-term use.

IN PRACTICE:

“Initiatives to reduce GC [glucocorticoid] exposure among patients with eRA [early RA] will likely require attention to rheumatology workforce shortages and close collaboration between rheumatologists and primary care clinicians to expedite referrals to rheumatology care,” the authors wrote.

SOURCE:

This study was led by Andriko Palmowski, MD, Department of Rheumatology and Clinical Immunology, Charité – Universitätsmedizin Berlin in Germany, and was published online in Seminars in Arthritis and Rheumatism.

LIMITATIONS:

The observational nature of this study limited the ability to establish causality between early glucocorticoid initiation and the prolonged use of glucocorticoids. Moreover, the study population was limited to older adults, which affected the generalizability of the findings to younger populations. It also did not account for the fact that patients with more severe early RA were more likely to start glucocorticoid therapy early and continue it for longer durations.

DISCLOSURES:

The study was supported by research grants from the Deutsche Autoimmun-Stiftung and other sources. Some authors declared receiving grant support, consultancy fees, honoraria, and travel expenses and had other ties with various pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A substantial proportion of older adults with early rheumatoid arthritis (RA) initiate glucocorticoids before receiving care from a rheumatologist. The early initiation of glucocorticoids in this group is associated with prolonged use.

METHODOLOGY:

• Researchers analyzed data from Medicare claims and Rheumatology Informatics System for Effectiveness registry of the American College of Rheumatology from 2016 to 2018 to assess the relationship between the timing of glucocorticoid initiation and the subsequent duration of glucocorticoid use in older adults with early RA in the United States.
• They included 1733 patients aged ≥ 65 years (mean age, 76 years; 67% women) with early RA.
• Glucocorticoid initiation was defined as the first use between 3 months before and 6 months after entrance into rheumatology care.
• The continuous administration of glucocorticoid therapy was monitored for all individuals who initiated glucocorticoid treatment for up to 12 months after entering rheumatology care.
• The primary outcome was the duration of continuous glucocorticoid use after entering rheumatology care.

TAKEAWAY:

• Glucocorticoids were initiated in 41% of patients, with 65% starting them before the initial RA diagnosis by a rheumatologist. The median duration of glucocorticoid use was 157 days.
• Patients with early RA who initiated glucocorticoids before entering rheumatology care showed a significantly longer duration of glucocorticoid use than those who initiated it later (median, 186 vs 97 days; P < .0001).
• Patients who initiated glucocorticoids before entering rheumatology care were 39% less likely to stop its use within 1 year (hazard ratio, 0.61; 95% CI, 0.51-0.74).
• The mean daily dose of glucocorticoids was < 5 mg/d for patients who received them for at least 3 months, indicating a trend toward low-dose, long-term use.

IN PRACTICE:

“Initiatives to reduce GC [glucocorticoid] exposure among patients with eRA [early RA] will likely require attention to rheumatology workforce shortages and close collaboration between rheumatologists and primary care clinicians to expedite referrals to rheumatology care,” the authors wrote.

SOURCE:

This study was led by Andriko Palmowski, MD, Department of Rheumatology and Clinical Immunology, Charité – Universitätsmedizin Berlin in Germany, and was published online in Seminars in Arthritis and Rheumatism.

LIMITATIONS:

The observational nature of this study limited the ability to establish causality between early glucocorticoid initiation and the prolonged use of glucocorticoids. Moreover, the study population was limited to older adults, which affected the generalizability of the findings to younger populations. It also did not account for the fact that patients with more severe early RA were more likely to start glucocorticoid therapy early and continue it for longer durations.

DISCLOSURES:

The study was supported by research grants from the Deutsche Autoimmun-Stiftung and other sources. Some authors declared receiving grant support, consultancy fees, honoraria, and travel expenses and had other ties with various pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Middle-aged adults who consume more ultra-processed foods have an elevated risk for rheumatoid arthritis (RA) that is mediated in part through circulating biomarkers.

METHODOLOGY: 

• Investigators conducted a retrospective cohort study of 207,012 middle-aged adults without RA from the UK Biobank who completed 24-hour dietary recalls.
• Foods and beverages were classified as (1) unprocessed or minimally processed foods, (2) processed culinary ingredients, (3) processed foods, or (4) ultra-processed foods (eg, soft drinks, sweet or savory packaged snacks, reconstituted meat products, pre-prepared frozen dishes).
• The main outcome was the incident RA based on hospital diagnoses.

TAKEAWAY:

• Overall, 0.9% of participants received an RA diagnosis during a median follow-up of about 12 years.
• Relative to peers in the lowest quintile of ultra-processed food consumption, participants in the highest quintile had a 17% greater adjusted risk for RA.
• The risk rose across quintile (P < .05) and increased by 6% with each standard deviation increase in ultra-processed food intake.
• Mediation analyses suggested that inflammatory, lipid, and liver enzyme biomarkers explained 3.1%-14.8% of the association between ultra-processed food intake and RA risk.
• Findings were similar regardless of participants’ age, sex, body mass index, smoking status, household income, and healthy diet score.

IN PRACTICE: 

“Lower [ultra-processed food] consumption is recommended to reduce RA incidence,” the authors wrote, noting that up to half of the food consumed in the United Kingdom now falls into the ultra-processed category. “Dietary guidelines should prominently feature the detrimental effects of [ultra-processed foods], and recommendations to curtail their consumption should be integrated into public health initiatives, to mitigate the risk of RA,” they added.

SOURCE:

The study was led by Haodong Zhao, Soochow University, Suzhou, China, and was published online in The American Journal of Clinical Nutrition. 

LIMITATIONS:

Limitations included possible recall and social desirability biases, potential residual confounding, and uncertain causality of the observed associations.

DISCLOSURES:

The study was funded by grants from the National Natural Science Foundation of China and other institutions. The authors reported no conflicts of interest.

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

TOPLINE:

Middle-aged adults who consume more ultra-processed foods have an elevated risk for rheumatoid arthritis (RA) that is mediated in part through circulating biomarkers.

METHODOLOGY: 

• Investigators conducted a retrospective cohort study of 207,012 middle-aged adults without RA from the UK Biobank who completed 24-hour dietary recalls.
• Foods and beverages were classified as (1) unprocessed or minimally processed foods, (2) processed culinary ingredients, (3) processed foods, or (4) ultra-processed foods (eg, soft drinks, sweet or savory packaged snacks, reconstituted meat products, pre-prepared frozen dishes).
• The main outcome was the incident RA based on hospital diagnoses.

TAKEAWAY:

• Overall, 0.9% of participants received an RA diagnosis during a median follow-up of about 12 years.
• Relative to peers in the lowest quintile of ultra-processed food consumption, participants in the highest quintile had a 17% greater adjusted risk for RA.
• The risk rose across quintile (P < .05) and increased by 6% with each standard deviation increase in ultra-processed food intake.
• Mediation analyses suggested that inflammatory, lipid, and liver enzyme biomarkers explained 3.1%-14.8% of the association between ultra-processed food intake and RA risk.
• Findings were similar regardless of participants’ age, sex, body mass index, smoking status, household income, and healthy diet score.

IN PRACTICE: 

“Lower [ultra-processed food] consumption is recommended to reduce RA incidence,” the authors wrote, noting that up to half of the food consumed in the United Kingdom now falls into the ultra-processed category. “Dietary guidelines should prominently feature the detrimental effects of [ultra-processed foods], and recommendations to curtail their consumption should be integrated into public health initiatives, to mitigate the risk of RA,” they added.

SOURCE:

The study was led by Haodong Zhao, Soochow University, Suzhou, China, and was published online in The American Journal of Clinical Nutrition. 

LIMITATIONS:

Limitations included possible recall and social desirability biases, potential residual confounding, and uncertain causality of the observed associations.

DISCLOSURES:

The study was funded by grants from the National Natural Science Foundation of China and other institutions. The authors reported no conflicts of interest.

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

TOPLINE:

Middle-aged adults who consume more ultra-processed foods have an elevated risk for rheumatoid arthritis (RA) that is mediated in part through circulating biomarkers.

METHODOLOGY: 

• Investigators conducted a retrospective cohort study of 207,012 middle-aged adults without RA from the UK Biobank who completed 24-hour dietary recalls.
• Foods and beverages were classified as (1) unprocessed or minimally processed foods, (2) processed culinary ingredients, (3) processed foods, or (4) ultra-processed foods (eg, soft drinks, sweet or savory packaged snacks, reconstituted meat products, pre-prepared frozen dishes).
• The main outcome was the incident RA based on hospital diagnoses.

TAKEAWAY:

• Overall, 0.9% of participants received an RA diagnosis during a median follow-up of about 12 years.
• Relative to peers in the lowest quintile of ultra-processed food consumption, participants in the highest quintile had a 17% greater adjusted risk for RA.
• The risk rose across quintile (P < .05) and increased by 6% with each standard deviation increase in ultra-processed food intake.
• Mediation analyses suggested that inflammatory, lipid, and liver enzyme biomarkers explained 3.1%-14.8% of the association between ultra-processed food intake and RA risk.
• Findings were similar regardless of participants’ age, sex, body mass index, smoking status, household income, and healthy diet score.

IN PRACTICE: 

“Lower [ultra-processed food] consumption is recommended to reduce RA incidence,” the authors wrote, noting that up to half of the food consumed in the United Kingdom now falls into the ultra-processed category. “Dietary guidelines should prominently feature the detrimental effects of [ultra-processed foods], and recommendations to curtail their consumption should be integrated into public health initiatives, to mitigate the risk of RA,” they added.

SOURCE:

The study was led by Haodong Zhao, Soochow University, Suzhou, China, and was published online in The American Journal of Clinical Nutrition. 

LIMITATIONS:

Limitations included possible recall and social desirability biases, potential residual confounding, and uncertain causality of the observed associations.

DISCLOSURES:

The study was funded by grants from the National Natural Science Foundation of China and other institutions. The authors reported no conflicts of interest.

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

TOPLINE:

Higher rheumatoid arthritis (RA) disease activity is associated with an accelerated kidney function decline and increased risk for chronic kidney disease (CKD) stages G3a and G3b.

METHODOLOGY:

• Researchers analyzed data from the CorEvitas RA registry, a prospective observational cohort in the United States, between 2001 and 2022, to evaluate the longitudinal association between RA disease activity and changes in kidney function.
• They included 31,129 patients with RA (median age, 58 years; 76.3% women) who had a baseline estimated glomerular filtration rate (eGFR) ≥ 60 mL/min per 1.73 m² and received treatment with disease-modifying antirheumatic drugs (DMARDs).
• The participants were categorized into those in remission (n = 6647) and those with low (n = 10,028), moderate (n = 8548), and high (n = 5906) disease activity based on the time-averaged Clinical Disease Activity Index and followed for a median duration of 3.5 years.
• The primary outcome was a longitudinal change in eGFR, and the secondary outcomes were the development of CKD stage G3a (eGFR < 60 mL/min/1.73 m2) and stage G3b (eGFR < 45 mL/min/1.73 m2).

TAKEAWAY:

• Higher RA disease activity was associated with a faster decline in eGFR, with those having moderate and high RA disease activity experiencing an additional mean annual decline of 0.17 mL/min per 1.73 m² and 0.18 mL/min per 1.73 m², respectively, compared with those in remission.
• The decline in annual eGFR was even more accelerated when patients had consistently high disease activity since the time of enrollment (−0.43 mL/min per 1.73 m²).
• Patients with high RA disease activity had a 1.27 times (adjusted hazard ratio, 1.27; 95% CI, 1.05-1.52) higher risk of developing CKD stage G3a and a 1.93 times (aHR, 1.93; 95% CI, 1.16-3.20) higher risk for CKD stage G3b, compared with those in remission.

IN PRACTICE:

“This study suggests that controlling disease activity may potentially contribute to preserving kidney function in patients with RA,” the authors wrote.

SOURCE:

This study was led by Sho Fukui, MD, Division of Rheumatology, Inflammation, and Immunity, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, Massachusetts, and was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

This study relied on serum creatinine and not cystatin C to estimate kidney function. It also did not collect information on the severity of comorbidities, which may have introduced residual confounding. Further studies are warranted to check the effect of DMARD therapy on renal function.

DISCLOSURES:

The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Some authors reported serving as scientific advisers or consultants, receiving consulting fees or salary support, or having other ties with pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Higher rheumatoid arthritis (RA) disease activity is associated with an accelerated kidney function decline and increased risk for chronic kidney disease (CKD) stages G3a and G3b.

METHODOLOGY:

• Researchers analyzed data from the CorEvitas RA registry, a prospective observational cohort in the United States, between 2001 and 2022, to evaluate the longitudinal association between RA disease activity and changes in kidney function.
• They included 31,129 patients with RA (median age, 58 years; 76.3% women) who had a baseline estimated glomerular filtration rate (eGFR) ≥ 60 mL/min per 1.73 m² and received treatment with disease-modifying antirheumatic drugs (DMARDs).
• The participants were categorized into those in remission (n = 6647) and those with low (n = 10,028), moderate (n = 8548), and high (n = 5906) disease activity based on the time-averaged Clinical Disease Activity Index and followed for a median duration of 3.5 years.
• The primary outcome was a longitudinal change in eGFR, and the secondary outcomes were the development of CKD stage G3a (eGFR < 60 mL/min/1.73 m2) and stage G3b (eGFR < 45 mL/min/1.73 m2).

TAKEAWAY:

• Higher RA disease activity was associated with a faster decline in eGFR, with those having moderate and high RA disease activity experiencing an additional mean annual decline of 0.17 mL/min per 1.73 m² and 0.18 mL/min per 1.73 m², respectively, compared with those in remission.
• The decline in annual eGFR was even more accelerated when patients had consistently high disease activity since the time of enrollment (−0.43 mL/min per 1.73 m²).
• Patients with high RA disease activity had a 1.27 times (adjusted hazard ratio, 1.27; 95% CI, 1.05-1.52) higher risk of developing CKD stage G3a and a 1.93 times (aHR, 1.93; 95% CI, 1.16-3.20) higher risk for CKD stage G3b, compared with those in remission.

IN PRACTICE:

“This study suggests that controlling disease activity may potentially contribute to preserving kidney function in patients with RA,” the authors wrote.

SOURCE:

This study was led by Sho Fukui, MD, Division of Rheumatology, Inflammation, and Immunity, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, Massachusetts, and was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

This study relied on serum creatinine and not cystatin C to estimate kidney function. It also did not collect information on the severity of comorbidities, which may have introduced residual confounding. Further studies are warranted to check the effect of DMARD therapy on renal function.

DISCLOSURES:

The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Some authors reported serving as scientific advisers or consultants, receiving consulting fees or salary support, or having other ties with pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Higher rheumatoid arthritis (RA) disease activity is associated with an accelerated kidney function decline and increased risk for chronic kidney disease (CKD) stages G3a and G3b.

METHODOLOGY:

• Researchers analyzed data from the CorEvitas RA registry, a prospective observational cohort in the United States, between 2001 and 2022, to evaluate the longitudinal association between RA disease activity and changes in kidney function.
• They included 31,129 patients with RA (median age, 58 years; 76.3% women) who had a baseline estimated glomerular filtration rate (eGFR) ≥ 60 mL/min per 1.73 m² and received treatment with disease-modifying antirheumatic drugs (DMARDs).
• The participants were categorized into those in remission (n = 6647) and those with low (n = 10,028), moderate (n = 8548), and high (n = 5906) disease activity based on the time-averaged Clinical Disease Activity Index and followed for a median duration of 3.5 years.
• The primary outcome was a longitudinal change in eGFR, and the secondary outcomes were the development of CKD stage G3a (eGFR < 60 mL/min/1.73 m2) and stage G3b (eGFR < 45 mL/min/1.73 m2).

TAKEAWAY:

• Higher RA disease activity was associated with a faster decline in eGFR, with those having moderate and high RA disease activity experiencing an additional mean annual decline of 0.17 mL/min per 1.73 m² and 0.18 mL/min per 1.73 m², respectively, compared with those in remission.
• The decline in annual eGFR was even more accelerated when patients had consistently high disease activity since the time of enrollment (−0.43 mL/min per 1.73 m²).
• Patients with high RA disease activity had a 1.27 times (adjusted hazard ratio, 1.27; 95% CI, 1.05-1.52) higher risk of developing CKD stage G3a and a 1.93 times (aHR, 1.93; 95% CI, 1.16-3.20) higher risk for CKD stage G3b, compared with those in remission.

IN PRACTICE:

“This study suggests that controlling disease activity may potentially contribute to preserving kidney function in patients with RA,” the authors wrote.

SOURCE:

This study was led by Sho Fukui, MD, Division of Rheumatology, Inflammation, and Immunity, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, Massachusetts, and was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

This study relied on serum creatinine and not cystatin C to estimate kidney function. It also did not collect information on the severity of comorbidities, which may have introduced residual confounding. Further studies are warranted to check the effect of DMARD therapy on renal function.

DISCLOSURES:

The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Some authors reported serving as scientific advisers or consultants, receiving consulting fees or salary support, or having other ties with pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE: 

Patients with both rheumatoid arthritis (RA) and atrial fibrillation (AF) have a higher risk for ischemic stroke than those with only AF. They are also less likely to receive oral anticoagulant treatment, which may contribute to this increased stroke risk.

METHODOLOGY:

• Researchers conducted a registry-based retrospective cohort study using the Norwegian Cardio-Rheuma Register to evaluate the risk for ischemic stroke following the diagnosis of AF in patients with or without RA.
• They included 163,595 patients with newly diagnosed AF between 2010 and 2017, of whom 2750 had RA. Patients had to be diagnosed with RA before the diagnosis of AF.
• They also assessed whether patients with RA were less likely to receive oral anticoagulants for stroke prevention within 3 months of AF diagnosis than those without RA.
• The median follow-up time was 2.5 years for patients with RA and 3.0 years for those without RA.
• The primary endpoint was ischemic stroke, which was identified through hospital admissions and visits.

TAKEAWAY:

• At 5 years, patients with both RA and AF showed a higher cumulative incidence of ischemic stroke than those with only AF (7.3% vs 5.0%).
• Among patients with AF, the risk of having a stroke was 25% higher in those with RA than in those without RA (adjusted hazard ratio, 1.25; 95% CI, 1.05-1.50).
• Patients with RA were also less likely to receive treatment with oral anticoagulants than those without RA, driven by concerns over potential interactions with RA medications, bleeding risk, or other factors (adjusted odds ratio, 0.88; 95% CI, 0.80-0.97). 

IN PRACTICE:

“Our study prompts preventive measures such as meticulous cardiovascular risk factor control among patients with RA and AF and raises the question whether the presence of RA should be taken into account when considering OAC [oral anticoagulant] treatment for AF patients,” the authors wrote.

SOURCE:

This study was led by Anne M. Kerola, MD, PhD, Helsinki University Hospital and University of Helsinki in Finland. It was published online in Rheumatology.

LIMITATIONS: 

This study lacked data on smoking, blood pressure measurements, alcohol use, and obesity, which may have affected the comprehensiveness of the findings. The study population was limited to Norway and may not be generalizable to other populations.

DISCLOSURES:

This study was supported by the Olav Thon Foundation, the Research Council of Norway, and the Foundation for Research in Rheumatology. Some authors received speaker fees, participated in advisory boards, served as consultants, or had other ties with some pharmaceutical companies and institutions.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE: 

Patients with both rheumatoid arthritis (RA) and atrial fibrillation (AF) have a higher risk for ischemic stroke than those with only AF. They are also less likely to receive oral anticoagulant treatment, which may contribute to this increased stroke risk.

METHODOLOGY:

• Researchers conducted a registry-based retrospective cohort study using the Norwegian Cardio-Rheuma Register to evaluate the risk for ischemic stroke following the diagnosis of AF in patients with or without RA.
• They included 163,595 patients with newly diagnosed AF between 2010 and 2017, of whom 2750 had RA. Patients had to be diagnosed with RA before the diagnosis of AF.
• They also assessed whether patients with RA were less likely to receive oral anticoagulants for stroke prevention within 3 months of AF diagnosis than those without RA.
• The median follow-up time was 2.5 years for patients with RA and 3.0 years for those without RA.
• The primary endpoint was ischemic stroke, which was identified through hospital admissions and visits.

TAKEAWAY:

• At 5 years, patients with both RA and AF showed a higher cumulative incidence of ischemic stroke than those with only AF (7.3% vs 5.0%).
• Among patients with AF, the risk of having a stroke was 25% higher in those with RA than in those without RA (adjusted hazard ratio, 1.25; 95% CI, 1.05-1.50).
• Patients with RA were also less likely to receive treatment with oral anticoagulants than those without RA, driven by concerns over potential interactions with RA medications, bleeding risk, or other factors (adjusted odds ratio, 0.88; 95% CI, 0.80-0.97). 

IN PRACTICE:

“Our study prompts preventive measures such as meticulous cardiovascular risk factor control among patients with RA and AF and raises the question whether the presence of RA should be taken into account when considering OAC [oral anticoagulant] treatment for AF patients,” the authors wrote.

SOURCE:

This study was led by Anne M. Kerola, MD, PhD, Helsinki University Hospital and University of Helsinki in Finland. It was published online in Rheumatology.

LIMITATIONS: 

This study lacked data on smoking, blood pressure measurements, alcohol use, and obesity, which may have affected the comprehensiveness of the findings. The study population was limited to Norway and may not be generalizable to other populations.

DISCLOSURES:

This study was supported by the Olav Thon Foundation, the Research Council of Norway, and the Foundation for Research in Rheumatology. Some authors received speaker fees, participated in advisory boards, served as consultants, or had other ties with some pharmaceutical companies and institutions.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE: 

Patients with both rheumatoid arthritis (RA) and atrial fibrillation (AF) have a higher risk for ischemic stroke than those with only AF. They are also less likely to receive oral anticoagulant treatment, which may contribute to this increased stroke risk.

METHODOLOGY:

• Researchers conducted a registry-based retrospective cohort study using the Norwegian Cardio-Rheuma Register to evaluate the risk for ischemic stroke following the diagnosis of AF in patients with or without RA.
• They included 163,595 patients with newly diagnosed AF between 2010 and 2017, of whom 2750 had RA. Patients had to be diagnosed with RA before the diagnosis of AF.
• They also assessed whether patients with RA were less likely to receive oral anticoagulants for stroke prevention within 3 months of AF diagnosis than those without RA.
• The median follow-up time was 2.5 years for patients with RA and 3.0 years for those without RA.
• The primary endpoint was ischemic stroke, which was identified through hospital admissions and visits.

TAKEAWAY:

• At 5 years, patients with both RA and AF showed a higher cumulative incidence of ischemic stroke than those with only AF (7.3% vs 5.0%).
• Among patients with AF, the risk of having a stroke was 25% higher in those with RA than in those without RA (adjusted hazard ratio, 1.25; 95% CI, 1.05-1.50).
• Patients with RA were also less likely to receive treatment with oral anticoagulants than those without RA, driven by concerns over potential interactions with RA medications, bleeding risk, or other factors (adjusted odds ratio, 0.88; 95% CI, 0.80-0.97). 

IN PRACTICE:

“Our study prompts preventive measures such as meticulous cardiovascular risk factor control among patients with RA and AF and raises the question whether the presence of RA should be taken into account when considering OAC [oral anticoagulant] treatment for AF patients,” the authors wrote.

SOURCE:

This study was led by Anne M. Kerola, MD, PhD, Helsinki University Hospital and University of Helsinki in Finland. It was published online in Rheumatology.

LIMITATIONS: 

This study lacked data on smoking, blood pressure measurements, alcohol use, and obesity, which may have affected the comprehensiveness of the findings. The study population was limited to Norway and may not be generalizable to other populations.

DISCLOSURES:

This study was supported by the Olav Thon Foundation, the Research Council of Norway, and the Foundation for Research in Rheumatology. Some authors received speaker fees, participated in advisory boards, served as consultants, or had other ties with some pharmaceutical companies and institutions.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE: 

Teclistamab, a T-cell engager that targets B-cell maturation antigen (BCMA), improved disease activity in four patients with refractory autoimmune conditions. In a separately published case report, teclistamab treatment induced remission in a patient with refractory systemic lupus erythematosus (SLE).

BACKGROUND: 

• Chimeric antigen receptor (CAR) T cells or T-cell engagers against CD19 have been effective in small studies of patients with treatment-resistant autoimmune diseases.
• Some patients have disease rooted in long-lived plasma cells that express BCMA but not CD19, making them resistant to CD19 CAR T-cell therapy.
• Teclistamab acts on T cells through CD3 and targets plasmablasts and plasma cells through BCMA.

METHODOLOGY:

• In one case series, researchers administered teclistamab subcutaneously to four patients with autoimmune diseases resistant to more than five immunosuppressants, including rituximab.
• Patient 1 had systemic sclerosis, patient 2 had primary Sjögren disease, patient 3 had idiopathic inflammatory myositis, and patient 4 had rheumatoid arthritis.
• Researchers incrementally increased teclistamab dosage in an inpatient setting: 0.06 mg/kg on day 1, 0.3 mg/kg on day 3, and 1.5 mg/kg on day 5. Patients 2, 3, and 4 received one maintenance dose of 1.5 mg/kg after 4 weeks, and patient 1 received a 1.5-mg/kg dose after 12 weeks.
• In the single case report, the patient with SLE received a step-up dosage of teclistamab (0.06 mg/kg and 0.3 mg/kg) followed by 0.8 mg/kg on day 7. She received 1.5 mg/kg at weeks 2 and 5.

TAKEAWAY: 

• Teclistamab therapy led to significant improvements in disease activity in all four patients, with notable reductions in skin disease, arthritis, and lung function scores.
• Teclistamab therapy had a good safety profile, with no neurotoxicity or myelotoxicity and only lower-grade cytokine release syndrome reported.
• Researchers observed seroconversion of PM-Scl-75, PM-Scl-100, rheumatoid factor, and autoantibodies against mutated citrullinated vimentin and lower levels of autoantibodies ANA, MDAS, SS-A/Ro, SS-B/La, and PL-7 after treatment.
• In the separate case report, the patient reached complete drug-free remission by week 6, as defined by the Systemic Lupus Erythematosus Disease Activity Index 2000.
• The level of anti–double-stranded DNA antibodies in the patient with SLE decreased rapidly, reaching normal range by week 5 and remaining undetectable through week 16.

IN PRACTICE:

“These data show that the targeting of the plasma-cell compartment by a BCMA-targeted T-cell engager is feasible in patients with autoimmune disease. Whether such therapy results in sustained clinical remission warrants further study,” write the authors of the four-patient case series.

SOURCE: 

Melanie Hagen, MD, Friedrich Alexander University Erlangen–Nuremberg, Germany, and colleagues reported their case series online in The New England Journal of Medicine. Tobias Alexander, MD, and colleagues at Charité–Universitätsmedizin Berlin, Germany, also described their single case report in The New England Journal of Medicine.

LIMITATIONS:

The small number of patients limits the generalizability of the findings. The short duration of follow-up may not capture long-term effects and potential late-onset adverse events. The lack of a control group makes it difficult to attribute improvements solely to teclistamab therapy.

DISCLOSURES:

The four-patient case series was supported by grants from the Deutsche Forschungsgemeinschaft, Bundesministerium für Bildung und Forschung, and the European Union. The single case report was supported by grants from the Deutsche Forschungsgemeinschaft and the European Union. Several authors have disclosed financial relationships with pharmaceutical companies, including Janssen Biotech, which markets teclistamab.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE: 

Teclistamab, a T-cell engager that targets B-cell maturation antigen (BCMA), improved disease activity in four patients with refractory autoimmune conditions. In a separately published case report, teclistamab treatment induced remission in a patient with refractory systemic lupus erythematosus (SLE).

BACKGROUND: 

• Chimeric antigen receptor (CAR) T cells or T-cell engagers against CD19 have been effective in small studies of patients with treatment-resistant autoimmune diseases.
• Some patients have disease rooted in long-lived plasma cells that express BCMA but not CD19, making them resistant to CD19 CAR T-cell therapy.
• Teclistamab acts on T cells through CD3 and targets plasmablasts and plasma cells through BCMA.

METHODOLOGY:

• In one case series, researchers administered teclistamab subcutaneously to four patients with autoimmune diseases resistant to more than five immunosuppressants, including rituximab.
• Patient 1 had systemic sclerosis, patient 2 had primary Sjögren disease, patient 3 had idiopathic inflammatory myositis, and patient 4 had rheumatoid arthritis.
• Researchers incrementally increased teclistamab dosage in an inpatient setting: 0.06 mg/kg on day 1, 0.3 mg/kg on day 3, and 1.5 mg/kg on day 5. Patients 2, 3, and 4 received one maintenance dose of 1.5 mg/kg after 4 weeks, and patient 1 received a 1.5-mg/kg dose after 12 weeks.
• In the single case report, the patient with SLE received a step-up dosage of teclistamab (0.06 mg/kg and 0.3 mg/kg) followed by 0.8 mg/kg on day 7. She received 1.5 mg/kg at weeks 2 and 5.

TAKEAWAY: 

• Teclistamab therapy led to significant improvements in disease activity in all four patients, with notable reductions in skin disease, arthritis, and lung function scores.
• Teclistamab therapy had a good safety profile, with no neurotoxicity or myelotoxicity and only lower-grade cytokine release syndrome reported.
• Researchers observed seroconversion of PM-Scl-75, PM-Scl-100, rheumatoid factor, and autoantibodies against mutated citrullinated vimentin and lower levels of autoantibodies ANA, MDAS, SS-A/Ro, SS-B/La, and PL-7 after treatment.
• In the separate case report, the patient reached complete drug-free remission by week 6, as defined by the Systemic Lupus Erythematosus Disease Activity Index 2000.
• The level of anti–double-stranded DNA antibodies in the patient with SLE decreased rapidly, reaching normal range by week 5 and remaining undetectable through week 16.

IN PRACTICE:

“These data show that the targeting of the plasma-cell compartment by a BCMA-targeted T-cell engager is feasible in patients with autoimmune disease. Whether such therapy results in sustained clinical remission warrants further study,” write the authors of the four-patient case series.

SOURCE: 

Melanie Hagen, MD, Friedrich Alexander University Erlangen–Nuremberg, Germany, and colleagues reported their case series online in The New England Journal of Medicine. Tobias Alexander, MD, and colleagues at Charité–Universitätsmedizin Berlin, Germany, also described their single case report in The New England Journal of Medicine.

LIMITATIONS:

The small number of patients limits the generalizability of the findings. The short duration of follow-up may not capture long-term effects and potential late-onset adverse events. The lack of a control group makes it difficult to attribute improvements solely to teclistamab therapy.

DISCLOSURES:

The four-patient case series was supported by grants from the Deutsche Forschungsgemeinschaft, Bundesministerium für Bildung und Forschung, and the European Union. The single case report was supported by grants from the Deutsche Forschungsgemeinschaft and the European Union. Several authors have disclosed financial relationships with pharmaceutical companies, including Janssen Biotech, which markets teclistamab.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE: 

Teclistamab, a T-cell engager that targets B-cell maturation antigen (BCMA), improved disease activity in four patients with refractory autoimmune conditions. In a separately published case report, teclistamab treatment induced remission in a patient with refractory systemic lupus erythematosus (SLE).

BACKGROUND: 

• Chimeric antigen receptor (CAR) T cells or T-cell engagers against CD19 have been effective in small studies of patients with treatment-resistant autoimmune diseases.
• Some patients have disease rooted in long-lived plasma cells that express BCMA but not CD19, making them resistant to CD19 CAR T-cell therapy.
• Teclistamab acts on T cells through CD3 and targets plasmablasts and plasma cells through BCMA.

METHODOLOGY:

• In one case series, researchers administered teclistamab subcutaneously to four patients with autoimmune diseases resistant to more than five immunosuppressants, including rituximab.
• Patient 1 had systemic sclerosis, patient 2 had primary Sjögren disease, patient 3 had idiopathic inflammatory myositis, and patient 4 had rheumatoid arthritis.
• Researchers incrementally increased teclistamab dosage in an inpatient setting: 0.06 mg/kg on day 1, 0.3 mg/kg on day 3, and 1.5 mg/kg on day 5. Patients 2, 3, and 4 received one maintenance dose of 1.5 mg/kg after 4 weeks, and patient 1 received a 1.5-mg/kg dose after 12 weeks.
• In the single case report, the patient with SLE received a step-up dosage of teclistamab (0.06 mg/kg and 0.3 mg/kg) followed by 0.8 mg/kg on day 7. She received 1.5 mg/kg at weeks 2 and 5.

TAKEAWAY: 

• Teclistamab therapy led to significant improvements in disease activity in all four patients, with notable reductions in skin disease, arthritis, and lung function scores.
• Teclistamab therapy had a good safety profile, with no neurotoxicity or myelotoxicity and only lower-grade cytokine release syndrome reported.
• Researchers observed seroconversion of PM-Scl-75, PM-Scl-100, rheumatoid factor, and autoantibodies against mutated citrullinated vimentin and lower levels of autoantibodies ANA, MDAS, SS-A/Ro, SS-B/La, and PL-7 after treatment.
• In the separate case report, the patient reached complete drug-free remission by week 6, as defined by the Systemic Lupus Erythematosus Disease Activity Index 2000.
• The level of anti–double-stranded DNA antibodies in the patient with SLE decreased rapidly, reaching normal range by week 5 and remaining undetectable through week 16.

IN PRACTICE:

“These data show that the targeting of the plasma-cell compartment by a BCMA-targeted T-cell engager is feasible in patients with autoimmune disease. Whether such therapy results in sustained clinical remission warrants further study,” write the authors of the four-patient case series.

SOURCE: 

Melanie Hagen, MD, Friedrich Alexander University Erlangen–Nuremberg, Germany, and colleagues reported their case series online in The New England Journal of Medicine. Tobias Alexander, MD, and colleagues at Charité–Universitätsmedizin Berlin, Germany, also described their single case report in The New England Journal of Medicine.

LIMITATIONS:

The small number of patients limits the generalizability of the findings. The short duration of follow-up may not capture long-term effects and potential late-onset adverse events. The lack of a control group makes it difficult to attribute improvements solely to teclistamab therapy.

DISCLOSURES:

The four-patient case series was supported by grants from the Deutsche Forschungsgemeinschaft, Bundesministerium für Bildung und Forschung, and the European Union. The single case report was supported by grants from the Deutsche Forschungsgemeinschaft and the European Union. Several authors have disclosed financial relationships with pharmaceutical companies, including Janssen Biotech, which markets teclistamab.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

We know exercise can be a powerful medical intervention. Now scientists are finally starting to understand why.

A recent study in rats found that exercise positively changes virtually every tissue in the body. The research was part of a large National Institutes of Health initiative called MoTrPAC (Molecular Transducers of Physical Activity Consortium) to understand how physical activity improves health and prevents disease. As part of the project, a large human study is also underway.

“What was mind-blowing to me was just how much every organ changed,” said cardiologist Euan A. Ashley, MD, professor of medicine at Stanford University, Stanford, California, and the study’s lead author. “You really are a different person on exercise.”

The study examined hundreds of previously sedentary rats that exercised on a treadmill for 8 weeks. Their tissues were compared with a control group of rats that stayed sedentary.

Your patients, unlike lab animals, can’t be randomly assigned to run on a treadmill until you switch the machine off.

So how do you persuade your patients to become more active?

We asked seven doctors what works for them. They shared 10 of their most effective persuasion tactics.
 

1. Focus on the First Step

“It’s easy to say you want to change behavior,” said Jordan Metzl, MD, a sports medicine specialist at the Hospital for Special Surgery in New York City who instructs medical students on how to prescribe exercise. “It’s much more difficult to do it.”

He compares it with moving a tractor tire from point A to point B. The hardest part is lifting the tire off the ground and starting to move it. “Once it’s rolling, it takes much less effort to keep it going in the same direction,” he said.

How much exercise a patient does is irrelevant until they’ve given that tire its first push.

“Any amount of exercise is better than nothing,” Dr. Ashley said. “Let’s just start with that. Making the move from sitting a lot to standing more has genuine health benefits.” 
 

2. Mind Your Language

Many patients have a deep-rooted aversion to words and phrases associated with physical activity.

“Exercise” is one. “Working out” is another.

“I often tell them they just have to start moving,” said Chris Raynor, MD, an orthopedic surgeon based in Ottawa, Ontario. “Don’t think about it as working out. Think about it as just moving. Start with something they already like doing and work from there.”
 

3. Make It Manageable

This also applies to patients who’re injured and either waiting for or recovering from surgery.

“Joints like motion,” said Rachel M. Frank, MD, an orthopedic surgeon at the University of Colorado Sports Medicine, Denver, Colorado. “The more mobile you can be, the easier your recovery’s going to be.”

That can be a challenge for a patient who wasn’t active before the injury, especially if he or she is fixed on the idea that exercise doesn’t matter unless they do it for 30-45 minutes at a time.

“I try to break it down into manageable bits they can do at home,” Dr. Frank said. “I say, ‘Look, you brush your teeth twice a day, right? Can you do these exercises for 5 or 10 minutes before or after you brush your teeth?’ ”
 

4. Connect Their Interests to Their Activity Level

Chad Waterbury, DPT, thought he knew how to motivate a postsurgical patient to become more active and improve her odds for a full recovery. He told her she’d feel better and have more energy — all the usual selling points.

None of it impressed her.

But one day she mentioned that she’d recently become a grandmother for the first time. Dr. Waterbury, a physical therapist based in Los Angeles, noticed how she lit up when she talked about her new granddaughter.

“So I started giving her scenarios, like taking her daughter to Disneyland when she’s 9 or 10. You have to be somewhat fit to do something like that.”

It worked, and Dr. Waterbury learned a fundamental lesson in motivation. “You have to connect the exercise to something that’s important in their life,” he said.
 

5. Don’t Let a Crisis Go to Waste

“There are very few things more motivating than having a heart attack,” Dr. Ashley said. “For the vast majority of people, that’s a very sobering moment where they reassess everything in their lives.”

There’ll never be a better time to persuade a patient to become more active. In his cardiology practice, Dr. Ashley has seen a lot of patients make that switch.

“They really do start to prioritize their health in a way they never did before,” he said.
 

6. Emphasize the Practical Over the Ideal

Not all patients attach negative feelings to working out. For some, it’s the goal.

Todd Ivan, MD, calls it the “ ’I need to get to the gym’ lament”: Something they’ve aspired to but rarely if ever done.

“I tell them I’d welcome a half-hour walk every day to get started,” said Dr. Ivan, a consultation-liaison psychiatrist at Summa Health in Akron, Ohio. “It’s a way to introduce the idea that fitness begins with small adjustments.”
 

7. Go Beneath the Surface

“Exercise doesn’t generally result in great weight loss,” said endocrinologist Karl Nadolsky, DO, an obesity specialist and co-host of the Docs Who Lift podcast.

But a lot of his patients struggle to break that connection. It’s understandable, given how many times they’ve been told they’d weigh less if they moved more.

Dr. Nadolsky tells them it’s what’s on the inside that counts. “I explain it as very literal, meaning their physical health, metabolic health, and mental health.”

By reframing physical activity with an internal rather than external focus — the plumbing and wiring vs the shutters and shingles — he gives them permission to approach exercise as a health upgrade rather than yet another part of their lifelong struggle to lose weight.

“A significant number of our patients respond well to that,” he said.
 

8. Appeal to Their Intellect

Some patients think like doctors: No matter how reluctant they may be to change their mind about something, they’ll respond to evidence.

Dr. Frank has learned to identify these scientifically inclined patients. “I’ll flood them with data,” she said. “I’ll say, ‘These studies show that if you do x, y, z, your outcome will be better.’ ”

Dr. Ashley takes a similar approach when his patients give him the most common reason for not exercising: “I don’t have time.”

He tells them that exercise doesn’t take time. It gives you time.

That’s according to a 2012 study of more than 650,000 adults that associated physical activity with an increased lifespan.

As one of the authors said in an interview, a middle-aged person who gets 150 minutes a week of moderate exercise will, on average, gain 7 more minutes of life for each minute of exercise, compared with someone who doesn’t get any exercise.

The strategy works because it brings patients out of their day-to-day lives and into the future, Dr. Ashley said.

“What about your entire life?” he asks them. “You’re actually in this world for 80-plus years, you hope. How are you going to spend that? You have to think about that when you’re in your 40s and 50s.”
 

9. Show Them the Money

Illness and injury, on top of everything else, can be really expensive.

Even with good insurance, a health problem that requires surgery and/or hospitalization might cost thousands of dollars out of pocket. With mediocre insurance, it might be tens of thousands.

Sometimes, Dr. Frank said, it helps to remind patients of the price they paid for their treatment. “I’ll say, ‘Let’s get moving so you don’t have to pay for this again.’ ”

Protecting their investment can be a powerful motivation.
 

10. Make It a Team Effort

While the doctors we interviewed have a wide range of specialties — cardiology, sports medicine, psychiatry, endocrinology, orthopedics, and physical therapy — their patients have one thing in common.

They don’t want to be in a doctor’s office. It means they have something, need something, or broke something.

It might be a treatable condition that’s merely inconvenient or a life-threatening event that’s flat-out terrifying.

Whatever it is, it pulls them out of their normal world. It can be a lonely, disorienting experience.

Sometimes the best thing a doctor can do is stay connected with the patient. “This is like a team sport,” Dr. Frank tells her patients. “I’m going to be your coach, but you’re the captain of the team.”

In some cases, she’ll ask the patient to message her on the portal after completing the daily or weekly exercises. That alone might motivate the patient — especially when she responds to their messages.

After all, nobody wants to let the coach down.
 

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

We know exercise can be a powerful medical intervention. Now scientists are finally starting to understand why.

A recent study in rats found that exercise positively changes virtually every tissue in the body. The research was part of a large National Institutes of Health initiative called MoTrPAC (Molecular Transducers of Physical Activity Consortium) to understand how physical activity improves health and prevents disease. As part of the project, a large human study is also underway.

“What was mind-blowing to me was just how much every organ changed,” said cardiologist Euan A. Ashley, MD, professor of medicine at Stanford University, Stanford, California, and the study’s lead author. “You really are a different person on exercise.”

The study examined hundreds of previously sedentary rats that exercised on a treadmill for 8 weeks. Their tissues were compared with a control group of rats that stayed sedentary.

Your patients, unlike lab animals, can’t be randomly assigned to run on a treadmill until you switch the machine off.

So how do you persuade your patients to become more active?

We asked seven doctors what works for them. They shared 10 of their most effective persuasion tactics.
 

1. Focus on the First Step

“It’s easy to say you want to change behavior,” said Jordan Metzl, MD, a sports medicine specialist at the Hospital for Special Surgery in New York City who instructs medical students on how to prescribe exercise. “It’s much more difficult to do it.”

He compares it with moving a tractor tire from point A to point B. The hardest part is lifting the tire off the ground and starting to move it. “Once it’s rolling, it takes much less effort to keep it going in the same direction,” he said.

How much exercise a patient does is irrelevant until they’ve given that tire its first push.

“Any amount of exercise is better than nothing,” Dr. Ashley said. “Let’s just start with that. Making the move from sitting a lot to standing more has genuine health benefits.” 
 

2. Mind Your Language

Many patients have a deep-rooted aversion to words and phrases associated with physical activity.

“Exercise” is one. “Working out” is another.

“I often tell them they just have to start moving,” said Chris Raynor, MD, an orthopedic surgeon based in Ottawa, Ontario. “Don’t think about it as working out. Think about it as just moving. Start with something they already like doing and work from there.”
 

3. Make It Manageable

This also applies to patients who’re injured and either waiting for or recovering from surgery.

“Joints like motion,” said Rachel M. Frank, MD, an orthopedic surgeon at the University of Colorado Sports Medicine, Denver, Colorado. “The more mobile you can be, the easier your recovery’s going to be.”

That can be a challenge for a patient who wasn’t active before the injury, especially if he or she is fixed on the idea that exercise doesn’t matter unless they do it for 30-45 minutes at a time.

“I try to break it down into manageable bits they can do at home,” Dr. Frank said. “I say, ‘Look, you brush your teeth twice a day, right? Can you do these exercises for 5 or 10 minutes before or after you brush your teeth?’ ”
 

4. Connect Their Interests to Their Activity Level

Chad Waterbury, DPT, thought he knew how to motivate a postsurgical patient to become more active and improve her odds for a full recovery. He told her she’d feel better and have more energy — all the usual selling points.

None of it impressed her.

But one day she mentioned that she’d recently become a grandmother for the first time. Dr. Waterbury, a physical therapist based in Los Angeles, noticed how she lit up when she talked about her new granddaughter.

“So I started giving her scenarios, like taking her daughter to Disneyland when she’s 9 or 10. You have to be somewhat fit to do something like that.”

It worked, and Dr. Waterbury learned a fundamental lesson in motivation. “You have to connect the exercise to something that’s important in their life,” he said.
 

5. Don’t Let a Crisis Go to Waste

“There are very few things more motivating than having a heart attack,” Dr. Ashley said. “For the vast majority of people, that’s a very sobering moment where they reassess everything in their lives.”

There’ll never be a better time to persuade a patient to become more active. In his cardiology practice, Dr. Ashley has seen a lot of patients make that switch.

“They really do start to prioritize their health in a way they never did before,” he said.
 

6. Emphasize the Practical Over the Ideal

Not all patients attach negative feelings to working out. For some, it’s the goal.

Todd Ivan, MD, calls it the “ ’I need to get to the gym’ lament”: Something they’ve aspired to but rarely if ever done.

“I tell them I’d welcome a half-hour walk every day to get started,” said Dr. Ivan, a consultation-liaison psychiatrist at Summa Health in Akron, Ohio. “It’s a way to introduce the idea that fitness begins with small adjustments.”
 

7. Go Beneath the Surface

“Exercise doesn’t generally result in great weight loss,” said endocrinologist Karl Nadolsky, DO, an obesity specialist and co-host of the Docs Who Lift podcast.

But a lot of his patients struggle to break that connection. It’s understandable, given how many times they’ve been told they’d weigh less if they moved more.

Dr. Nadolsky tells them it’s what’s on the inside that counts. “I explain it as very literal, meaning their physical health, metabolic health, and mental health.”

By reframing physical activity with an internal rather than external focus — the plumbing and wiring vs the shutters and shingles — he gives them permission to approach exercise as a health upgrade rather than yet another part of their lifelong struggle to lose weight.

“A significant number of our patients respond well to that,” he said.
 

8. Appeal to Their Intellect

Some patients think like doctors: No matter how reluctant they may be to change their mind about something, they’ll respond to evidence.

Dr. Frank has learned to identify these scientifically inclined patients. “I’ll flood them with data,” she said. “I’ll say, ‘These studies show that if you do x, y, z, your outcome will be better.’ ”

Dr. Ashley takes a similar approach when his patients give him the most common reason for not exercising: “I don’t have time.”

He tells them that exercise doesn’t take time. It gives you time.

That’s according to a 2012 study of more than 650,000 adults that associated physical activity with an increased lifespan.

As one of the authors said in an interview, a middle-aged person who gets 150 minutes a week of moderate exercise will, on average, gain 7 more minutes of life for each minute of exercise, compared with someone who doesn’t get any exercise.

The strategy works because it brings patients out of their day-to-day lives and into the future, Dr. Ashley said.

“What about your entire life?” he asks them. “You’re actually in this world for 80-plus years, you hope. How are you going to spend that? You have to think about that when you’re in your 40s and 50s.”
 

9. Show Them the Money

Illness and injury, on top of everything else, can be really expensive.

Even with good insurance, a health problem that requires surgery and/or hospitalization might cost thousands of dollars out of pocket. With mediocre insurance, it might be tens of thousands.

Sometimes, Dr. Frank said, it helps to remind patients of the price they paid for their treatment. “I’ll say, ‘Let’s get moving so you don’t have to pay for this again.’ ”

Protecting their investment can be a powerful motivation.
 

10. Make It a Team Effort

While the doctors we interviewed have a wide range of specialties — cardiology, sports medicine, psychiatry, endocrinology, orthopedics, and physical therapy — their patients have one thing in common.

They don’t want to be in a doctor’s office. It means they have something, need something, or broke something.

It might be a treatable condition that’s merely inconvenient or a life-threatening event that’s flat-out terrifying.

Whatever it is, it pulls them out of their normal world. It can be a lonely, disorienting experience.

Sometimes the best thing a doctor can do is stay connected with the patient. “This is like a team sport,” Dr. Frank tells her patients. “I’m going to be your coach, but you’re the captain of the team.”

In some cases, she’ll ask the patient to message her on the portal after completing the daily or weekly exercises. That alone might motivate the patient — especially when she responds to their messages.

After all, nobody wants to let the coach down.
 

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

We know exercise can be a powerful medical intervention. Now scientists are finally starting to understand why.

A recent study in rats found that exercise positively changes virtually every tissue in the body. The research was part of a large National Institutes of Health initiative called MoTrPAC (Molecular Transducers of Physical Activity Consortium) to understand how physical activity improves health and prevents disease. As part of the project, a large human study is also underway.

“What was mind-blowing to me was just how much every organ changed,” said cardiologist Euan A. Ashley, MD, professor of medicine at Stanford University, Stanford, California, and the study’s lead author. “You really are a different person on exercise.”

The study examined hundreds of previously sedentary rats that exercised on a treadmill for 8 weeks. Their tissues were compared with a control group of rats that stayed sedentary.

Your patients, unlike lab animals, can’t be randomly assigned to run on a treadmill until you switch the machine off.

So how do you persuade your patients to become more active?

We asked seven doctors what works for them. They shared 10 of their most effective persuasion tactics.
 

1. Focus on the First Step

“It’s easy to say you want to change behavior,” said Jordan Metzl, MD, a sports medicine specialist at the Hospital for Special Surgery in New York City who instructs medical students on how to prescribe exercise. “It’s much more difficult to do it.”

He compares it with moving a tractor tire from point A to point B. The hardest part is lifting the tire off the ground and starting to move it. “Once it’s rolling, it takes much less effort to keep it going in the same direction,” he said.

How much exercise a patient does is irrelevant until they’ve given that tire its first push.

“Any amount of exercise is better than nothing,” Dr. Ashley said. “Let’s just start with that. Making the move from sitting a lot to standing more has genuine health benefits.” 
 

2. Mind Your Language

Many patients have a deep-rooted aversion to words and phrases associated with physical activity.

“Exercise” is one. “Working out” is another.

“I often tell them they just have to start moving,” said Chris Raynor, MD, an orthopedic surgeon based in Ottawa, Ontario. “Don’t think about it as working out. Think about it as just moving. Start with something they already like doing and work from there.”
 

3. Make It Manageable

This also applies to patients who’re injured and either waiting for or recovering from surgery.

“Joints like motion,” said Rachel M. Frank, MD, an orthopedic surgeon at the University of Colorado Sports Medicine, Denver, Colorado. “The more mobile you can be, the easier your recovery’s going to be.”

That can be a challenge for a patient who wasn’t active before the injury, especially if he or she is fixed on the idea that exercise doesn’t matter unless they do it for 30-45 minutes at a time.

“I try to break it down into manageable bits they can do at home,” Dr. Frank said. “I say, ‘Look, you brush your teeth twice a day, right? Can you do these exercises for 5 or 10 minutes before or after you brush your teeth?’ ”
 

4. Connect Their Interests to Their Activity Level

Chad Waterbury, DPT, thought he knew how to motivate a postsurgical patient to become more active and improve her odds for a full recovery. He told her she’d feel better and have more energy — all the usual selling points.

None of it impressed her.

But one day she mentioned that she’d recently become a grandmother for the first time. Dr. Waterbury, a physical therapist based in Los Angeles, noticed how she lit up when she talked about her new granddaughter.

“So I started giving her scenarios, like taking her daughter to Disneyland when she’s 9 or 10. You have to be somewhat fit to do something like that.”

It worked, and Dr. Waterbury learned a fundamental lesson in motivation. “You have to connect the exercise to something that’s important in their life,” he said.
 

5. Don’t Let a Crisis Go to Waste

“There are very few things more motivating than having a heart attack,” Dr. Ashley said. “For the vast majority of people, that’s a very sobering moment where they reassess everything in their lives.”

There’ll never be a better time to persuade a patient to become more active. In his cardiology practice, Dr. Ashley has seen a lot of patients make that switch.

“They really do start to prioritize their health in a way they never did before,” he said.
 

6. Emphasize the Practical Over the Ideal

Not all patients attach negative feelings to working out. For some, it’s the goal.

Todd Ivan, MD, calls it the “ ’I need to get to the gym’ lament”: Something they’ve aspired to but rarely if ever done.

“I tell them I’d welcome a half-hour walk every day to get started,” said Dr. Ivan, a consultation-liaison psychiatrist at Summa Health in Akron, Ohio. “It’s a way to introduce the idea that fitness begins with small adjustments.”
 

7. Go Beneath the Surface

“Exercise doesn’t generally result in great weight loss,” said endocrinologist Karl Nadolsky, DO, an obesity specialist and co-host of the Docs Who Lift podcast.

But a lot of his patients struggle to break that connection. It’s understandable, given how many times they’ve been told they’d weigh less if they moved more.

Dr. Nadolsky tells them it’s what’s on the inside that counts. “I explain it as very literal, meaning their physical health, metabolic health, and mental health.”

By reframing physical activity with an internal rather than external focus — the plumbing and wiring vs the shutters and shingles — he gives them permission to approach exercise as a health upgrade rather than yet another part of their lifelong struggle to lose weight.

“A significant number of our patients respond well to that,” he said.
 

8. Appeal to Their Intellect

Some patients think like doctors: No matter how reluctant they may be to change their mind about something, they’ll respond to evidence.

Dr. Frank has learned to identify these scientifically inclined patients. “I’ll flood them with data,” she said. “I’ll say, ‘These studies show that if you do x, y, z, your outcome will be better.’ ”

Dr. Ashley takes a similar approach when his patients give him the most common reason for not exercising: “I don’t have time.”

He tells them that exercise doesn’t take time. It gives you time.

That’s according to a 2012 study of more than 650,000 adults that associated physical activity with an increased lifespan.

As one of the authors said in an interview, a middle-aged person who gets 150 minutes a week of moderate exercise will, on average, gain 7 more minutes of life for each minute of exercise, compared with someone who doesn’t get any exercise.

The strategy works because it brings patients out of their day-to-day lives and into the future, Dr. Ashley said.

“What about your entire life?” he asks them. “You’re actually in this world for 80-plus years, you hope. How are you going to spend that? You have to think about that when you’re in your 40s and 50s.”
 

9. Show Them the Money

Illness and injury, on top of everything else, can be really expensive.

Even with good insurance, a health problem that requires surgery and/or hospitalization might cost thousands of dollars out of pocket. With mediocre insurance, it might be tens of thousands.

Sometimes, Dr. Frank said, it helps to remind patients of the price they paid for their treatment. “I’ll say, ‘Let’s get moving so you don’t have to pay for this again.’ ”

Protecting their investment can be a powerful motivation.
 

10. Make It a Team Effort

While the doctors we interviewed have a wide range of specialties — cardiology, sports medicine, psychiatry, endocrinology, orthopedics, and physical therapy — their patients have one thing in common.

They don’t want to be in a doctor’s office. It means they have something, need something, or broke something.

It might be a treatable condition that’s merely inconvenient or a life-threatening event that’s flat-out terrifying.

Whatever it is, it pulls them out of their normal world. It can be a lonely, disorienting experience.

Sometimes the best thing a doctor can do is stay connected with the patient. “This is like a team sport,” Dr. Frank tells her patients. “I’m going to be your coach, but you’re the captain of the team.”

In some cases, she’ll ask the patient to message her on the portal after completing the daily or weekly exercises. That alone might motivate the patient — especially when she responds to their messages.

After all, nobody wants to let the coach down.
 

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

TOPLINE:

Treatment with etanercept led to faster disease control initially in patients with early rheumatoid arthritis (RA) who had an insufficient early response to methotrexate and bridging glucocorticoids therapy, but more patients achieved disease control with leflunomide at 104 weeks.

METHODOLOGY:

• Researchers conducted CareRA2020, a randomized controlled trial including 276 patients with early RA who were initially treated with oral methotrexate 15 mg/wk and a step-down prednisone scheme, with early insufficient responders (n = 110) randomized to add etanercept 50 mg/wk or leflunomide 10 mg/d for 24 weeks.
• Patients were classified as early insufficient responders if they did not achieve a 28-joint Disease Activity Score with C-reactive protein (DAS28-CRP) < 3.2 between weeks 8 and 32 or < 2.6 at week 32, despite an increase in methotrexate dose to 20 mg/wk.
• The primary outcome was the longitudinal disease activity measured by DAS28-CRP over 104 weeks.
• The secondary outcomes included disease control at 28 weeks post randomization and the use of biologic or targeted synthetic disease-modifying antirheumatic drugs at week 104.

TAKEAWAY:

• Early introduction of etanercept in patients with RA did not show long-term superiority over leflunomide in disease control over 2 years (P = .157).
• At 28 weeks post randomization, the percentage of patients who achieved a DAS28-CRP < 2.6 was higher in the etanercept group than in the leflunomide group (59% vs 44%).
• After stopping etanercept, disease activity scores worsened, and a lower proportion of patients achieved DAS28-CRP < 2.6 in the etanercept group than in the leflunomide group (55% vs 69%) at week 104.
• Even after treatment with etanercept or leflunomide, the 110 early insufficient responders never reached the same level of disease control as the 142 patients who responded to methotrexate and bridging glucocorticoids within weeks 8-32.

IN PRACTICE:

“The CareRA2020 trial did not completely solve the unmet need of patients responding insufficiently to conventional initial therapy for early RA, but it provides opportunities to further optimize the treatment approach in this population, for instance, by focusing on the identification of potential subgroups with different disease activity trajectories within the early insufficient responder group,” wrote the authors.

SOURCE:

The study was led by Delphine Bertrand of the Skeletal Biology and Engineering Research Center in the Department of Development and Regeneration at KU Leuven in Belgium, and was published online on August 7, 2024, in RMD Open.

LIMITATIONS:

The open-label design of the study may have introduced bias, as patients and investigators were aware of the treatment. The temporary administration of etanercept may not have reflected its long-term effects. The study was conducted in Belgium, which limited the generalizability of the findings to other populations.

DISCLOSURES:

The study was supported by the Belgian Health Care Knowledge Centre. Some authors reported serving as speakers or receiving grants, consulting fees, honoraria, or meeting or travel support from financial ties with Novartis, Pfizer, Amgen, and other pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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

TOPLINE:

Treatment with etanercept led to faster disease control initially in patients with early rheumatoid arthritis (RA) who had an insufficient early response to methotrexate and bridging glucocorticoids therapy, but more patients achieved disease control with leflunomide at 104 weeks.

METHODOLOGY:

• Researchers conducted CareRA2020, a randomized controlled trial including 276 patients with early RA who were initially treated with oral methotrexate 15 mg/wk and a step-down prednisone scheme, with early insufficient responders (n = 110) randomized to add etanercept 50 mg/wk or leflunomide 10 mg/d for 24 weeks.
• Patients were classified as early insufficient responders if they did not achieve a 28-joint Disease Activity Score with C-reactive protein (DAS28-CRP) < 3.2 between weeks 8 and 32 or < 2.6 at week 32, despite an increase in methotrexate dose to 20 mg/wk.
• The primary outcome was the longitudinal disease activity measured by DAS28-CRP over 104 weeks.
• The secondary outcomes included disease control at 28 weeks post randomization and the use of biologic or targeted synthetic disease-modifying antirheumatic drugs at week 104.

TAKEAWAY:

• Early introduction of etanercept in patients with RA did not show long-term superiority over leflunomide in disease control over 2 years (P = .157).
• At 28 weeks post randomization, the percentage of patients who achieved a DAS28-CRP < 2.6 was higher in the etanercept group than in the leflunomide group (59% vs 44%).
• After stopping etanercept, disease activity scores worsened, and a lower proportion of patients achieved DAS28-CRP < 2.6 in the etanercept group than in the leflunomide group (55% vs 69%) at week 104.
• Even after treatment with etanercept or leflunomide, the 110 early insufficient responders never reached the same level of disease control as the 142 patients who responded to methotrexate and bridging glucocorticoids within weeks 8-32.

IN PRACTICE:

“The CareRA2020 trial did not completely solve the unmet need of patients responding insufficiently to conventional initial therapy for early RA, but it provides opportunities to further optimize the treatment approach in this population, for instance, by focusing on the identification of potential subgroups with different disease activity trajectories within the early insufficient responder group,” wrote the authors.

SOURCE:

The study was led by Delphine Bertrand of the Skeletal Biology and Engineering Research Center in the Department of Development and Regeneration at KU Leuven in Belgium, and was published online on August 7, 2024, in RMD Open.

LIMITATIONS:

The open-label design of the study may have introduced bias, as patients and investigators were aware of the treatment. The temporary administration of etanercept may not have reflected its long-term effects. The study was conducted in Belgium, which limited the generalizability of the findings to other populations.

DISCLOSURES:

The study was supported by the Belgian Health Care Knowledge Centre. Some authors reported serving as speakers or receiving grants, consulting fees, honoraria, or meeting or travel support from financial ties with Novartis, Pfizer, Amgen, and other pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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

TOPLINE:

Treatment with etanercept led to faster disease control initially in patients with early rheumatoid arthritis (RA) who had an insufficient early response to methotrexate and bridging glucocorticoids therapy, but more patients achieved disease control with leflunomide at 104 weeks.

METHODOLOGY:

• Researchers conducted CareRA2020, a randomized controlled trial including 276 patients with early RA who were initially treated with oral methotrexate 15 mg/wk and a step-down prednisone scheme, with early insufficient responders (n = 110) randomized to add etanercept 50 mg/wk or leflunomide 10 mg/d for 24 weeks.
• Patients were classified as early insufficient responders if they did not achieve a 28-joint Disease Activity Score with C-reactive protein (DAS28-CRP) < 3.2 between weeks 8 and 32 or < 2.6 at week 32, despite an increase in methotrexate dose to 20 mg/wk.
• The primary outcome was the longitudinal disease activity measured by DAS28-CRP over 104 weeks.
• The secondary outcomes included disease control at 28 weeks post randomization and the use of biologic or targeted synthetic disease-modifying antirheumatic drugs at week 104.

TAKEAWAY:

• Early introduction of etanercept in patients with RA did not show long-term superiority over leflunomide in disease control over 2 years (P = .157).
• At 28 weeks post randomization, the percentage of patients who achieved a DAS28-CRP < 2.6 was higher in the etanercept group than in the leflunomide group (59% vs 44%).
• After stopping etanercept, disease activity scores worsened, and a lower proportion of patients achieved DAS28-CRP < 2.6 in the etanercept group than in the leflunomide group (55% vs 69%) at week 104.
• Even after treatment with etanercept or leflunomide, the 110 early insufficient responders never reached the same level of disease control as the 142 patients who responded to methotrexate and bridging glucocorticoids within weeks 8-32.

IN PRACTICE:

“The CareRA2020 trial did not completely solve the unmet need of patients responding insufficiently to conventional initial therapy for early RA, but it provides opportunities to further optimize the treatment approach in this population, for instance, by focusing on the identification of potential subgroups with different disease activity trajectories within the early insufficient responder group,” wrote the authors.

SOURCE:

The study was led by Delphine Bertrand of the Skeletal Biology and Engineering Research Center in the Department of Development and Regeneration at KU Leuven in Belgium, and was published online on August 7, 2024, in RMD Open.

LIMITATIONS:

The open-label design of the study may have introduced bias, as patients and investigators were aware of the treatment. The temporary administration of etanercept may not have reflected its long-term effects. The study was conducted in Belgium, which limited the generalizability of the findings to other populations.

DISCLOSURES:

The study was supported by the Belgian Health Care Knowledge Centre. Some authors reported serving as speakers or receiving grants, consulting fees, honoraria, or meeting or travel support from financial ties with Novartis, Pfizer, Amgen, and other pharmaceutical companies.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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

TOPLINE:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A smartphone app that delivers acceptance and commitment therapy (ACT), a type of cognitive behavioral therapy, improves overall well-being and reduces the severity of pain, fatigue, sleep issues, and depression to a greater extent than daily symptom tracking in patients with fibromyalgia.

METHODOLOGY:

• Researchers conducted the phase 3 PROSPER-FM trial at 25 community sites in the United States to assess the efficacy and safety of digital ACT for patients with fibromyalgia.
• A total of 275 adult patients aged 22-75 years with fibromyalgia were randomly assigned to either the digital ACT group (n = 140) or the active control group (n = 135) for 12 weeks.
• Patients in the digital ACT group received a self-guided, smartphone-delivered program in which they learned and practiced the core ACT skills of acceptance, values, mindfulness, defusion, self as context, and willingness and committed action to build psychological flexibility, while the control group underwent daily symptom tracking and received educational materials.
• The primary endpoint was the response rate on the Patient Global Impression of Change (PGIC) at week 12, which is an indicator of patient well-being.
• The secondary endpoints included changes in the Revised Fibromyalgia Impact Questionnaire (FIQ-R) total score and pain intensity, pain interference, and sleep interference scores.

TAKEAWAY:

• At week 12, 71% of the patients in the digital ACT group responded with a minimally improved or better change in the PGIC response, compared with only 22% of the patients in the control group (P < .0001).
• The digital ACT group showed a significant reduction in the impact of fibromyalgia, with a between-group effect size of d = 0.65 (P < .0001) at week 12. The FIQ-R total score significantly improved within 3 weeks of using the self-guided digital ACT app.
• The use of digital ACT also demonstrated positive effects on the levels of weekly pain intensity (P = .001) and depression (P < .0001), compared with the control group.
• No serious adverse effects related to the app were reported, and both groups demonstrated high rates of adherence, with most (72%) participants in the digital ACT group completing at least 42 sessions.

IN PRACTICE:

“The results found in the study are essential for professionals who care for patients with fibromyalgia as they present a new viable treatment alternative,” Guilherme Torres Vilarino, PhD, Santa Catarina State University, Florianópolis, Brazil, wrote in an accompanying editorial.

SOURCE:

This study was led by R. Michael Gendreau, MD, PhD, Gendreau Consulting, Poway, California. It was published online  in The Lancet.

LIMITATIONS:

The study population predominantly consisted of women and White individuals, which may limit the generalizability of the findings to more diverse populations. Additionally, the study was conducted in the United States, and the results may thus not be applicable to other countries with different racial, ethnic, educational, and economic characteristics. The study duration was 12 weeks, and the long-term benefits of digital ACT have not yet been shown.

DISCLOSURES:

This study was funded by Swing Therapeutics. Seven authors declared having stock options and/or receiving salary from Swing Therapeutics. Other authors reported having many ties with several sources, including Swing Therapeutics.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A smartphone app that delivers acceptance and commitment therapy (ACT), a type of cognitive behavioral therapy, improves overall well-being and reduces the severity of pain, fatigue, sleep issues, and depression to a greater extent than daily symptom tracking in patients with fibromyalgia.

METHODOLOGY:

• Researchers conducted the phase 3 PROSPER-FM trial at 25 community sites in the United States to assess the efficacy and safety of digital ACT for patients with fibromyalgia.
• A total of 275 adult patients aged 22-75 years with fibromyalgia were randomly assigned to either the digital ACT group (n = 140) or the active control group (n = 135) for 12 weeks.
• Patients in the digital ACT group received a self-guided, smartphone-delivered program in which they learned and practiced the core ACT skills of acceptance, values, mindfulness, defusion, self as context, and willingness and committed action to build psychological flexibility, while the control group underwent daily symptom tracking and received educational materials.
• The primary endpoint was the response rate on the Patient Global Impression of Change (PGIC) at week 12, which is an indicator of patient well-being.
• The secondary endpoints included changes in the Revised Fibromyalgia Impact Questionnaire (FIQ-R) total score and pain intensity, pain interference, and sleep interference scores.

TAKEAWAY:

• At week 12, 71% of the patients in the digital ACT group responded with a minimally improved or better change in the PGIC response, compared with only 22% of the patients in the control group (P < .0001).
• The digital ACT group showed a significant reduction in the impact of fibromyalgia, with a between-group effect size of d = 0.65 (P < .0001) at week 12. The FIQ-R total score significantly improved within 3 weeks of using the self-guided digital ACT app.
• The use of digital ACT also demonstrated positive effects on the levels of weekly pain intensity (P = .001) and depression (P < .0001), compared with the control group.
• No serious adverse effects related to the app were reported, and both groups demonstrated high rates of adherence, with most (72%) participants in the digital ACT group completing at least 42 sessions.

IN PRACTICE:

“The results found in the study are essential for professionals who care for patients with fibromyalgia as they present a new viable treatment alternative,” Guilherme Torres Vilarino, PhD, Santa Catarina State University, Florianópolis, Brazil, wrote in an accompanying editorial.

SOURCE:

This study was led by R. Michael Gendreau, MD, PhD, Gendreau Consulting, Poway, California. It was published online  in The Lancet.

LIMITATIONS:

The study population predominantly consisted of women and White individuals, which may limit the generalizability of the findings to more diverse populations. Additionally, the study was conducted in the United States, and the results may thus not be applicable to other countries with different racial, ethnic, educational, and economic characteristics. The study duration was 12 weeks, and the long-term benefits of digital ACT have not yet been shown.

DISCLOSURES:

This study was funded by Swing Therapeutics. Seven authors declared having stock options and/or receiving salary from Swing Therapeutics. Other authors reported having many ties with several sources, including Swing Therapeutics.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A smartphone app that delivers acceptance and commitment therapy (ACT), a type of cognitive behavioral therapy, improves overall well-being and reduces the severity of pain, fatigue, sleep issues, and depression to a greater extent than daily symptom tracking in patients with fibromyalgia.

METHODOLOGY:

• Researchers conducted the phase 3 PROSPER-FM trial at 25 community sites in the United States to assess the efficacy and safety of digital ACT for patients with fibromyalgia.
• A total of 275 adult patients aged 22-75 years with fibromyalgia were randomly assigned to either the digital ACT group (n = 140) or the active control group (n = 135) for 12 weeks.
• Patients in the digital ACT group received a self-guided, smartphone-delivered program in which they learned and practiced the core ACT skills of acceptance, values, mindfulness, defusion, self as context, and willingness and committed action to build psychological flexibility, while the control group underwent daily symptom tracking and received educational materials.
• The primary endpoint was the response rate on the Patient Global Impression of Change (PGIC) at week 12, which is an indicator of patient well-being.
• The secondary endpoints included changes in the Revised Fibromyalgia Impact Questionnaire (FIQ-R) total score and pain intensity, pain interference, and sleep interference scores.

TAKEAWAY:

• At week 12, 71% of the patients in the digital ACT group responded with a minimally improved or better change in the PGIC response, compared with only 22% of the patients in the control group (P < .0001).
• The digital ACT group showed a significant reduction in the impact of fibromyalgia, with a between-group effect size of d = 0.65 (P < .0001) at week 12. The FIQ-R total score significantly improved within 3 weeks of using the self-guided digital ACT app.
• The use of digital ACT also demonstrated positive effects on the levels of weekly pain intensity (P = .001) and depression (P < .0001), compared with the control group.
• No serious adverse effects related to the app were reported, and both groups demonstrated high rates of adherence, with most (72%) participants in the digital ACT group completing at least 42 sessions.

IN PRACTICE:

“The results found in the study are essential for professionals who care for patients with fibromyalgia as they present a new viable treatment alternative,” Guilherme Torres Vilarino, PhD, Santa Catarina State University, Florianópolis, Brazil, wrote in an accompanying editorial.

SOURCE:

This study was led by R. Michael Gendreau, MD, PhD, Gendreau Consulting, Poway, California. It was published online  in The Lancet.

LIMITATIONS:

The study population predominantly consisted of women and White individuals, which may limit the generalizability of the findings to more diverse populations. Additionally, the study was conducted in the United States, and the results may thus not be applicable to other countries with different racial, ethnic, educational, and economic characteristics. The study duration was 12 weeks, and the long-term benefits of digital ACT have not yet been shown.

DISCLOSURES:

This study was funded by Swing Therapeutics. Seven authors declared having stock options and/or receiving salary from Swing Therapeutics. Other authors reported having many ties with several sources, including Swing Therapeutics.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Since the first Food and Drug Administration approval of a Janus kinase (JAK) inhibitor in 2011, the number of these medications available — and their treatment indications — have continued to grow. Prescribing physicians are familiar with the benefits and risks for these drugs, including higher risk for cardiac events and malignancy; however, one adverse effect may be overlooked, especially by specialties outside of dermatology: acne. Though less serious than some other side effects, JAK inhibitor–associated acne — JAKne, for short — can be a concern for patients.

“Your physical appearance and how you present yourself to the world is an important part of your self-confidence and living life on your own terms,” said Arash Mostaghimi, MD, the director of inpatient dermatology at Brigham and Women’s Hospital in Boston, Massachusetts. “I think letting people know about [JAKne] and then addressing it when it occurs should be a normal part of managing these medications.”
 

What Is JAKne?

JAKne generally looks like other kinds of acne, explained Janelle Nassim, MD, director of laser and cosmetic dermatology at the Indiana University School of Medicine, Indianapolis. “It can affect the same areas that typical acne affects, including the face, chest, back, neck, and upper shoulders.”

Though it appears like typical forms of acne, it is not clear what drives these skin eruptions in patients taking JAK inhibitors.

courtesy Brigham and Women&#039;s Hospital

“We don’t understand the underlying pathophysiology,” Dr. Mostaghimi said. “It looks like acne, but we don’t know if the exact underlying inflammatory process is the same or if it’s different.”

In a 2023 systematic review of clinical studies, Dr. Mostaghimi and colleagues found that patients on any JAK inhibitor were nearly four times more likely to experience acne than patients who received placebo, but risk varied between medications. Patients taking JAK inhibitors for skin conditions had higher risk for acne than those given the medications for other indications. However, Dr. Mostaghimi thinks this finding is the result of selection bias.

Participants may not mention side effects like acne in trials for rheumatologic or gastrointestinal conditions, he said, unlike in trials for skin conditions. “Clinically, I’ve seen it in patients across every indication.”

Patients with a history of acne seem to be more likely to develop this side effect, though formal studies looking into risk factors are lacking. In Dr. Mostaghimi’s own clinical experience, JAKne is also more common in younger patients, but it can happen to anyone. “I’ve seen 70-year-olds develop acne — patients who’ve never had an issue their whole life — when they’re taking a JAK inhibitor.”

This issue also appears to be more common earlier in treatment, he added, and may improve over time as a patient continues with the medication.
 

How Do You Treat It?

“I think in other specialties, you will often feel awkward addressing skin conditions or pointing out acne,” Dr. Mostaghimi said. The most important steps are being aware of this potential side effect, and if you see it practice, to bring it up.

“Say: I’m noticing there’s some changes in your skin. Some patients on JAK inhibitors develop more acne. Have you noticed this? And if so, is this bothering you?”

Generally, JAKne is mild to moderate, explained Dr. Nassim, and if non-dermatologists are comfortable, they can prescribe a first-line topical regimen for patients. Dr. Mostaghimi recommends prescribing a clindamycin 1% lotion or gel. In addition, patients can use a benzoyl peroxide wash (4% or 10%) combined with a gentle retinoid, such as adapalene. (Both of these treatments are now available over the counter.)

courtesy Harvard Medical School

In patients with scalp or hairline involvement, he often prescribes a ketoconazole 2% shampoo, which patients can use to wash their scalp, face, chest, and back in the shower.

If they aren’t responding to these initial treatments, then refer to a dermatologist for further assessment.

“Ultimately, referring to a dermatologist is the best course of action,” Dr. Nassim said. “I have had patients on JAK inhibitors who improved with topical acne treatments, and some that required more aggressive treatment with oral medications.”

Dr. Mostaghimi reported consulting fees from AbbVie, Concert Pharmaceuticals, Pfizer, and 3Derm Systems; research funding from Incyte, Aclaris Therapeutics, Eli Lilly, and Concert Pharmaceuticals; personal fees from Equillium, ASLAN Pharmaceuticals, ACOM, and Boehringer Ingelheim; and advisory board fees from Fig.1 Beauty, Eli Lilly, Pfizer, and Hims & Hers Health. Dr. Nassim had no relevant disclosures.

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

Since the first Food and Drug Administration approval of a Janus kinase (JAK) inhibitor in 2011, the number of these medications available — and their treatment indications — have continued to grow. Prescribing physicians are familiar with the benefits and risks for these drugs, including higher risk for cardiac events and malignancy; however, one adverse effect may be overlooked, especially by specialties outside of dermatology: acne. Though less serious than some other side effects, JAK inhibitor–associated acne — JAKne, for short — can be a concern for patients.

“Your physical appearance and how you present yourself to the world is an important part of your self-confidence and living life on your own terms,” said Arash Mostaghimi, MD, the director of inpatient dermatology at Brigham and Women’s Hospital in Boston, Massachusetts. “I think letting people know about [JAKne] and then addressing it when it occurs should be a normal part of managing these medications.”
 

What Is JAKne?

JAKne generally looks like other kinds of acne, explained Janelle Nassim, MD, director of laser and cosmetic dermatology at the Indiana University School of Medicine, Indianapolis. “It can affect the same areas that typical acne affects, including the face, chest, back, neck, and upper shoulders.”

Though it appears like typical forms of acne, it is not clear what drives these skin eruptions in patients taking JAK inhibitors.

courtesy Brigham and Women&#039;s Hospital

“We don’t understand the underlying pathophysiology,” Dr. Mostaghimi said. “It looks like acne, but we don’t know if the exact underlying inflammatory process is the same or if it’s different.”

In a 2023 systematic review of clinical studies, Dr. Mostaghimi and colleagues found that patients on any JAK inhibitor were nearly four times more likely to experience acne than patients who received placebo, but risk varied between medications. Patients taking JAK inhibitors for skin conditions had higher risk for acne than those given the medications for other indications. However, Dr. Mostaghimi thinks this finding is the result of selection bias.

Participants may not mention side effects like acne in trials for rheumatologic or gastrointestinal conditions, he said, unlike in trials for skin conditions. “Clinically, I’ve seen it in patients across every indication.”

Patients with a history of acne seem to be more likely to develop this side effect, though formal studies looking into risk factors are lacking. In Dr. Mostaghimi’s own clinical experience, JAKne is also more common in younger patients, but it can happen to anyone. “I’ve seen 70-year-olds develop acne — patients who’ve never had an issue their whole life — when they’re taking a JAK inhibitor.”

This issue also appears to be more common earlier in treatment, he added, and may improve over time as a patient continues with the medication.
 

How Do You Treat It?

“I think in other specialties, you will often feel awkward addressing skin conditions or pointing out acne,” Dr. Mostaghimi said. The most important steps are being aware of this potential side effect, and if you see it practice, to bring it up.

“Say: I’m noticing there’s some changes in your skin. Some patients on JAK inhibitors develop more acne. Have you noticed this? And if so, is this bothering you?”

Generally, JAKne is mild to moderate, explained Dr. Nassim, and if non-dermatologists are comfortable, they can prescribe a first-line topical regimen for patients. Dr. Mostaghimi recommends prescribing a clindamycin 1% lotion or gel. In addition, patients can use a benzoyl peroxide wash (4% or 10%) combined with a gentle retinoid, such as adapalene. (Both of these treatments are now available over the counter.)

courtesy Harvard Medical School

In patients with scalp or hairline involvement, he often prescribes a ketoconazole 2% shampoo, which patients can use to wash their scalp, face, chest, and back in the shower.

If they aren’t responding to these initial treatments, then refer to a dermatologist for further assessment.

“Ultimately, referring to a dermatologist is the best course of action,” Dr. Nassim said. “I have had patients on JAK inhibitors who improved with topical acne treatments, and some that required more aggressive treatment with oral medications.”

Dr. Mostaghimi reported consulting fees from AbbVie, Concert Pharmaceuticals, Pfizer, and 3Derm Systems; research funding from Incyte, Aclaris Therapeutics, Eli Lilly, and Concert Pharmaceuticals; personal fees from Equillium, ASLAN Pharmaceuticals, ACOM, and Boehringer Ingelheim; and advisory board fees from Fig.1 Beauty, Eli Lilly, Pfizer, and Hims & Hers Health. Dr. Nassim had no relevant disclosures.

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

Since the first Food and Drug Administration approval of a Janus kinase (JAK) inhibitor in 2011, the number of these medications available — and their treatment indications — have continued to grow. Prescribing physicians are familiar with the benefits and risks for these drugs, including higher risk for cardiac events and malignancy; however, one adverse effect may be overlooked, especially by specialties outside of dermatology: acne. Though less serious than some other side effects, JAK inhibitor–associated acne — JAKne, for short — can be a concern for patients.

“Your physical appearance and how you present yourself to the world is an important part of your self-confidence and living life on your own terms,” said Arash Mostaghimi, MD, the director of inpatient dermatology at Brigham and Women’s Hospital in Boston, Massachusetts. “I think letting people know about [JAKne] and then addressing it when it occurs should be a normal part of managing these medications.”
 

What Is JAKne?

JAKne generally looks like other kinds of acne, explained Janelle Nassim, MD, director of laser and cosmetic dermatology at the Indiana University School of Medicine, Indianapolis. “It can affect the same areas that typical acne affects, including the face, chest, back, neck, and upper shoulders.”

Though it appears like typical forms of acne, it is not clear what drives these skin eruptions in patients taking JAK inhibitors.

courtesy Brigham and Women&#039;s Hospital

“We don’t understand the underlying pathophysiology,” Dr. Mostaghimi said. “It looks like acne, but we don’t know if the exact underlying inflammatory process is the same or if it’s different.”

In a 2023 systematic review of clinical studies, Dr. Mostaghimi and colleagues found that patients on any JAK inhibitor were nearly four times more likely to experience acne than patients who received placebo, but risk varied between medications. Patients taking JAK inhibitors for skin conditions had higher risk for acne than those given the medications for other indications. However, Dr. Mostaghimi thinks this finding is the result of selection bias.

Participants may not mention side effects like acne in trials for rheumatologic or gastrointestinal conditions, he said, unlike in trials for skin conditions. “Clinically, I’ve seen it in patients across every indication.”

Patients with a history of acne seem to be more likely to develop this side effect, though formal studies looking into risk factors are lacking. In Dr. Mostaghimi’s own clinical experience, JAKne is also more common in younger patients, but it can happen to anyone. “I’ve seen 70-year-olds develop acne — patients who’ve never had an issue their whole life — when they’re taking a JAK inhibitor.”

This issue also appears to be more common earlier in treatment, he added, and may improve over time as a patient continues with the medication.
 

How Do You Treat It?

“I think in other specialties, you will often feel awkward addressing skin conditions or pointing out acne,” Dr. Mostaghimi said. The most important steps are being aware of this potential side effect, and if you see it practice, to bring it up.

“Say: I’m noticing there’s some changes in your skin. Some patients on JAK inhibitors develop more acne. Have you noticed this? And if so, is this bothering you?”

Generally, JAKne is mild to moderate, explained Dr. Nassim, and if non-dermatologists are comfortable, they can prescribe a first-line topical regimen for patients. Dr. Mostaghimi recommends prescribing a clindamycin 1% lotion or gel. In addition, patients can use a benzoyl peroxide wash (4% or 10%) combined with a gentle retinoid, such as adapalene. (Both of these treatments are now available over the counter.)

courtesy Harvard Medical School

In patients with scalp or hairline involvement, he often prescribes a ketoconazole 2% shampoo, which patients can use to wash their scalp, face, chest, and back in the shower.

If they aren’t responding to these initial treatments, then refer to a dermatologist for further assessment.

“Ultimately, referring to a dermatologist is the best course of action,” Dr. Nassim said. “I have had patients on JAK inhibitors who improved with topical acne treatments, and some that required more aggressive treatment with oral medications.”

Dr. Mostaghimi reported consulting fees from AbbVie, Concert Pharmaceuticals, Pfizer, and 3Derm Systems; research funding from Incyte, Aclaris Therapeutics, Eli Lilly, and Concert Pharmaceuticals; personal fees from Equillium, ASLAN Pharmaceuticals, ACOM, and Boehringer Ingelheim; and advisory board fees from Fig.1 Beauty, Eli Lilly, Pfizer, and Hims & Hers Health. Dr. Nassim had no relevant disclosures.

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