Key clinical point: Rheumatoid arthritis (RA) is associated with a significant increase in the risk for ischemic heart disease (IHD) and myocardial infarction (MI), and managing RA activity may reduce the risk for cardiovascular diseases.

Major finding: RA is significantly associated with an increased risk for IHD (odds ratio [OR] 1.0006; P  =  .001551915) and MI (OR 1.0458; P  =  .001636), but not arrhythmia and atrial fibrillation.

Study details: Findings are from a two-sample Mendelian randomization study including patients and matched control individuals for RA (n = 14,361 and n = 43,923, respectively), MI (n = 12,801 and n = 187,840, respectively), IHD (n = 5861 and n = 457,149, respectively), atrial fibrillation (n = 60,620 and n = 970,216, respectively), and arrhythmia (n = 2545 and n = 460,388, respectively).

Disclosures: This study was supported by the Young Talent Development Plan of Changzhou Health Commission, China, and other sources. The authors declared no conflicts of interest.

Source: Wang M et al. Relationship between rheumatoid arthritis and cardiovascular comorbidity, causation or co-occurrence: A Mendelian randomization study. Front Cardiovasc Med. 2023;10:1099861 (Mar 17). Doi: 10.3389/fcvm.2023.1099861

Key clinical point: Rheumatoid arthritis (RA) is associated with a significant increase in the risk for ischemic heart disease (IHD) and myocardial infarction (MI), and managing RA activity may reduce the risk for cardiovascular diseases.

Major finding: RA is significantly associated with an increased risk for IHD (odds ratio [OR] 1.0006; P  =  .001551915) and MI (OR 1.0458; P  =  .001636), but not arrhythmia and atrial fibrillation.

Study details: Findings are from a two-sample Mendelian randomization study including patients and matched control individuals for RA (n = 14,361 and n = 43,923, respectively), MI (n = 12,801 and n = 187,840, respectively), IHD (n = 5861 and n = 457,149, respectively), atrial fibrillation (n = 60,620 and n = 970,216, respectively), and arrhythmia (n = 2545 and n = 460,388, respectively).

Disclosures: This study was supported by the Young Talent Development Plan of Changzhou Health Commission, China, and other sources. The authors declared no conflicts of interest.

Source: Wang M et al. Relationship between rheumatoid arthritis and cardiovascular comorbidity, causation or co-occurrence: A Mendelian randomization study. Front Cardiovasc Med. 2023;10:1099861 (Mar 17). Doi: 10.3389/fcvm.2023.1099861

Key clinical point: Rheumatoid arthritis (RA) is associated with a significant increase in the risk for ischemic heart disease (IHD) and myocardial infarction (MI), and managing RA activity may reduce the risk for cardiovascular diseases.

Major finding: RA is significantly associated with an increased risk for IHD (odds ratio [OR] 1.0006; P  =  .001551915) and MI (OR 1.0458; P  =  .001636), but not arrhythmia and atrial fibrillation.

Study details: Findings are from a two-sample Mendelian randomization study including patients and matched control individuals for RA (n = 14,361 and n = 43,923, respectively), MI (n = 12,801 and n = 187,840, respectively), IHD (n = 5861 and n = 457,149, respectively), atrial fibrillation (n = 60,620 and n = 970,216, respectively), and arrhythmia (n = 2545 and n = 460,388, respectively).

Disclosures: This study was supported by the Young Talent Development Plan of Changzhou Health Commission, China, and other sources. The authors declared no conflicts of interest.

Source: Wang M et al. Relationship between rheumatoid arthritis and cardiovascular comorbidity, causation or co-occurrence: A Mendelian randomization study. Front Cardiovasc Med. 2023;10:1099861 (Mar 17). Doi: 10.3389/fcvm.2023.1099861

Key clinical point: Mortality risk varied with time and increased only during the second not the first decade after the diagnosis of rheumatoid arthritis (RA), with respiratory diseases potentially surpassing cardiovascular diseases as major attributable factors.

Major finding: Increase in mortality was observed at 20 years (standardized mortality ratio [SMR] 1.49; P < .001) but not during the first 10 years (P  =  .44) after RA diagnosis, with pneumonia (cause-specific SMR 5.22; 95% CI 2.26-10.29) and interstitial lung disease (cause-specific SMR 7.64; 95% CI 2.98-14.69) being major contributors.

Study details: Findings are from an analysis of 1895 patients with RA from the Australian Rheumatology Association Database (ARAD) registry who received biologic, targeted synthetic, or conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: ARAD received support through the Australian Rheumatology Association from various sources. Three authors declared receiving grants, funding, or honoraria from different sources unrelated to this study.

Source: Black RJ et al. Mortality estimates and excess mortality in rheumatoid arthritis. Rheumatology (Oxford). 2023 (Mar 15). Doi: 10.1093/rheumatology/kead106

Key clinical point: Mortality risk varied with time and increased only during the second not the first decade after the diagnosis of rheumatoid arthritis (RA), with respiratory diseases potentially surpassing cardiovascular diseases as major attributable factors.

Major finding: Increase in mortality was observed at 20 years (standardized mortality ratio [SMR] 1.49; P < .001) but not during the first 10 years (P  =  .44) after RA diagnosis, with pneumonia (cause-specific SMR 5.22; 95% CI 2.26-10.29) and interstitial lung disease (cause-specific SMR 7.64; 95% CI 2.98-14.69) being major contributors.

Study details: Findings are from an analysis of 1895 patients with RA from the Australian Rheumatology Association Database (ARAD) registry who received biologic, targeted synthetic, or conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: ARAD received support through the Australian Rheumatology Association from various sources. Three authors declared receiving grants, funding, or honoraria from different sources unrelated to this study.

Source: Black RJ et al. Mortality estimates and excess mortality in rheumatoid arthritis. Rheumatology (Oxford). 2023 (Mar 15). Doi: 10.1093/rheumatology/kead106

Key clinical point: Mortality risk varied with time and increased only during the second not the first decade after the diagnosis of rheumatoid arthritis (RA), with respiratory diseases potentially surpassing cardiovascular diseases as major attributable factors.

Major finding: Increase in mortality was observed at 20 years (standardized mortality ratio [SMR] 1.49; P < .001) but not during the first 10 years (P  =  .44) after RA diagnosis, with pneumonia (cause-specific SMR 5.22; 95% CI 2.26-10.29) and interstitial lung disease (cause-specific SMR 7.64; 95% CI 2.98-14.69) being major contributors.

Study details: Findings are from an analysis of 1895 patients with RA from the Australian Rheumatology Association Database (ARAD) registry who received biologic, targeted synthetic, or conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: ARAD received support through the Australian Rheumatology Association from various sources. Three authors declared receiving grants, funding, or honoraria from different sources unrelated to this study.

Source: Black RJ et al. Mortality estimates and excess mortality in rheumatoid arthritis. Rheumatology (Oxford). 2023 (Mar 15). Doi: 10.1093/rheumatology/kead106

Key clinical point: Rheumatoid arthritis (RA) was significantly associated with an increased risk for bronchial asthma, allergic rhinitis, and sinusitis, and a notable interrelation was observed between the presence of asthma and obesity in patients with RA.

Major finding: Presence of RA significantly increased the risk for asthma (odds ratio [OR] 2.32; 95% CI 1.51-3.57), allergic rhinitis (OR 1.51; 95% CI 1.08-2.10), and sinusitis (OR 1.64; 95% CI 1.08-2.50) in the whole cohort and the prevalence of obesity in patients with asthma (64.0% vs 40.2%; P  =  .034).

Study details: This population-based cross-sectional study included 14,272 participants, of which 334 had RA.

Disclosures: This study was supported by the National Research Foundation of Korea grant funded by the Korean Government. The authors declared no conflicts of interest.

Source: Kim JG et al. Association of rheumatoid arthritis with bronchial asthma and asthma-related comorbidities: A population-based national surveillance study. Front Med (Lausanne). 2023;10:1006290 (Mar 10). Doi: 10.3389/fmed.2023.1006290

Key clinical point: Rheumatoid arthritis (RA) was significantly associated with an increased risk for bronchial asthma, allergic rhinitis, and sinusitis, and a notable interrelation was observed between the presence of asthma and obesity in patients with RA.

Major finding: Presence of RA significantly increased the risk for asthma (odds ratio [OR] 2.32; 95% CI 1.51-3.57), allergic rhinitis (OR 1.51; 95% CI 1.08-2.10), and sinusitis (OR 1.64; 95% CI 1.08-2.50) in the whole cohort and the prevalence of obesity in patients with asthma (64.0% vs 40.2%; P  =  .034).

Study details: This population-based cross-sectional study included 14,272 participants, of which 334 had RA.

Disclosures: This study was supported by the National Research Foundation of Korea grant funded by the Korean Government. The authors declared no conflicts of interest.

Source: Kim JG et al. Association of rheumatoid arthritis with bronchial asthma and asthma-related comorbidities: A population-based national surveillance study. Front Med (Lausanne). 2023;10:1006290 (Mar 10). Doi: 10.3389/fmed.2023.1006290

Key clinical point: Rheumatoid arthritis (RA) was significantly associated with an increased risk for bronchial asthma, allergic rhinitis, and sinusitis, and a notable interrelation was observed between the presence of asthma and obesity in patients with RA.

Major finding: Presence of RA significantly increased the risk for asthma (odds ratio [OR] 2.32; 95% CI 1.51-3.57), allergic rhinitis (OR 1.51; 95% CI 1.08-2.10), and sinusitis (OR 1.64; 95% CI 1.08-2.50) in the whole cohort and the prevalence of obesity in patients with asthma (64.0% vs 40.2%; P  =  .034).

Study details: This population-based cross-sectional study included 14,272 participants, of which 334 had RA.

Disclosures: This study was supported by the National Research Foundation of Korea grant funded by the Korean Government. The authors declared no conflicts of interest.

Source: Kim JG et al. Association of rheumatoid arthritis with bronchial asthma and asthma-related comorbidities: A population-based national surveillance study. Front Med (Lausanne). 2023;10:1006290 (Mar 10). Doi: 10.3389/fmed.2023.1006290

Key clinical point: Abatacept with or without conventional synthetic disease-modifying antirheumatic drugs (csDMARD) demonstrated better efficacy and favorable safety outcomes compared with placebo, csDMARD, or other biologic DMARD (bDMARD) in patients with rheumatoid arthritis (RA).

Major finding: Patients treated with abatacept with or without csDMARD vs placebo, csDMARD, or other bDMARD were more likely to achieve American College of Rheumatology (ACR) 20 (relative risk [RR] 1.57; 95% CI 1.27-1.93), ACR50 (RR 1.84; 95% CI 1.38-2.44), and ACR70 (RR 2.36; 95% CI 1.60-3.47) responses, as well as were less likely to experience adverse events (RR 0.93; 95% CI 0.84-1.03).

Study details: Findings are from a systematic review and meta-analysis of 13 randomized controlled trials including 5978 patients with RA who were randomly assigned to receive abatacept alone, abatacept with csDMARD, placebo, csDMARD, or other bDMARD.

Disclosures: This study was supported by the National Key R&D Program of China. The authors did not report conflicts of interest.

Source: Ahamada MM and Wu X. Analysis of efficacy and safety of abatacept for rheumatoid arthritis: Systematic review and meta-analysis. Clin Exp Rheumatol. 2023 (Mar 7). Doi: 10.55563/clinexprheumatol/2xjg0d

Key clinical point: Abatacept with or without conventional synthetic disease-modifying antirheumatic drugs (csDMARD) demonstrated better efficacy and favorable safety outcomes compared with placebo, csDMARD, or other biologic DMARD (bDMARD) in patients with rheumatoid arthritis (RA).

Major finding: Patients treated with abatacept with or without csDMARD vs placebo, csDMARD, or other bDMARD were more likely to achieve American College of Rheumatology (ACR) 20 (relative risk [RR] 1.57; 95% CI 1.27-1.93), ACR50 (RR 1.84; 95% CI 1.38-2.44), and ACR70 (RR 2.36; 95% CI 1.60-3.47) responses, as well as were less likely to experience adverse events (RR 0.93; 95% CI 0.84-1.03).

Study details: Findings are from a systematic review and meta-analysis of 13 randomized controlled trials including 5978 patients with RA who were randomly assigned to receive abatacept alone, abatacept with csDMARD, placebo, csDMARD, or other bDMARD.

Disclosures: This study was supported by the National Key R&D Program of China. The authors did not report conflicts of interest.

Source: Ahamada MM and Wu X. Analysis of efficacy and safety of abatacept for rheumatoid arthritis: Systematic review and meta-analysis. Clin Exp Rheumatol. 2023 (Mar 7). Doi: 10.55563/clinexprheumatol/2xjg0d

Key clinical point: Abatacept with or without conventional synthetic disease-modifying antirheumatic drugs (csDMARD) demonstrated better efficacy and favorable safety outcomes compared with placebo, csDMARD, or other biologic DMARD (bDMARD) in patients with rheumatoid arthritis (RA).

Major finding: Patients treated with abatacept with or without csDMARD vs placebo, csDMARD, or other bDMARD were more likely to achieve American College of Rheumatology (ACR) 20 (relative risk [RR] 1.57; 95% CI 1.27-1.93), ACR50 (RR 1.84; 95% CI 1.38-2.44), and ACR70 (RR 2.36; 95% CI 1.60-3.47) responses, as well as were less likely to experience adverse events (RR 0.93; 95% CI 0.84-1.03).

Study details: Findings are from a systematic review and meta-analysis of 13 randomized controlled trials including 5978 patients with RA who were randomly assigned to receive abatacept alone, abatacept with csDMARD, placebo, csDMARD, or other bDMARD.

Disclosures: This study was supported by the National Key R&D Program of China. The authors did not report conflicts of interest.

Source: Ahamada MM and Wu X. Analysis of efficacy and safety of abatacept for rheumatoid arthritis: Systematic review and meta-analysis. Clin Exp Rheumatol. 2023 (Mar 7). Doi: 10.55563/clinexprheumatol/2xjg0d

Key clinical point: Factors like age ≥65 years or current or former smoking accounted for excess risk with tofacitinib vs tumor necrosis factor inhibitor (TNFi) use in patients with rheumatoid arthritis (RA).

Major finding: Tofacitinib vs TNFi significantly increased the risk for malignancies (hazard ratio [HR] 1.55; 95% CI 1.05-2.30), venous thromboembolism (HR 5.19; 95% CI 1.86-14.46), and all-cause death (HR 2.24; 95% CI 1.20-4.19) among patients who were ≥65 years old or ever smokers, but not among those aged <65 years and never smokers.

Study details: Findings are from a post hoc analysis of the ORAL Surveillance trial including patients with RA (n = 4362) treated with tofacitinib or TNFi and an exploratory analysis of RA, PsA, and ulcerative colitis (UC) development programs including tofacitinib-exposed patients with RA (n = 7964), psoriatic arthritis (n = 783), and UC (n = 1157).

Disclosures: This study was sponsored by Pfizer Inc. Six authors declared being employees and stockholders of Pfizer. Two authors declared receiving speaking, consulting, or lecture fees or research grants from Pfizer and other sources.

Source: Kristensen LE et al. Identification of two tofacitinib subpopulations with different relative risk versus TNF inhibitors: An analysis of the open label, randomised controlled study ORAL Surveillance. Ann Rheum Dis. 2023 (Mar 17). Doi: 10.1136/ard-2022-223715

Key clinical point: Factors like age ≥65 years or current or former smoking accounted for excess risk with tofacitinib vs tumor necrosis factor inhibitor (TNFi) use in patients with rheumatoid arthritis (RA).

Major finding: Tofacitinib vs TNFi significantly increased the risk for malignancies (hazard ratio [HR] 1.55; 95% CI 1.05-2.30), venous thromboembolism (HR 5.19; 95% CI 1.86-14.46), and all-cause death (HR 2.24; 95% CI 1.20-4.19) among patients who were ≥65 years old or ever smokers, but not among those aged <65 years and never smokers.

Study details: Findings are from a post hoc analysis of the ORAL Surveillance trial including patients with RA (n = 4362) treated with tofacitinib or TNFi and an exploratory analysis of RA, PsA, and ulcerative colitis (UC) development programs including tofacitinib-exposed patients with RA (n = 7964), psoriatic arthritis (n = 783), and UC (n = 1157).

Disclosures: This study was sponsored by Pfizer Inc. Six authors declared being employees and stockholders of Pfizer. Two authors declared receiving speaking, consulting, or lecture fees or research grants from Pfizer and other sources.

Source: Kristensen LE et al. Identification of two tofacitinib subpopulations with different relative risk versus TNF inhibitors: An analysis of the open label, randomised controlled study ORAL Surveillance. Ann Rheum Dis. 2023 (Mar 17). Doi: 10.1136/ard-2022-223715

Key clinical point: Factors like age ≥65 years or current or former smoking accounted for excess risk with tofacitinib vs tumor necrosis factor inhibitor (TNFi) use in patients with rheumatoid arthritis (RA).

Major finding: Tofacitinib vs TNFi significantly increased the risk for malignancies (hazard ratio [HR] 1.55; 95% CI 1.05-2.30), venous thromboembolism (HR 5.19; 95% CI 1.86-14.46), and all-cause death (HR 2.24; 95% CI 1.20-4.19) among patients who were ≥65 years old or ever smokers, but not among those aged <65 years and never smokers.

Study details: Findings are from a post hoc analysis of the ORAL Surveillance trial including patients with RA (n = 4362) treated with tofacitinib or TNFi and an exploratory analysis of RA, PsA, and ulcerative colitis (UC) development programs including tofacitinib-exposed patients with RA (n = 7964), psoriatic arthritis (n = 783), and UC (n = 1157).

Disclosures: This study was sponsored by Pfizer Inc. Six authors declared being employees and stockholders of Pfizer. Two authors declared receiving speaking, consulting, or lecture fees or research grants from Pfizer and other sources.

Source: Kristensen LE et al. Identification of two tofacitinib subpopulations with different relative risk versus TNF inhibitors: An analysis of the open label, randomised controlled study ORAL Surveillance. Ann Rheum Dis. 2023 (Mar 17). Doi: 10.1136/ard-2022-223715

Key clinical point: Risk for severe infections significantly increased in patients who were newly diagnosed with rheumatoid arthritis (RA) after initiating biologic disease-modifying antirheumatic drugs (bDMARD).

Major finding: Over a period of 8 years, severe infection rates significantly increased in patients who were newly diagnosed with RA after initiating bDMARD (adjusted difference between pre- and post-bDMARD rates [Δ] 1.85; P  =  .001), whereas no significant change was observed in control individuals from the general population (Δ 0.12; P  =  .29).

Study details: Findings are from a population-based retrospective cohort study including 60,226 patients with newly diagnosed RA and 588,499 age- and sex-matched control individuals without any inflammatory arthritis from the general population who initiated bDMARD.

Disclosures: This study was supported by the Canadian Institute of Health Research and other sources. The authors declared no conflicts of interest.

Source: Zhou VY et al. Risk of severe infections after the introduction of biologic DMARDs in people with newly diagnosed rheumatoid arthritis: A population-based interrupted time-series analysis. Rheumatology (Oxford). 2023 (Apr 4). Doi: 10.1093/rheumatology/kead158

Key clinical point: Risk for severe infections significantly increased in patients who were newly diagnosed with rheumatoid arthritis (RA) after initiating biologic disease-modifying antirheumatic drugs (bDMARD).

Major finding: Over a period of 8 years, severe infection rates significantly increased in patients who were newly diagnosed with RA after initiating bDMARD (adjusted difference between pre- and post-bDMARD rates [Δ] 1.85; P  =  .001), whereas no significant change was observed in control individuals from the general population (Δ 0.12; P  =  .29).

Study details: Findings are from a population-based retrospective cohort study including 60,226 patients with newly diagnosed RA and 588,499 age- and sex-matched control individuals without any inflammatory arthritis from the general population who initiated bDMARD.

Disclosures: This study was supported by the Canadian Institute of Health Research and other sources. The authors declared no conflicts of interest.

Source: Zhou VY et al. Risk of severe infections after the introduction of biologic DMARDs in people with newly diagnosed rheumatoid arthritis: A population-based interrupted time-series analysis. Rheumatology (Oxford). 2023 (Apr 4). Doi: 10.1093/rheumatology/kead158

Key clinical point: Risk for severe infections significantly increased in patients who were newly diagnosed with rheumatoid arthritis (RA) after initiating biologic disease-modifying antirheumatic drugs (bDMARD).

Major finding: Over a period of 8 years, severe infection rates significantly increased in patients who were newly diagnosed with RA after initiating bDMARD (adjusted difference between pre- and post-bDMARD rates [Δ] 1.85; P  =  .001), whereas no significant change was observed in control individuals from the general population (Δ 0.12; P  =  .29).

Study details: Findings are from a population-based retrospective cohort study including 60,226 patients with newly diagnosed RA and 588,499 age- and sex-matched control individuals without any inflammatory arthritis from the general population who initiated bDMARD.

Disclosures: This study was supported by the Canadian Institute of Health Research and other sources. The authors declared no conflicts of interest.

Source: Zhou VY et al. Risk of severe infections after the introduction of biologic DMARDs in people with newly diagnosed rheumatoid arthritis: A population-based interrupted time-series analysis. Rheumatology (Oxford). 2023 (Apr 4). Doi: 10.1093/rheumatology/kead158

Key clinical point: Patients with rheumatoid arthritis (RA) treated with tofacitinib had a 69% lower risk of developing interstitial lung disease (ILD) than those treated with adalimumab.

Major finding: Compared with adalimumab, tofacitinib resulted in the lowest incidence of ILD (incidence rate ratio 0.43; 95% CI 0.18-1.05), followed by abatacept, tocilizumab, and rituximab. Tofacitinib was associated with a significant 69% reduced risk of developing ILD compared with adalimumab (adjusted hazard ratio 0.31; P  =  .009).

Study details: Findings are from a retrospective cohort study including 28,559 patients with RA without preexisting ILD who were newly administered adalimumab, abatacept, rituximab, tocilizumab, or tofacitinib, of which 276 patients were diagnosed with incident ILD.

Disclosures: This study was supported by the US National Institutes of Health and other sources. The authors did not report conflicts of interest.

Source: Baker MC et al. Incidence of interstitial lung disease in patients with rheumatoid arthritis treated with biologic and targeted synthetic disease-modifying antirheumatic drugs. JAMA Netw Open. 2023;6(3):e233640 (Mar 20). Doi: 10.1001/jamanetworkopen.2023.3640

Key clinical point: Patients with rheumatoid arthritis (RA) treated with tofacitinib had a 69% lower risk of developing interstitial lung disease (ILD) than those treated with adalimumab.

Major finding: Compared with adalimumab, tofacitinib resulted in the lowest incidence of ILD (incidence rate ratio 0.43; 95% CI 0.18-1.05), followed by abatacept, tocilizumab, and rituximab. Tofacitinib was associated with a significant 69% reduced risk of developing ILD compared with adalimumab (adjusted hazard ratio 0.31; P  =  .009).

Study details: Findings are from a retrospective cohort study including 28,559 patients with RA without preexisting ILD who were newly administered adalimumab, abatacept, rituximab, tocilizumab, or tofacitinib, of which 276 patients were diagnosed with incident ILD.

Disclosures: This study was supported by the US National Institutes of Health and other sources. The authors did not report conflicts of interest.

Source: Baker MC et al. Incidence of interstitial lung disease in patients with rheumatoid arthritis treated with biologic and targeted synthetic disease-modifying antirheumatic drugs. JAMA Netw Open. 2023;6(3):e233640 (Mar 20). Doi: 10.1001/jamanetworkopen.2023.3640

Key clinical point: Patients with rheumatoid arthritis (RA) treated with tofacitinib had a 69% lower risk of developing interstitial lung disease (ILD) than those treated with adalimumab.

Major finding: Compared with adalimumab, tofacitinib resulted in the lowest incidence of ILD (incidence rate ratio 0.43; 95% CI 0.18-1.05), followed by abatacept, tocilizumab, and rituximab. Tofacitinib was associated with a significant 69% reduced risk of developing ILD compared with adalimumab (adjusted hazard ratio 0.31; P  =  .009).

Study details: Findings are from a retrospective cohort study including 28,559 patients with RA without preexisting ILD who were newly administered adalimumab, abatacept, rituximab, tocilizumab, or tofacitinib, of which 276 patients were diagnosed with incident ILD.

Disclosures: This study was supported by the US National Institutes of Health and other sources. The authors did not report conflicts of interest.

Source: Baker MC et al. Incidence of interstitial lung disease in patients with rheumatoid arthritis treated with biologic and targeted synthetic disease-modifying antirheumatic drugs. JAMA Netw Open. 2023;6(3):e233640 (Mar 20). Doi: 10.1001/jamanetworkopen.2023.3640

Key clinical point: Continuation of conventional synthetic disease-modifying antirheumatic drugs (csDMARD) was not superior to withdrawal in patients with rheumatoid arthritis (RA) in sustained remission with half-dose csDMARD, suggesting withdrawal of half-dose csDMARD is feasible in some patients.

Major finding: Although discontinuing vs continuing half-dose csDMARD led to a numerically higher risk for flares within 12 months (risk difference 21.5%; 95% CI −3.4% to 49.7%), more patients discontinuing vs continuing half-dose csDMARD showed no radiographic joint damage progression (risk difference 13.9%; 95% CI −10.6% to 38.3%) and regained Disease Activity Score-based remission (80.0% [95% CI 44.4%-97.5%] vs 66.7% [95% CI 9.5%-99.2%]) at the first visit after flare.

Study details: This open-label trial, a part of the ARCTIC REWIND project, included 56 patients with RA who were in sustained remission for ≥12 months with half-dose csDMARD and were randomly assigned to discontinue or continue half-dose csDMARD.

Disclosures: This study was funded by the Research Council of Norway and other sources. Several authors declared receiving research grants or personal fees from various sources.

Source: Lillegraven S et al. Discontinuation of conventional synthetic disease-modifying antirheumatic drugs in patients with rheumatoid arthritis and excellent disease control. JAMA. 2023;329(12):1024-1026 (Mar 28). Doi: 10.1001/jama.2023.0492

Key clinical point: Continuation of conventional synthetic disease-modifying antirheumatic drugs (csDMARD) was not superior to withdrawal in patients with rheumatoid arthritis (RA) in sustained remission with half-dose csDMARD, suggesting withdrawal of half-dose csDMARD is feasible in some patients.

Major finding: Although discontinuing vs continuing half-dose csDMARD led to a numerically higher risk for flares within 12 months (risk difference 21.5%; 95% CI −3.4% to 49.7%), more patients discontinuing vs continuing half-dose csDMARD showed no radiographic joint damage progression (risk difference 13.9%; 95% CI −10.6% to 38.3%) and regained Disease Activity Score-based remission (80.0% [95% CI 44.4%-97.5%] vs 66.7% [95% CI 9.5%-99.2%]) at the first visit after flare.

Study details: This open-label trial, a part of the ARCTIC REWIND project, included 56 patients with RA who were in sustained remission for ≥12 months with half-dose csDMARD and were randomly assigned to discontinue or continue half-dose csDMARD.

Disclosures: This study was funded by the Research Council of Norway and other sources. Several authors declared receiving research grants or personal fees from various sources.

Source: Lillegraven S et al. Discontinuation of conventional synthetic disease-modifying antirheumatic drugs in patients with rheumatoid arthritis and excellent disease control. JAMA. 2023;329(12):1024-1026 (Mar 28). Doi: 10.1001/jama.2023.0492

Key clinical point: Continuation of conventional synthetic disease-modifying antirheumatic drugs (csDMARD) was not superior to withdrawal in patients with rheumatoid arthritis (RA) in sustained remission with half-dose csDMARD, suggesting withdrawal of half-dose csDMARD is feasible in some patients.

Major finding: Although discontinuing vs continuing half-dose csDMARD led to a numerically higher risk for flares within 12 months (risk difference 21.5%; 95% CI −3.4% to 49.7%), more patients discontinuing vs continuing half-dose csDMARD showed no radiographic joint damage progression (risk difference 13.9%; 95% CI −10.6% to 38.3%) and regained Disease Activity Score-based remission (80.0% [95% CI 44.4%-97.5%] vs 66.7% [95% CI 9.5%-99.2%]) at the first visit after flare.

Study details: This open-label trial, a part of the ARCTIC REWIND project, included 56 patients with RA who were in sustained remission for ≥12 months with half-dose csDMARD and were randomly assigned to discontinue or continue half-dose csDMARD.

Disclosures: This study was funded by the Research Council of Norway and other sources. Several authors declared receiving research grants or personal fees from various sources.

Source: Lillegraven S et al. Discontinuation of conventional synthetic disease-modifying antirheumatic drugs in patients with rheumatoid arthritis and excellent disease control. JAMA. 2023;329(12):1024-1026 (Mar 28). Doi: 10.1001/jama.2023.0492

Key clinical point: Preexisting rheumatoid arthritis (RA) did not increase the risk for mortality or severe immune-related adverse events (AE) in patients initiating immune checkpoint inhibitors for cancer treatment and thus, should not be considered as a contraindication for initiating immune checkpoint inhibitors.

Major finding: Among patients initiating immune checkpoint inhibitors for cancer treatment, those with and without preexisting RA had comparable risks for mortality (adjusted hazard ratio [aHR] 1.16; P  =  .30) and severe grade ≥3 immune-related AE (aHR 1.06; P  =  .83).

Study details: Findings are from a retrospective, comparative, cohort study including 11,901 patients who initiated immune checkpoint inhibitors for cancer treatment, of which 87 patients with preexisting RA were matched to 203 patients without preexisting autoimmune diseases (comparator group).

Disclosures: This study did not receive any specific funding. Several authors declared being employed and owning stock options or receiving partial salary support, honoraria, consulting fees, research grants, or royalties from different sources.

Source: McCarter KR et al. Mortality and immune-related adverse events after immune checkpoint inhibitor initiation for cancer among patients with pre-existing rheumatoid arthritis: A retrospective, comparative, cohort study. Lancet Rheumatol. 2023 (Mar 27). Doi: 10.1016/S2665-9913(23)00064-4

Key clinical point: Preexisting rheumatoid arthritis (RA) did not increase the risk for mortality or severe immune-related adverse events (AE) in patients initiating immune checkpoint inhibitors for cancer treatment and thus, should not be considered as a contraindication for initiating immune checkpoint inhibitors.

Major finding: Among patients initiating immune checkpoint inhibitors for cancer treatment, those with and without preexisting RA had comparable risks for mortality (adjusted hazard ratio [aHR] 1.16; P  =  .30) and severe grade ≥3 immune-related AE (aHR 1.06; P  =  .83).

Study details: Findings are from a retrospective, comparative, cohort study including 11,901 patients who initiated immune checkpoint inhibitors for cancer treatment, of which 87 patients with preexisting RA were matched to 203 patients without preexisting autoimmune diseases (comparator group).

Disclosures: This study did not receive any specific funding. Several authors declared being employed and owning stock options or receiving partial salary support, honoraria, consulting fees, research grants, or royalties from different sources.

Source: McCarter KR et al. Mortality and immune-related adverse events after immune checkpoint inhibitor initiation for cancer among patients with pre-existing rheumatoid arthritis: A retrospective, comparative, cohort study. Lancet Rheumatol. 2023 (Mar 27). Doi: 10.1016/S2665-9913(23)00064-4

Key clinical point: Preexisting rheumatoid arthritis (RA) did not increase the risk for mortality or severe immune-related adverse events (AE) in patients initiating immune checkpoint inhibitors for cancer treatment and thus, should not be considered as a contraindication for initiating immune checkpoint inhibitors.

Major finding: Among patients initiating immune checkpoint inhibitors for cancer treatment, those with and without preexisting RA had comparable risks for mortality (adjusted hazard ratio [aHR] 1.16; P  =  .30) and severe grade ≥3 immune-related AE (aHR 1.06; P  =  .83).

Study details: Findings are from a retrospective, comparative, cohort study including 11,901 patients who initiated immune checkpoint inhibitors for cancer treatment, of which 87 patients with preexisting RA were matched to 203 patients without preexisting autoimmune diseases (comparator group).

Disclosures: This study did not receive any specific funding. Several authors declared being employed and owning stock options or receiving partial salary support, honoraria, consulting fees, research grants, or royalties from different sources.

Source: McCarter KR et al. Mortality and immune-related adverse events after immune checkpoint inhibitor initiation for cancer among patients with pre-existing rheumatoid arthritis: A retrospective, comparative, cohort study. Lancet Rheumatol. 2023 (Mar 27). Doi: 10.1016/S2665-9913(23)00064-4

BOSTON – Noninvasive tests performed in midlife may help identify people who are at risk of late-onset epilepsy, a new study suggests. New data from the Framingham Heart Study show those who scored better on a neurocognitive test that measures executive function were 75% less likely to develop late-onset epilepsy.

An analysis of MRI revealed that those with higher cortical volumes also had a lower risk of epilepsy later in life, while those with higher white matter hyperintensities had an increased risk.

The study could help identify at-risk individuals years before symptoms of epilepsy appear.

“We present possible markers that could potentially identify patients at risk for developing late-onset epilepsy, even in the preclinical phase and before the clinical manifestation of conditions like stroke and dementia that are known now to be linked with the condition,” said lead investigator Maria Stefanidou, MD, assistant professor of neurology at Boston University.

The findings were presented at the 2023 annual meeting of the American Academy of Neurology.
 

Protection against late-onset epilepsy?

Hypertension and stroke are known risk factors for late-onset epilepsy. Dementia is also a known risk factor. But in about 30% of cases, the cause of epilepsy in older individuals is unknown.

For this study, investigators analyzed data from the offspring cohort of the Framingham Heart Study. Participants were at least 45 years old; underwent neuropsychological evaluation and brain MRI; and had no prior history of stroke, dementia, or epilepsy. Cognitive measures included Visual Reproductions Delayed Recall, Logical Memory Delayed Recall, Similarities, Trail Making B-A (TrB-TrA), and the Hooper Visual Organization Test.

Participants also underwent an MRI to measure total cerebral brain volume, cortical gray matter volume, white matter hyperintensities, and hippocampal volume.

After a mean follow-up of 13.5 years, late-onset epilepsy was diagnosed in 31 of participants who underwent neuropsychological testing (n = 2,349) and in 27 of those who underwent MRI (n = 2,056).

Better performance on the TrB-TrA test (a measure of executive function, processing speed, and occult vascular injury) was associated with a reduced risk of late-onset epilepsy (adjusted hazard ratio, 0.25; P = .011).

The findings held even after adjusting for age, sex, educational level, and known risk factors for late-onset epilepsy, such as hypertension (aHR, 0.30; P = .0401).

Higher white matter hyperintensities, a measure of occult vascular injury, was associated with increased epilepsy risk (aHR, 1.5; P = .042) when adjusted only for age, sex, and education, but was no longer significant after adjusting for hypertension and other risk factors (aHR, 1.47; P = .065).

The analysis also revealed that participants with a higher cortical gray matter volume had a lower risk for late-onset epilepsy (aHR, 0.73; P = .001).

“There is increasing literature supporting that late-onset epilepsy may be secondary to accumulative occult cerebrovascular and neurodegenerative processes that occur during aging,” Dr. Stefanidou said. “Our findings likely reflect that a lesser degree of occult vascular brain injury in midlife may be protective against late-onset epilepsy.”

However, the epidemiological study points to association, not causation, Dr. Stefanidou cautions.

“Further studies will be needed to study our observations in the clinical setting,” she said.
 

‘Intriguing’ findings

Commenting on the findings, Joseph Sirven, MD, a neurologist at the Mayo Clinic in Jacksonville, Fla., said the findings are “intriguing,” but also raise some questions. “Late-onset epilepsy remains an issue for many and it’s common,” said Dr. Sirven, who has patients with late-onset epilepsy.

Dr. Sirven was particularly interested in the findings on white matter hyperintensities. “Hippocampal volumes have been used but not so much cortical volumes,” he said. “I would like to know more about how white matter changes suggest pathology that would explain epilepsy.”

Study funding was not disclosed. Dr. Stefanidou and Dr. Sirven report no relevant financial relationships.

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

BOSTON – Noninvasive tests performed in midlife may help identify people who are at risk of late-onset epilepsy, a new study suggests. New data from the Framingham Heart Study show those who scored better on a neurocognitive test that measures executive function were 75% less likely to develop late-onset epilepsy.

An analysis of MRI revealed that those with higher cortical volumes also had a lower risk of epilepsy later in life, while those with higher white matter hyperintensities had an increased risk.

The study could help identify at-risk individuals years before symptoms of epilepsy appear.

“We present possible markers that could potentially identify patients at risk for developing late-onset epilepsy, even in the preclinical phase and before the clinical manifestation of conditions like stroke and dementia that are known now to be linked with the condition,” said lead investigator Maria Stefanidou, MD, assistant professor of neurology at Boston University.

The findings were presented at the 2023 annual meeting of the American Academy of Neurology.
 

Protection against late-onset epilepsy?

Hypertension and stroke are known risk factors for late-onset epilepsy. Dementia is also a known risk factor. But in about 30% of cases, the cause of epilepsy in older individuals is unknown.

For this study, investigators analyzed data from the offspring cohort of the Framingham Heart Study. Participants were at least 45 years old; underwent neuropsychological evaluation and brain MRI; and had no prior history of stroke, dementia, or epilepsy. Cognitive measures included Visual Reproductions Delayed Recall, Logical Memory Delayed Recall, Similarities, Trail Making B-A (TrB-TrA), and the Hooper Visual Organization Test.

Participants also underwent an MRI to measure total cerebral brain volume, cortical gray matter volume, white matter hyperintensities, and hippocampal volume.

After a mean follow-up of 13.5 years, late-onset epilepsy was diagnosed in 31 of participants who underwent neuropsychological testing (n = 2,349) and in 27 of those who underwent MRI (n = 2,056).

Better performance on the TrB-TrA test (a measure of executive function, processing speed, and occult vascular injury) was associated with a reduced risk of late-onset epilepsy (adjusted hazard ratio, 0.25; P = .011).

The findings held even after adjusting for age, sex, educational level, and known risk factors for late-onset epilepsy, such as hypertension (aHR, 0.30; P = .0401).

Higher white matter hyperintensities, a measure of occult vascular injury, was associated with increased epilepsy risk (aHR, 1.5; P = .042) when adjusted only for age, sex, and education, but was no longer significant after adjusting for hypertension and other risk factors (aHR, 1.47; P = .065).

The analysis also revealed that participants with a higher cortical gray matter volume had a lower risk for late-onset epilepsy (aHR, 0.73; P = .001).

“There is increasing literature supporting that late-onset epilepsy may be secondary to accumulative occult cerebrovascular and neurodegenerative processes that occur during aging,” Dr. Stefanidou said. “Our findings likely reflect that a lesser degree of occult vascular brain injury in midlife may be protective against late-onset epilepsy.”

However, the epidemiological study points to association, not causation, Dr. Stefanidou cautions.

“Further studies will be needed to study our observations in the clinical setting,” she said.
 

‘Intriguing’ findings

Commenting on the findings, Joseph Sirven, MD, a neurologist at the Mayo Clinic in Jacksonville, Fla., said the findings are “intriguing,” but also raise some questions. “Late-onset epilepsy remains an issue for many and it’s common,” said Dr. Sirven, who has patients with late-onset epilepsy.

Dr. Sirven was particularly interested in the findings on white matter hyperintensities. “Hippocampal volumes have been used but not so much cortical volumes,” he said. “I would like to know more about how white matter changes suggest pathology that would explain epilepsy.”

Study funding was not disclosed. Dr. Stefanidou and Dr. Sirven report no relevant financial relationships.

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

BOSTON – Noninvasive tests performed in midlife may help identify people who are at risk of late-onset epilepsy, a new study suggests. New data from the Framingham Heart Study show those who scored better on a neurocognitive test that measures executive function were 75% less likely to develop late-onset epilepsy.

An analysis of MRI revealed that those with higher cortical volumes also had a lower risk of epilepsy later in life, while those with higher white matter hyperintensities had an increased risk.

The study could help identify at-risk individuals years before symptoms of epilepsy appear.

“We present possible markers that could potentially identify patients at risk for developing late-onset epilepsy, even in the preclinical phase and before the clinical manifestation of conditions like stroke and dementia that are known now to be linked with the condition,” said lead investigator Maria Stefanidou, MD, assistant professor of neurology at Boston University.

The findings were presented at the 2023 annual meeting of the American Academy of Neurology.
 

Protection against late-onset epilepsy?

Hypertension and stroke are known risk factors for late-onset epilepsy. Dementia is also a known risk factor. But in about 30% of cases, the cause of epilepsy in older individuals is unknown.

For this study, investigators analyzed data from the offspring cohort of the Framingham Heart Study. Participants were at least 45 years old; underwent neuropsychological evaluation and brain MRI; and had no prior history of stroke, dementia, or epilepsy. Cognitive measures included Visual Reproductions Delayed Recall, Logical Memory Delayed Recall, Similarities, Trail Making B-A (TrB-TrA), and the Hooper Visual Organization Test.

Participants also underwent an MRI to measure total cerebral brain volume, cortical gray matter volume, white matter hyperintensities, and hippocampal volume.

After a mean follow-up of 13.5 years, late-onset epilepsy was diagnosed in 31 of participants who underwent neuropsychological testing (n = 2,349) and in 27 of those who underwent MRI (n = 2,056).

Better performance on the TrB-TrA test (a measure of executive function, processing speed, and occult vascular injury) was associated with a reduced risk of late-onset epilepsy (adjusted hazard ratio, 0.25; P = .011).

The findings held even after adjusting for age, sex, educational level, and known risk factors for late-onset epilepsy, such as hypertension (aHR, 0.30; P = .0401).

Higher white matter hyperintensities, a measure of occult vascular injury, was associated with increased epilepsy risk (aHR, 1.5; P = .042) when adjusted only for age, sex, and education, but was no longer significant after adjusting for hypertension and other risk factors (aHR, 1.47; P = .065).

The analysis also revealed that participants with a higher cortical gray matter volume had a lower risk for late-onset epilepsy (aHR, 0.73; P = .001).

“There is increasing literature supporting that late-onset epilepsy may be secondary to accumulative occult cerebrovascular and neurodegenerative processes that occur during aging,” Dr. Stefanidou said. “Our findings likely reflect that a lesser degree of occult vascular brain injury in midlife may be protective against late-onset epilepsy.”

However, the epidemiological study points to association, not causation, Dr. Stefanidou cautions.

“Further studies will be needed to study our observations in the clinical setting,” she said.
 

‘Intriguing’ findings

Commenting on the findings, Joseph Sirven, MD, a neurologist at the Mayo Clinic in Jacksonville, Fla., said the findings are “intriguing,” but also raise some questions. “Late-onset epilepsy remains an issue for many and it’s common,” said Dr. Sirven, who has patients with late-onset epilepsy.

Dr. Sirven was particularly interested in the findings on white matter hyperintensities. “Hippocampal volumes have been used but not so much cortical volumes,” he said. “I would like to know more about how white matter changes suggest pathology that would explain epilepsy.”

Study funding was not disclosed. Dr. Stefanidou and Dr. Sirven report no relevant financial relationships.

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