The National Databank for Rheumatic Diseases

Smoking presents significant challenges for individuals with rheumatoid arthritis (RA) yet understanding of their smoking habits and perceptions remains limited. This study explores preferences regarding tobacco cessation strategies, barriers to success in cessation, and perceived needs in this population. We conducted qualitative semi-structured interviews with 16 people with RA (9 past and 7 current tobacco users). Data were analyzed to identify common themes and patterns related to smoking behaviors and perceptions. Most participants did not alter their smoking habits after developing RA, and common triggers for smoking included alcohol consumption, coffee, stress, and RA symptoms. Few used non-combustible tobacco products, but many attempted nicotine replacement methods. Participants generally perceived smoking as having no role in RA development, although they recognized its negative health impacts, including respiratory and cardiovascular issues. Despite advice from healthcare providers, many participants were not ready to quit smoking, citing addiction, past failures, and challenges in replacing smoking with other activities as major barriers. Motivations and facilitators for quitting included family needs and support, health concerns, and financial savings. Successful quitters identified the need for strong personal commitment, use of medical aids, behavioral changes, and social support. Effective cessation programs should include education about health impacts and medication use, interactive discussions, support groups, and flexible formats, participants said. Smoking behaviors in individuals with RA are influenced by multiple factors, including stress, RA symptoms, and addiction. Effective cessation programs should address these specific challenges by incorporating personalized education, behavioral support, and flexible formats. Understanding these dynamics can improve targeted interventions to support RA patients in quitting smoking and managing their health more effectively.

Background: Deucravacitinib is the first oral tyrosine kinase 2 inhibitor approved by the US Food and Drug Administration (FDA) for moderate-to-severe plaque psoriasis (PsO). Phase 2 and Phase 3 clinical trials have shown clinical efficacy across various endpoints. Long-term clinical trial data of deucravacitinib in moderate-to-severe plaque PsO also show that treatment efficacy is durable. However, real-world evidence regarding the patient-reported outcomes (PROs) of patients treated with deucravacitinib for PsO is limited. Objective: The goal of this PRO study is to understand the impact of deucravacitinib on improvement of PsO signs and symptoms. Methods: Patients were recruited from U.S dermatology offices as a part of a national practice group, through a patient support program for deucravacitinib, and online from the FORWARD registry website. Patients were enrolled between August 2023 and November 2024. Inclusion criteria were adult patients initiating deucravacitinib ≤14 days of survey enrollment. We descriptively report demographics, disease characteristics, current treatments, and comorbidities for participants at enrollment as well as mean change in key PROs and patient-reported psoriasis severity at 6 months among the subset of patients who were persistent on deucravacitinib at 6 months. Psoriasis Symptoms and Signs Diary (PSSD) score was the primary outcome (range 0-100), and a meaningful change was set to be at least 15 point improvement. [Papp JAMA Dermatol 2023] Results: Among 306 patients with PsO initiating deucravacitinib, 81 (20.9%) had completed a 6-month follow up. Among these, 51 (63.0%) were persistent on therapy. Baseline demographics for these 51 persistent patients did not differ substantially from the overall cohort of initiators. The mean baseline PSSD was 32.2 (SD: 24) and change from baseline to 6 months was -19.0, which is above the set point for meaningful change. For overall global assessment of psoriasis severity (range 0-100), baseline was 42.7 (SD: 28.7), and average change from baseline was -25.3 (SD: 27.4). Dermatology Life Quality Index (DLQI) was 8.5 (SD: 4.7) at baseline and changed -4.3 (5.4). The global assessment of itch (numeric rating score) was 4.3 (SD 3.0) at baseline and changed -2.7 (3.2). For patient global assessment of nail disease (range 0-100), baseline was 25.6 (SD: 31.9), and changed -10.2 (SD: 25.8). Body surface area of psoriasis improved as well. At baseline 5.9% had a BSA<1% whereas at 6 months, 45.1% achieved BSA <1%. Treatment satisfaction also improved with 69% indicating they were satisfied or highly satisfied at follow up on deucravacitinib, compared with 33% at baseline. Conclusions: Deucravacitinib was associated with improvements in psoriasis severity and patient-reported outcomes in a real-world setting.

Background:Inflammatory Arthritides (IA) cause complex flares, partly explained by factors like diet, lifestyle, and medications, prompting speculation about the influence of seasonality. Studies suggest that winter and spring trigger most exacerbations, but findings are contentious due to symptom overlap with Seasonal Affective Disorder (SAD). It remains unclear whether seasons directly impact disease activity or through SAD-related symptoms.Objectives:To assess the seasonal variation in PROs in patients with IA.Methods:Study data came from adults in the Forward Databank registry diagnosed with IA (RA, SLE, PsA, AS). They provided biannual questionnaires with completed Patient Activity Score-II (PAS-II) scores from 1998 to 2023. PAS-II, averaging pain VAS, patient global VAS, and HAQ-II, was the primary outcome with season as the exposure. When HAQ-II was missing, HAQ-DI substituted for PAS-II imputation. Descriptive statistics characterized patients at baseline and by season, averaging patient-reported outcomes (PROs). Gaussian GEE models, with robust standard errors, assessed PAS-II and season association. Five models adjusted for demographics, clinical variables, other PROs (fatigue, sleep), comorbidities, and treatment. The best models were selected using the QIC criteria.Results:47,052 total participants with IA contributed 406,215 observations with mean age of 58, males 19%, and RA 84% (Table 1). Mean values of PROs over the follow-up are presented in Table 1. Higher PROs, indicating worse disease, were more frequently observed in the spring and fall. Figure 1 illustrates the five models that assess the impact of seasonal variation on PAS-II scores. The QIC scores decrease as more variables are introduced, indicating the increasing strength of the correlation structure. No difference in PAS-II is seen between winter and summer. Spring and fall have the highest coefficients in Model 1, with a PAS-II 0.13 (95% CI 0.11 – 0.14) and 0.10 (95% CI 0.09 – 0.12) higher PAS-II than in the summer. This association continues till Model 4, but in Model 5, winter, spring, and fall had the same coefficient impact on PAS-II estimates, with about a 0.04 increase in PAS2 when compared to the summer. The important factors in predicting the seasonal variation of PAS-II scores are fatigue (Z-score 149), followed by sleep (Z-score of 74.86), education (Z-score of -34.91), MCS (Z-score -32.04), RD comorbidity index (Z score 27.02), IA duration (Z-score 21.53), employment (Z-score -22.45), and prednisone use (Z score 22.7).Table 1.Descriptive statistics of the sample at baseline and by season throughout the follow-upAt baseline(N=47,052)During follow-up(mean (SD overall))Winter, mean, SDSpring, mean, SDSummer, mean, SDFall, mean, SDRA (%)83.7RA (N=39,390)145226781109847103SLE (%)5.4SLE (N=2,475;)647488845495Other inflammatory arthritis- (%)11.0PsA, AS, Fib (N=5,187)203210361255864Age (years), SD57.70, 13.59Pain (0-10), mean, SD3.84, 2.784.32, 2.913.82, 2.784.28, 2.91Male (%)18.51Fatigue (0-10), mean, SD4.31, 3.024.97, 3.164.45, 3.024.90, 3.15Education (years), SD13.62, 2.43Sleep (0-10)3.75, 3.064.12, 3.143.81, 3.064.12, 3.16Disease duration (years), SD12.63, 11.08Global Severity (0-10)3.64, 2.484.02, 2.563.69, 2.513.98, 2.59Total income (103US dollars), SD48,78,32,05PAS-II (0-10), mean, SD3.60, 2.203.98, 2.303.61, 2.203.94, 2.31BMI, SD28.60, 7.14Mental Component Summary (MCS)49.36,11.3847.16, 11.7949.25, 11.3747.82, 11.72Married (%)66.97PHQ8 depression (%)4.89, 4.755.29, 4.904.92, 4.765.37, 4.95Current smoker14.58GAD2 Score - Anxiety (%).85, 1.401.00, 1.53.86, 1.391.05, 1.57Employed (%)32.00Vitality (SF-36)44.15, 11.3042.60, 11.2143.83,11.2743.01, 11.24DMARD use (%)62.13DMARD use (%)63.7458.2664.0860.69Biologic use (%)31.11Biologic use (%)37.9442.9938.4342.28TNF use (%)26.91TNF use (%)32.1835.9332.4235.27NTNF use (%)4.81NTNF use (%)6.257.606.527.60Conclusion:We identified a seasonal correlation with PROs, impacted by factors like fatigue and sleep. Future work will explore SAD and inflammation components, using varied outcomes and consider regional weather.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of Interests:None declared.

ObjectivesThis study aims to evaluate non-melanoma skin cancer (NMSC) risk associated with abatacept treatment for rheumatoid arthritis (RA).MethodsThis evaluation included 16 abatacept RA clinical trials and 6 observational studies. NMSC incidence rates (IRs)/1000 patient-years (p-y) of exposure were compared between patients treated with abatacept versus placebo, conventional synthetic (cs) disease-modifying antirheumatic drugs (DMARDs) and other biological/targeted synthetic (b/ts)DMARDs. For observational studies, a random-effects model was used to pool rate ratios (RRs).Results~49 000 patients receiving abatacept were analysed from clinical trials (~7000) and observational studies (~42 000). In randomised trials (n=4138; median abatacept exposure, 12 (range 2–30) months), NMSC IRs (95% CIs) were not significantly different for abatacept (6.0 (3.3 to 10.0)) and placebo (4.0 (1.3 to 9.3)) and remained stable throughout the long-term, open-label period (median cumulative exposure, 28 (range 2–130 months); 21 335 p-y of exposure (7044 patients over 3 years)). For registry databases, NMSC IRs/1000 p-y were 5–12 (abatacept), 1.6–10 (csDMARDs) and 3–8 (other b/tsDMARDs). Claims database IRs were 19–22 (abatacept), 15–18 (csDMARDs) and 14–17 (other b/tsDMARDs). Pooled RRs (95% CIs) from observational studies for NMSC in patients receiving abatacept were 1.84 (1.00 to 3.37) vs csDMARDs and 1.11 (0.98 to 1.26) vs other b/tsDMARDs.ConclusionsConsistent with the warnings and precautions of the abatacept label, this analysis suggests a potential increase in NMSC risk with abatacept use compared with csDMARDs. No significant increase was observed compared with b/tsDMARDs, but the lower limit of the 95% CI was close to unity.

ObjectiveAssess major adverse cardiovascular event (MACE) risk with opioids compared with non-steroidal anti-inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis (RA)MethodsWe conducted a new-user active comparator cohort study among patients with RA within FORWARD, The National Databank for Rheumatic Diseases, with ≥1 year participation between 1998 and 2021. Each opioid initiator was matched to two NSAID initiators by propensity scores (PSs). Patients were followed until the occurrence of the composite endpoint of MACE (myocardial infarction, stroke, heart failure, cardiovascular disease (CVD) death, venous thromboembolism (VTE)) and all-cause mortality. The risk of outcomes was estimated using Cox proportional hazards with adjustment for PS weights and imbalanced covariables.ResultsAmong 6866 opioid initiators and 13 689 NSAID initiators, 212 vs 253 MACE (20.6/1000 person-years (PY) vs 18.9/1000 PY) and 144 vs 150 deaths (13.5/1000 PY vs 10.8/1000 PY) occurred, respectively. The risk of MACE with opioids was similar to NSAIDs (HR=1.02, 95% CI 0.85 to 1.22), whereas all-cause mortality with opioids was 33% higher than NSAIDs (HR=1.33, 95% CI 1.06 to 1.67) in PS-weighted models. Among the individual outcomes of MACE, VTE risk tended to be higher in opioid initiators than NSAID initiators (HR=1.41, 95% CI 0.84 to 2.35). Strong opioids had a higher risk for all-cause mortality and VTE than weak opioids compared with NSAIDs suggesting a dose-dependent association.ConclusionOpioids had similar MACE risk compared with NSAIDs in patients with RA with increased all-cause mortality and likely VTE, which suggests that opioids are not safer than NSAIDs, as clinicians have perceived.

ObjectiveTo evaluate the risk of malignancy (overall, breast, lung, and lymphoma) in patients with rheumatoid arthritis treated with abatacept, conventional synthetic (cs) disease-modifying antirheumatic drugs (DMARDs), and other biologic/targeted synthetic (b/ts)DMARDs in clinical practice. MethodsFour international observational data sources were included: ARTIS (Sweden), RABBIT (Germany), FORWARD (USA), and BC (Canada). Crude incidence rates (IRs) per 1000 patient-years of exposure with 95% confidence intervals (CIs) for a malignancy event were calculated; rate ratios (RRs) were estimated and adjusted for demographics, comorbidities, and other potential confounders. RRs were then pooled in a random-effects model. ResultsAcross data sources, mean follow-up for patients treated with abatacept (n = 5182), csDMARDs (n = 73,755), and other b/tsDMARDs (n = 37,195) was 3.0–3.7, 2.9–6.2, and 3.1–4.7 years, respectively. IRs per 1000 patient-years for overall malignancy ranged from 7.6–11.4 (abatacept), 8.6–13.2 (csDMARDs), and 5.0–11.8 (other b/tsDMARDs). IRs ranged from: 0–4.4, 0–3.3, and 0–2.5 (breast cancer); 0.1–2.8, 0–3.7, and 0.2–2.9 (lung cancer); and 0–1.1, 0–0.9, and 0–0.6 (lymphoma), respectively, for the three treatment groups. The numbers of individual cancers (breast, lung, and lymphoma) in some registries were low; RRs were not available. There were a few cases of lymphoma in some of the registries; ARTIS observed an RR of 2.8 (95% CI 1.1–6.8) with abatacept versus csDMARDs. The pooled RRs (95% CIs) for overall malignancy with abatacept were 1.1 (0.8–1.5) versus csDMARDs and 1.0 (0.8–1.3) versus b/tsDMARDs. ConclusionsThis international, post-marketing observational safety study did not find any statistically significant increase in the risk of overall malignancies in pooled data in patients treated with abatacept compared with csDMARDs or with other b/tsDMARDs. Assessment of larger populations is needed to further evaluate the risks for individual cancers, especially lymphoma.

IntroductionThe efficacy of abatacept is enhanced in anti-citrullinated protein antibody (ACPA) and rheumatoid factor (RF)-positive versus -negative patients with rheumatoid arthritis (RA). Four early RA abatacept trials were analyzed to understand the differential impact of abatacept among patients with SeroPositive Early and Active RA (SPEAR) compared to non-SPEAR patients.MethodsPooled patient-level data from AGREE, AMPLE, AVERT, and AVERT-2 were analyzed. Patients were classified as SPEAR if they were ACPA +, RF +, disease duration < 1 year, and Disease Activity Score-28 (DAS28) C-reactive protein (CRP) ≥ 3.2 at baseline; non-SPEAR otherwise. Outcomes included: American College of Rheumatology (ACR) 20/50/70 at week 24; mean change from baseline to week 24 for DAS28 (CRP), Simple Disease Activity Index (SDAI), ACR core components; DAS28 (CRP) and SDAI remission. Adjusted regression analyses among abatacept-treated patients compared SPEAR and non-SPEAR patients, and in full trial population estimating how the efficacy of abatacept versus comparators [adalimumab + methotrexate, methotrexate] was modified by SPEAR status.ResultsThe study included 1400 SPEAR and 673 non-SPEAR patients; most were female (79.35%), white (77.38%), and with a mean age 49.26 (SD 12.86) years old. Around half with non-SPEAR were RF + and three-quarters ACPA +. Stronger improvements from baseline to week 24 were observed in almost all outcomes for abatacept-treated SPEAR versus non-SPEAR patients or versus SPEAR patients treated with comparators. Larger improvements were observed for SPEAR patients among the abatacept-treated population, and more strongly improved efficacy among SPEAR patients for abatacept than comparators.ConclusionsThis analysis, including large patient numbers of early-RA abatacept trials, confirmed beneficial treatment effects of abatacept in patients with SPEAR versus non-SPEAR.