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ObjectivesTo determine factors associated with COVID-19-related death in people with rheumatic diseases.MethodsPhysician-reported registry of adults with rheumatic disease and confirmed or presumptive COVID-19 (from 24 March to 1 July 2020). The primary outcome was COVID-19-related death. Age, sex, smoking status, comorbidities, rheumatic disease diagnosis, disease activity and medications were included as covariates in multivariable logistic regression models. Analyses were further stratified according to rheumatic disease category.ResultsOf 3729 patients (mean age 57 years, 68% female), 390 (10.5%) died. Independent factors associated with COVID-19-related death were age (66–75 years: OR 3.00, 95% CI 2.13 to 4.22; >75 years: 6.18, 4.47 to 8.53; both vs ≤65 years), male sex (1.46, 1.11 to 1.91), hypertension combined with cardiovascular disease (1.89, 1.31 to 2.73), chronic lung disease (1.68, 1.26 to 2.25) and prednisolone-equivalent dosage >10 mg/day (1.69, 1.18 to 2.41; vs no glucocorticoid intake). Moderate/high disease activity (vs remission/low disease activity) was associated with higher odds of death (1.87, 1.27 to 2.77). Rituximab (4.04, 2.32 to 7.03), sulfasalazine (3.60, 1.66 to 7.78), immunosuppressants (azathioprine, cyclophosphamide, ciclosporin, mycophenolate or tacrolimus: 2.22, 1.43 to 3.46) and not receiving any disease-modifying anti-rheumatic drug (DMARD) (2.11, 1.48 to 3.01) were associated with higher odds of death, compared with methotrexate monotherapy. Other synthetic/biological DMARDs were not associated with COVID-19-related death.ConclusionAmong people with rheumatic disease, COVID-19-related death was associated with known general factors (older age, male sex and specific comorbidities) and disease-specific factors (disease activity and specific medications). The association with moderate/high disease activity highlights the importance of adequate disease control with DMARDs, preferably without increasing glucocorticoid dosages. Caution may be required with rituximab, sulfasalazine and some immunosuppressants.

ObjectivesCOVID-19 outcomes in people with rheumatic diseases remain poorly understood. The aim was to examine demographic and clinical factors associated with COVID-19 hospitalisation status in people with rheumatic disease.MethodsCase series of individuals with rheumatic disease and COVID-19 from the COVID-19 Global Rheumatology Alliance registry: 24 March 2020 to 20 April 2020. Multivariable logistic regression was used to estimate ORs and 95% CIs of hospitalisation. Age, sex, smoking status, rheumatic disease diagnosis, comorbidities and rheumatic disease medications taken immediately prior to infection were analysed.ResultsA total of 600 cases from 40 countries were included. Nearly half of the cases were hospitalised (277, 46%) and 55 (9%) died. In multivariable-adjusted models, prednisone dose ≥10 mg/day was associated with higher odds of hospitalisation (OR 2.05, 95% CI 1.06 to 3.96). Use of conventional disease-modifying antirheumatic drug (DMARD) alone or in combination with biologics/Janus Kinase inhibitors was not associated with hospitalisation (OR 1.23, 95% CI 0.70 to 2.17 and OR 0.74, 95% CI 0.37 to 1.46, respectively). Non-steroidal anti-inflammatory drug (NSAID) use was not associated with hospitalisation status (OR 0.64, 95% CI 0.39 to 1.06). Tumour necrosis factor inhibitor (anti-TNF) use was associated with a reduced odds of hospitalisation (OR 0.40, 95% CI 0.19 to 0.81), while no association with antimalarial use (OR 0.94, 95% CI 0.57 to 1.57) was observed.ConclusionsWe found that glucocorticoid exposure of ≥10 mg/day is associated with a higher odds of hospitalisation and anti-TNF with a decreased odds of hospitalisation in patients with rheumatic disease. Neither exposure to DMARDs nor NSAIDs were associated with increased odds of hospitalisation.

Purpose of Review Although intra-articular (IA) mineralization resulting from calcium crystal deposition is common in osteoarthritis (OA), its clinical significance remains unclear, including whether it is a cause or consequence of OA. This article reviews the current understanding of IA mineralization in OA including epidemiology, pathogenesis, and associations with clinical and structural OA outcomes. Recent Findings Many gaps in knowledge remain regarding the role in OA of calcium crystal deposition resulting in IA mineralization. However, recent studies have begun to further elucidate this role, including through use of advanced imaging modalities that can differentiate calcium crystal types, as well as basic science studies investigating whether calcium pyrophosphate (CPP) and basic calcium phosphate (BCP) depositions represent different phenotypes and endotypes in OA. Summary An improved understanding of the role of IA mineralization in OA may lead to development of targeted therapies with potential clinical and structural benefits for knee OA.

Despite gender parity in the rheumatology workforce, biases may persist in speaker introductions at professional rheumatology meetings, as observed in other specialties. We analyzed speaker introductions at an international rheumatology conference to assess the relationship between speaker and moderator gender on professional address. We analyzed video-archived speaker introductions from the 2022 American College of Rheumatology (ACR) Convergence meeting. Two reviewers coded speaker and moderator gender and form of address. We defined a “strict address” as use of “Doctor” or “Professor” and “lenient address” as full name with a professional title. Fisher’s exact tests and logistic regression analyses examined associations between gender and forms of address. We analyzed 355 speakers (52.7% female, 47.3% male). Female speakers were less likely to receive a strict address by male moderators than male speakers (42.1% versus 57.9%, χ 2 =4.20, p  = 0.030). In logistic regression models after adjusting for moderator gender, male speakers were 1.8 times more likely to receive a strict address versus female speakers [odds ratio (OR) 1.76; 95% confidence interval (CI) (1.10, 2.82)]. Male moderators were 64% less likely to provide a strict address than female moderators [OR 0.46; 95% CI (0.29, 0.73)], adjusting for speaker gender. At an international rheumatology meeting, male (versus female) speakers received formal introductions more frequently, and male (versus female) moderators were less likely to provide them. Our results suggest persistent gender bias in speaker introductions, highlighting a need for standardized practices for session moderators to improve gender equity.

BackgroundPreventing worsening osteoarthritis (OA) in persons with early OA is a major treatment goal. We evaluated if different early OA definitions yielded enough cases of worsening OA within 2–5 years to make trial testing treatments feasible.MethodsWe assessed different definitions of early OA using data from Multicenter Osteoarthritis (MOST) Study participants who were followed up longitudinally. We defined early OA as having at least minimal knee pain (WOMAC (Western Ontario and McMaster Universities Osteoarthritis Index) pain ≥3/20) with different levels of pre-radiographic OA. For MRI, we required knee pain and used MRI definitions with combinations of cartilage damage, osteophytes, bone marrow lesions and meniscus damage.The primary outcome, worsening OA at 2 or 5 years, combined structural (Kellgren and Lawrence grade ≥2 with joint space narrowing ≥1) and symptom (WOMAC pain ≥6 with increase ≥2 from baseline) outcomes. We also examined structural and symptom outcomes separately.ResultsFor worsening OA at 2 years, we included 750 participants (mean age 65 years, 60% female, 90% white, mean body mass index 29.2 kg/m2). Fewer than 10% of early OA knees had the combined outcome at 2 or 5 years. At 2 years, for several early OA definitions, roughly 20% of knees had either structural or symptom worsening outcomes. Two-year trials of either, but not both, outcomes would need to recruit over 1200 patients.ConclusionMost knees with early OA are stable and do not progress. Some painful knees experience worse pain but not structural progression and vice versa. Trial testing treatments to prevent OA illness or disease will be challenging.