Deflazacort and prednisone were given to 26 patients with rheumatoid arthritis, polymyalgia rheumatica, or other chronic inflammatory diseases, in a double-blind study. Deflazacort rapidly and effectively suppressed disease activity in a manner supporting its assumed therapeutic potency of 83% that of prednisone. Prednisone induced a rapid increase in the level of daily calcium excretion that was not evident with deflazacort. Cortisol secretion was acutely inhibited by prednisone, but not by deflazacort. Neither corticosteroid had a significant effect on glucose metabolism, at the doses studied. Treatment with deflazacort may be an effective alternative to prednisone treatment, with fewer adverse effects on levels of calcium and cortisol, in patients with
Objectives Registry data suggest that people with immune-mediated inflammatory diseases (IMIDs) receiving targeted systemic therapies have fewer adverse COVID-19 outcomes compared to patients receiving no systemic treatments. We used international patient survey data to explore the hypothesis that greater risk-mitigating behaviour in those receiving targeted therapies may account, at least in part, for this observation. Methods Online surveys were completed by individuals with Rheumatic and Musculoskeletal Diseases (RMD) (UK only) or psoriasis (globally) between 4th May and 7th September 2020. We used multiple logistic regression to assess the association between treatment type and risk-mitigating behaviour, adjusting for clinical and demographic characteristics. We characterised international variation in a mixed effects model. Results Of 3,720 participants (2,869 psoriasis, 851 RMD) from 74 countries, 2,262 (60.8%) reported the most stringent risk-mitigating behaviour (classified here under the umbrella term shielding). A greater proportion of those receiving targeted therapies (biologics and JAK inhibitors) reported shielding compared to those receiving no systemic therapy (adjusted odds ratio [OR] 1.63, 95% CI 1.35-1.97) and standard systemic agents (OR 1.39, 95% CI 1.22-1.56). Shielding was associated with established risk factors for severe COVID-19 (male sex [OR 1.14, 95% CI 1.05-1.24], obesity [OR 1.38, 95% CI 1.23-1.54], comorbidity burden [OR 1.43, 95% CI 1.15-1.78]), a primary indication of RMD (OR 1.37, 95% CI 1.27-1.48) and a positive anxiety or depression screen (OR 1.57, 95% CI 1.36-1.80). Modest differences in the proportion shielding were observed across nations. Conclusions Greater risk-mitigating behaviour among people with IMIDs receiving targeted therapies may contribute to the reported lower risk of adverse COVID-19 outcomes. The behaviour variation across treatment groups, IMIDs and nations reinforces the need for clear evidence-based patient communication on risk mitigation strategies and may help inform updated public health guidelines as the pandemic continues.
BackgroundIn the general population, polypharmacy (PP) is associated with increased risk of adverse events. The relationship between adverse outcomes and PP in Rheumatoid Arthritis (RA) has not been studied in depth. The mantra of treatment in RA encourages PP through combination Disease Modifying Anti-Rheumatic Drugs (DMARD).ObjectivesTo study the relationship between PP and serious adverse events in RA, including the influence of DMARDs within the PP count.MethodsData from the British Society for Rheumatology Biologics Register were analysed. PP was defined as number of drugs co-prescribed at baseline, with two models: (1) including DMARDs (2) excluding DMARDs from the medication count. PP was stratified by 0–5, 6–9 and >10. Patients were studied from initiation of 1st biologic until 1st serious adverse event (SAE), 3 years of follow up, or last available visit, whichever came first. A Cox-proportional hazard model was used, with adjustment for a priori selected cofounders.ResultsThis study included 15,004 patients commencing biologics. The demographics are shown in table 1. Excluding DMARDs from the PP cohort, 7,115 (47%) of the patients were taking up to 5 drugs; 6,010 (40%) were taking 6 to 9 drugs; 1,870 (12%) were taking 10 or more medications. Higher levels of PP associated with older age, more severe disease, and longer disease duration. PP predictably associated with comorbidities; the relationship was not linear: comorbidity count appeared to show a ceiling effect. The overall incidence of SAEs was 25.5/100 person years (95% CI 24.7–26.3). The rate of SAEs increased across the PP counts (See Table 1). The relationship remained significant after adjusting for comorbidities. Including DMARDs within the PP count attenuated the association.Table 1All Patients0–5 drugs6–9 drugs>10 drugs PP count excluding DMARDs N=15,004n=7,115n=6,019n=1,870 Baseline characteristics Mean Age in years56.354.057.661.0 Mean DAS 28 (SD)4.30 (1.76)4.17 (1.79)4.51 (1.67)4.88 (1.67) Mean HAQ (SD)1.93 (0.64)1.85 (0.65)2.10 (0.56)2.15 (0.58) Mean Disease Duration (SD) in years12.59 (9.72)11.96 (9.32)13.79 (10.26)14.67 (10.96) Comorbidity (SD)1.87 (0.80)1.65 (0.74)2.29 (0.73)2.57 (0.68)Analysis of Serious Adverse Events Exposure time (person-years)14,2009,6903,706804 Event count (single failure model)326120021251368 Incidence rate (95% CI)25.5 (24.7–26.3)20.6 (19.7–21.5)33.7 (31.9–35.6)45.7 (41.3–50.7) Including DMARDs in PP model Unadjusted HR (95% CI)–Ref1.20 (1.11–1.29)1.82 (1.66–1.99) Adjusted HR (95% CI)–Ref1.05 (0.97–1.13)1.39 (1.26–1.54) Excluding DMARDs in PP model Unadjusted HR (95% CI)–Ref1.63 (1.52–1.75)2.21 (1.98–2.47) Adjusted HR (95% CI)–Ref1.18 (1.09–1.28)1.35 (1.19–1.53)Adjusted for age, sex, DAS, HAQ, disease duration and comorbidities.ConclusionsPP is common in patients with RA and is associated with adverse outcomes especially when patients are on >10 drugs. Including or excluding DMARDs from the PP model had negligible impact on findings. The relationship between PP and comorbidity is worthy of further resea...
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