5,940 publications found
Sort by
Breakthrough COVID-19 after tixagevimab/cilgavimab among patients with systemic autoimmune rheumatic diseases.

To determine the incidence and baseline factors associated with breakthrough COVID-19 after pre-exposure prophylaxis (PrEP) with tixagevimab/cilgavimab among patients with systemic autoimmune rheumatic diseases (SARDs). We performed a retrospective cohort study among patients with SARDs who received tixagevimab/cilgavimab between January 2, 2022 and November 16, 2022. The primary outcome was breakthrough COVID-19 after tixagevimab/cilgavimab. We performed multivariable Cox regression models adjusted for baseline factors to identify risk factors for breakthrough COVID-19. We identified 444 SARD patients who received tixagevimab/cilgavimab (mean age 62.0 years, 78.2% female). There were 83 (18.7%) breakthrough COVID-19 cases (incidence rate 31.5 per 1000 person-months [95% CI 24.7 - 38.2]), 7 (1.6%) hospitalizations and 1 (0.2%) death. Older age was inversely associated with breakthrough COVID-19 (adjusted hazard ratio [aHR] 0.86 per 10 years, 95% CI 0.75 - 0.99). Higher baseline spike antibody levels were associated with lower risk of breakthrough COVID-19 (aHR 0.42, 95% CI 0.18 - 0.99 for spike antibody levels >200 vs. <0.4 units). CD20 inhibitor users had a similar risk of breakthrough COVID-19 (aHR 1.05, 95% CI 0.44 - 2.49) compared to conventional synthetic DMARD users. We found that SARD patients had frequent breakthrough COVID-19, but the proportion experiencing severe COVID-19 was low. DMARD type, including CD20 inhibitors, did not significantly affect risk of breakthrough COVID-19. Evidence of prior humoral immunity was protective against breakthrough infection, highlighting the continued need for a multimodal approach to prevent severe COVID-19 as novel PrEP therapies are being developed.

Open Access
Occurrence and prediction of flare after tapering of TNF inhibitors in patients with axial spondyloarthritis.

Patients with axial spondyloarthritis (axSpA) in clinical remission tapered Tumor Necrosis Factor inhibitor (TNFi) therapy according to a clinical guideline. During 2-years' follow-up, we aimed to investigate flare frequency, dose at which flare occurred, type of flare and predictors thereof. Patients in clinical remission (Bath ankylosing spondylitis disease activity index (BASDAI)<40, physician global score<40 and without disease activity the previous year) tapered TNFi to 2/3 standard dose at baseline, 1/2 at week (w) 16, 1/3 at w32 and discontinuationed at w48. Flare was defined as: BASDAI flare (BASDAI≥40 and Δ≥20) and/or clinical flare (development of inflammatory back pain, musculoskeletal or extra-articular manifestations and/or ASDAS-CRP increase ≥0.9) and/or MRI flare (≥2 new/worsened inflammatory lesions). Of 108 patients, 106 (99%) flared before 2 years: 29 patients (27%) at 2/3 standard dose, 21 (20%) at 1/2 dose, 29 (27%) at 1/3 dose and 27 (25%) after discontinuation. One-hundred-and-five (99%) had clinical flare, 25 (24%) BASDAI flare and 23 (29% of patients with MRI) MRI flare. Forty-one patients (41%) fulfilled the ASAS-definition of clinically important worsening (≥0.9 increase since baseline). Higher baseline physician global score was an independent predictor of flare after tapering to 2/3 (Odds ratio=1.19 (95% Confidence Interval=1.05-1.41);p=0.011). Changes in clinical and/or imaging variables in the 16 weeks prior to tapering did not predict flare. Almost all (99%) axSpA patients in clinical remission flared during tapering to discontinuation, but above half not before receiving 1/3 dose or less. Higher physician global score was an independent predictor of flare.

Risk factor and incidence of serious infections in systemic lupus erythematosus patients undergoing rituximab therapy.

To evaluate the risk and protective factors of serious infection (SI) in patients with systemic lupus erythematosus (SLE) after rituximab treatment within 180 days. SLE patients treated with rituximab were analyzed. SI was defined as any infectious disease requiring hospitalization. The clinical characteristics, laboratory profiles, medications, and incidence rate (IR) were presented. Multivariate Cox proportional hazards models and Kaplan-Meier analysis for risk factors of SI were performed. A total of 174 SLE patients receiving rituximab treatment were enrolled. The overall IR of SI was 51/100 patient-years. Pneumonia (30.4/100 patient-years), followed by soft tissue infections, intra-abdominal infections, and Pneumocystis jiroveci pneumonia (all 6.1/100 patient-years) were the leading types of SI. Twelve patients died during the 180-day follow-up (crude mortality rate: 14.6/100 patient-years). Chronic kidney disease (CKD), defined as an estimated glomerular filtration rate <60 mL/min/1.73m2 (hazard ratio [HR]: 2.88, 95% confidence interval [CI]: 1.3-6.38), and a background prednisolone equivalent dosage ≥15 mg/day (HR: 3.5, 95% CI: 1.57-7.78) were risk factors for SI among all SLE patients. Kaplan-Meier analysis confirmed the risk of SI for SLE patients with CKD and a background prednisolone equivalent dosage ≥15 mg/day (log-rank p = 0.001 and 0.019, respectively). Hydroxychloroquine reduced the risk of SI in SLE patients (HR: 0.35, 95% CI: 0.15-0.82; log-rank p = 0.003). SI was prevalent in SLE patients after rituximab treatment. SLE patients with CKD and high-dose glucocorticoid use required constant vigilance. Hydroxychloroquine may reduce the risk of SI among SLE patients administered rituximab.