Arthritis & Rheumatology最新文献

Objective: Real-world initial treatment strategies in SSc-PAH remain incompletely described. We aimed to characterise these strategies across haemodynamic thresholds and risk strata and evaluate outcome associations.

Methods: We analysed treatment-naïve SSc-PAH patients in EUSTAR (2000-2021) fulfilling the 2022 haemodynamic definition. Initial therapy comprised treatment initiated within 4 months of RHC. As-treated (AT) analyses were primary and intention-to-treat (ITT) analyses supportive. Outcomes were all-cause mortality and 36-month PAH progression.

Results: Among 301 patients, 198 (66%) initiated therapy and 170 maintained therapy for ≥3 months. Therapy was initiated in 31% with milder haemodynamic impairment (mPAP 21-24 mmHg and/or PVR 2-3 WU) versus 79% fulfilling the previous haemodynamic definition; combination therapy increased from 14% to 67% across low- to high-risk strata. Over a median 3.9 years, 125 (42%) died and 85/227 (37%) progressed. Adjusted ITT analyses showed no association with either outcome, whereas adjusted AT analyses showed lower mortality risk with sustained monotherapy and combination therapy (HR 0.50, 95% CI 0.27-0.92 and HR 0.40, 95% CI 0.18-0.88, respectively) and lower PAH progression risk with sustained initial therapy (HR 0.37, 95% CI 0.18-0.76). In the milder haemodynamic subgroup, the mortality estimate was directionally consistent but imprecise.

Conclusion: Initial treatment strategies reflected haemodynamic severity and baseline risk, while variation suggested potential implementation gaps. Sustained initial therapy was associated with lower risks of mortality and PAH progression. Contrasting ITT and AT estimates highlight challenges in observational treatment-outcome comparisons. Findings in the milder haemodynamic subgroup support dedicated prospective studies.

Background: Little is known about the prevalence of and factors associated with Long COVID in patients with autoimmune rheumatic diseases (AIRDs).

Methods: We conducted a retrospective cohort study using data from the National Clinical Cohort Collaborative (N3C). We included adults with a first documented SARS-CoV-2 infection between September 2021 and December 2023, with follow-up through December 2024. Long COVID was defined as ICD-10-CM code U09.9 or a Long COVID clinic visit occurring 28 to 365 days after first infection. We compared patients with AIRD with matched non-AIRD controls using 1:1 nearest-neighbor propensity score matching on age with exact matching on sex, race/ethnicity, SARS-CoV-2 variant-dominant period, and data-contributing organization. We estimated hazard ratios using multivariable Cox regression models. Among people with AIRD, we assessed risk by AIRD type and medication exposure before acute COVID-19.

Results: In the matched cohort of 187,106 patients, Long COVID occurred in 2.8% of AIRD patients and 1.5% among non-AIRD patients. In multivariable analyses, AIRD was associated with an increased risk of Long COVID compared with non-AIRD patients (aHR 1.56, 95% CI 1.45-1.67). Among patients with AIRD, higher acute COVID-19 severity, pulmonary disease, obesity, and exposure to rituximab or glucocorticoids were associated with an increased risk of Long COVID. Sjögren's syndrome was associated with a higher risk of Long COVID.

Conclusion: The higher risk of developing Long COVID among AIRD patients compared with those without AIRD underscores the need to identify potential risk factors for Long COVID in this population to minimize its long-term effects.

Expression of concern: M. M. Luchetti, G. Moroncini, M. Jose Escamez, S. Svegliati Baroni, T. Spadoni, A. Grieco, C. Paolini, A. Funaro, E. V. Avvedimento, F. Larcher, M. Del Rio, and A. Gabrielli, "Induction of Scleroderma Fibrosis in Skin-humanized Mice by Administration of Anti-platelet-derived Growth Factor Receptor Agonistic Autoantibodies," Arthritis & Rheumatology 68, no. 9 (2016): 2263-2273, https://doi.org/10.1002/art.39728. This Expression of Concern is for the above article, published online on 25 April 2016 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, S. Louis Bridges, Jr.; the American College of Rheumatology; and Wiley Periodicals LLC. Concerns were raised by a third party on PubPeer [1] regarding a high level of similarity between the beta-actin bands in Figures 1C and 2B. Additional investigation by the publisher also found that there was evidence of splicing in the PDGFR-alpha band in Figure 3B. The authors responded to an inquiry by the publisher and shared original data. However, original data were not available for the bands originally published in Figure 3B, and the authors supplied data from replicate experiments performed during the same period of the original experiments. A review of these data found that not all of the data could be verified. Therefore, this Expression of Concern has been agreed to in order to inform and alert readers as to the results of this investigation. The authors have been informed of the Expression of Concern.

Reference: 1. Psychotria siamica. Comments on "Induction of Scleroderma Fibrosis in Skin-Humanized Mice by Administration of Anti-Platelet-Derived Growth Factor Receptor Agonistic Autoantibodies," PubPeer, November 2025. https://pubpeer.com/publications/33B47982F70FD05FFA5D7CE38D417A.