Objective: This study examines the impact of dose step-down in patients with rheumatoid arthritis (RA) who achieved sustained disease control with baricitinib 4-mg once-daily up to 96-weeks.
Methods: Patients who completed a baricitinib phase 3 study could enter a long-term extension (LTE). In the LTE, patients who received baricitinib 4-mg for ≥15 months and maintained clinical disease activity index (CDAI) low disease activity (LDA) or remission (REM) were blindly randomized to continue 4-mg or taper to 2-mg.
Introduction: We aim to assess the association of patient-reported pain and remission or low disease activity (LDA) at 3 months (M) in patients receiving baricitinib or other treatments in RA-BE-REAL.
Methods: RA-BE-REAL reports on patients with rheumatoid arthritis (RA) who were prescribed, for the first time, baricitinib (cohort A) or a tumour necrosis factor inhibitor (TNFi) (cohort B-TNFi) or any other mode of action (OMA) (cohort B-OMA). Pain was measured using the visual analogue scale (VAS) (0-100 mm) and clinically meaningful pain improvement thresholds of ≥ 30%, ≥ 50% and ≥ 70% from baseline to 3, 6, 12 and 24 M.
Objective: Baricitinib is an oral, reversible and selective inhibitor of Janus kinase (JAK)1 and JAK2 that is approved as monotherapy or in combination with methotrexate for the treatment of adults with moderate-to-severe active rheumatoid arthritis (RA) who have responded inadequately to disease-modifying antirheumatic drugs. Evidence supporting the approved monotherapy indication is growing in real-world settings that reflect routine clinical practice.
Methods: Results of separate analyses of real-world data from the observational prospective RA-BE-REAL, Erlangen Baricitinib cohort, the BSRBR-RA, and Swiss Clinical Quality Management in Rheumatic Diseases (SCQM) registries, and the retrospective ORBIT-RA and SUSTAIN long-term chart reviews were reported, documenting baseline data and outcomes for a total of 932 patients with active RA receiving baricitinib as monotherapy.
The study aimed to explore the pontential impact of 10 polymorphisms within IFN-α, IFN-β1, IFN-γ and TLR3 genes on SLE phenotype and susceptibility and to study the relationship between specific genotypes and clinics. Whole blood samples from SLE patients and healthy controls was obtained. DNA was extracted from the peripheral blood by the QIAamp DNA Blood Mini Kit (Qiagen).
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