Objective: COMPLETE-PsA was an observational study of biologic-naïve Canadian adults with active psoriatic arthritis (PsA) treated with adalimumab (ADA) or a nonbiologic disease-modifying antirheumatic drug (nbDMARD) regimen, after inadequate response/intolerance to a current nbDMARD treatment regimen. The aim of this analysis was to assess the 12-month effectiveness of ADA vs nbDMARDs.
Methods: Patients enrolled between March 2012 and November 2017 were included. The following clinical variables and patient-reported outcomes were collected/calculated per routine care: Disease Activity Index for Psoriatic Arthritis in 28 joints (DAPSA28), Disease Activity Score in 28 joints (DAS28), erythrocyte sedimentation rate (ESR), C-reactive protein, physician global assessment (PGA), patient global assessment (PtGA), pain, Health Assessment Questionnaire-Disability Index (HAQ-DI), 12-item Short Form Health Survey, enthesitis, dactylitis, body surface area (BSA), and time to achieving American College of Rheumatology (ACR) 50, ACR70, and modified minimal disease activity (mMDA).
Results: Two hundred and seventy-seven ADA-treated and 148 nbDMARD-treated patients were included. At baseline, ADA-treated patients were less likely to be employed, had longer morning stiffness, higher DAPSA28, DAS28, PGA, PtGA, pain, and HAQ-DI, and lower prevalence of dactylitis (all < 0.05). ADA-treated patients showed lower baseline-adjusted DAPSA28 (16.5 vs 26.6), DAS28 (2.8 vs 3.9), PGA (25.3 vs 37.1), and ESR (10.4 vs 15.0 mm/h) after 3 months compared to nbDMARD-treated patients, with observed improvements maintained to month 12. Time to achievement of ACR50, ACR70, and mMDA was significantly shorter ( < 0.001) among ADA-treated patients, with the likelihood of having dactylitis (odds ratio [OR] 0.4, 95% CI 0.2-0.6) and BSA< 3% (OR 2.7, 95% CI 1.5-5.0) significantly lower and higher, respectively. Switching to another biologic was less likely in ADA-treated vs nbDMARD-treated patients (hazard ratio 0.3, 95% CI 0.2-0.5).
Conclusion: In a real-world Canadian population of patients with PsA, ADA was more effective than nbDMARDs at reducing disease activity and the severity of skin involvement, and demonstrated higher retention. [ClinicalTrials.gov: NCT01559038].
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http://dx.doi.org/10.3899/jrheum.200609 | DOI Listing |
Inflammopharmacology
December 2024
Riphah Institute of Pharmaceutical Sciences, Riphah International University, Lahore Campus, Lahore, 5400, Pakistan.
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December 2024
Department of Biotechnology, Science Campus, Alagappa University, Karaikudi, India.
Early childhood caries (ECC), a severe form of dental caries, is exacerbated by the synergistic interaction between Streptococcus mutans and Candida albicans, leading to greater disease severity than their individual effects. This underscores the need for more targeted and potent therapeutic alternatives. Given the promising anti-infective properties of quaternary ammonium surfactants (QAS), this study explores the microbicidal properties of one such QAS, cetyltrimethylammonium chloride (CTAC), against both individual- and dual-species cultures of S.
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Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Virus encephalitis (VE), recognized as one of the common kinds of central nervous system (CNS) diseases after virus infection, has a surprising correlation with autoimmune encephalitis (AE) when autoimmune antibodies emerge in cerebrospinal fluid (CSF) or serum. Herpes simplex virus and Epstein-Barr virus are the most critical agents worldwide. By molecular mimicry, herpes viruses can invade the brain directly or indirectly.
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December 2024
Department of Medicine, Division of Rheumatology, Queen's University, Kingston, ON, Canada.
Purpose Of Review: The canonical pathogenesis of spondyloarthritis (SpA) involves inflammation driven by HLA-B27, type 3 immunity, and gut microbial dysregulation. This review based on information presented at the SPARTAN meeting highlights studies on the pathogenesis of SpA from the past year, focusing on emerging mechanisms such as the roles of microbe-derived metabolites, microRNAs (miRNAs) and cytokines in plasma exosomes, specific T cell subsets, and neutrophils.
Recent Findings: The induction of arthritis in a preclinical model through microbiota-driven alterations in tryptophan catabolism provides new insights as to how intestinal dysbiosis may activate disease via the gut-joint axis.
Protein Sci
January 2025
Department of Neuroscience, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Human succinic semialdehyde dehydrogenase is a mitochondrial enzyme fundamental in the neurotransmitter γ-aminobutyric acid catabolism. It catalyzes the NAD-dependent oxidative degradation of its derivative, succinic semialdehyde, to succinic acid. Mutations in its gene lead to an inherited neurometabolic rare disease, succinic semialdehyde dehydrogenase deficiency, characterized by mental and developmental delay.
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