ReviewBioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy2026
Beyond the Prevention of Anti-drug Antibody Formation with Uricase Therapy: Mechanistic Roles of DMARDs in Modifying Gout Flare Risk.
Review in BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disease-modifying antirheumatic drugs (DMARDs) are immune-modifying agents that have shown efficacy in improving response rates and reducing infusion reactions associated with uricase therapy for uncontrolled gout by inhibiting anti-drug antibody (ADA) formation. However, increased gout flare rates following initiation of uricase therapy remain a concern, impacting patient quality of life and treatment adherence. Gout flares are an acute inflammatory reaction to monosodium urate crystals, driven by inflammasome activation. As such, it is possible that DMARDs could impact gout flare risk. In this hypothesis-generating narrative review, we have synthesized mechanistic data investigating the effects of the DMARDs methotrexate, mycophenolate mofetil, azathioprine, leflunomide, and sirolimus on mechanisms involved in gout flare such as NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome activation. The mechanisms by which DMARDs inhibit ADA formation appear to be distinct from those that may affect gout flares, but these may exist in balance with one another to form a distinct pharmacological profile for each agent. Paradoxically, preclinical evidence suggests that DMARDs may sometimes induce NLRP3 inflammasome activation, particularly at higher doses. We suggest that individual DMARDs' effect on inflammatory pathways relevant to gout flare may vary depending on the pathophysiological context and differences in their pharmacological profiles. Therefore, the inflammatory consequences of combining DMARDs with uricase therapy are likely to be specific to the individual agent. Understanding the mechanistic profile of each DMARD is key to optimizing both immunogenicity management and flare outcomes in patients receiving uricase therapy for uncontrolled gout.
Identifiers
42734877What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.