Abstract: Cold temperatures have been recognized as a possible catalyst for gouty arthritis exacerbations in individuals with hyperuricemia. The mechanisms underlying cold-induced gout are, however, minimally recognized. The article examines the pathophysiological connection between hyperuricemia and cold-induced gout flare triggers, emphasizing the molecular and physiological mechanisms involved. Genetic predisposition significantly influences an individual's risk of developing hyperuricemia and subsequent gout, underscoring the relevance of genetic variables in disease susceptibility. The diagnosis of gout depends on a combination of laboratory testing, such as blood uric acid levels, synovial fluid examination for urate crystals, and imaging to evaluate joint damage. Cold exposure is a significant environmental element that promotes the crystallization of monosodium urate in synovial fluid, initiating an inflammatory response. Activating the NLR family pyrin domain-containing 3 (NLRP3) inflammasome triggers the production of pro-inflammatory cytokines, consequently contributing to the pathophysiology of gout flares. The NLRP3 inflammatory system gets activated, leading to the secretion of pro-inflammatory cytokines. Low temperatures additionally impair blood circulation and the efficacy of immune cells, hence exacerbating inflammation. This review highlights the recent findings on epidemiology, pathophysiology, and diagnostic techniques of gouty arthritis, providing insights into prospective preventive strategies, therapies for those affected, and offering hope for the future. Overall, it provides an overview of the mechanisms behind cold-induced gout flares.
Lin et al. (Thu,) studied this question.