Pathogenetic and clinical features of comorbid conditions in gout

Gout is the most common inflammatory arthritis worldwide and represents a growing global health problem. It develops as a result of hyperuricemia caused by impaired purine metabolism, leading to the deposition of monosodium urate (MSU) crystals and recurrent inflammatory arthritis. Although hyperuricemia is the primary risk factor, genetic predisposition, impaired urate transport, and emerging factors such as the gut microbiota also contribute to disease development. Acute flares are mediated by activation of the NLRP3 inflammasome induced by MSU crystals and the subsequent production of interleukin-1β, whereas chronic inflammation leads to the formation of tophi and structural joint damage. Gout is closely associated with metabolic syndrome, chronic kidney disease, and cardiovascular diseases, which contribute to persistently elevated mortality. Although advances in imaging and pharmacological therapy have improved diagnosis and management, the real-world application of urate-lowering therapy remains suboptimal. Further research and continuous efforts by healthcare professionals are needed to improve long-term disease control.