Tophaceous wounds represent a severe complication of end-stage gout, characterized by the deposition of monosodium urate (MSU) crystals leading to localized tissue ischemia, chronic inflammation, and non-healing ulcers. The pathological mechanism involves the formation of MSU crystals under persistent hyperuricemia, inflammatory encapsulation, and mechanical compression of the vascular system due to tophus enlarge-ment, ultimately resulting in chronic non-healing ulcers. This article consolidates current evidence to outline an integrated management strategy for such wounds, combining systemic metabolic control with localized interventions. Effective treatment hinges on maintaining serum uric acid levels below 300 μmol/L through urate-lowering agents, including conventional drugs and novel urate transporter 1 inhibitors such as AR882, complemented by anti-inflammatory medications such as nonsteroidal anti-inflammatory drugs and glucocorticoid alleviate pain and reduce inflammation. Topical agents and advanced dressings are utilized to support healing and manage exudate. Debridement—encompassing sharp, ultrasonic, and micro-techniques—is essential for removing necrotic tissue and MSU deposits, with efficacy assessed via local uric acid monitoring. Surgical interventions, including flap transfers and tendon or ligament reconstruction, are indicated for significant tissue loss or functional impairment. Long-term management emphasizes continuous metabolic control, personalized rehabilitation, and lifestyle modification. The comprehensive treatment of tophaceous wounds requires multidisciplinary collaboration to balance local repair and systemic regulation for improved prognosis. Future research directions include gene therapy to regulate purine metabolism and artificial intelligence-assisted personalized treatment plans, aiming to achieve precision medicine for tophaceous wounds.
He et al. (Mon,) studied this question.