Comprehensive management of tophaceous wounds.

Q2 Medicine
Guoyu He, Shuliang Lu, Xinyi Lu, Yingkai Liu
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引用次数: 0

Abstract

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.

风疹伤口的综合处理。
白癜风伤口是终末期痛风的严重并发症,其特征是尿酸钠(MSU)晶体沉积导致局部组织缺血、慢性炎症和无法愈合的溃疡。其病理机制包括:在持续高尿酸血症、炎症包封和痛风疹增大对血管系统的机械压迫下形成MSU晶体,最终导致慢性无法愈合的溃疡。这篇文章整合了目前的证据,概述了这类伤口的综合管理策略,将全身代谢控制与局部干预相结合。有效的治疗取决于通过降尿酸剂(包括常规药物和新型尿酸转运蛋白1抑制剂如AR882)将血清尿酸水平维持在300 μmol/L以下,辅以非甾体抗炎药和糖皮质激素等抗炎药物,以减轻疼痛和炎症。局部药物和高级敷料用于支持愈合和管理渗出液。清创包括锐刀、超声和显微技术,对于清除坏死组织和MSU沉积物至关重要,通过局部尿酸监测评估其疗效。手术干预,包括皮瓣转移和肌腱或韧带重建,适用于显著的组织损失或功能损害。长期治疗强调持续的代谢控制、个性化康复和生活方式的改变。综合治疗石质伤口需要多学科合作,平衡局部修复和全身调节,以改善预后。未来的研究方向包括调节嘌呤代谢的基因治疗和人工智能辅助的个性化治疗方案,旨在实现对风疹伤口的精准医疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
67
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