Based on the excessive damage and subsequent regulation theory and the iron death mechanism, this paper discusses the etiology and pathogenesis of gouty arthritis and its diagnosis and treatment

Corresponding author: Li Yan, liyankm@126.com

DOI: 10.12201/bmr.202512.00037

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  Abstract: 痛风性关节炎(gouty arthritis, GA)是一种因嘌呤代谢紊乱、尿酸排泄减少导致血尿酸水平升高,单钠尿酸盐(monosodium urate, MSU)沉积于关节内及其周围组织而引起的炎症性疾病1。其主要临床表现为突发性关节红、肿、热、痛以及活动受限2。近年来,随着人们生活水平的提高和饮食结构的改变,痛风性关节炎的患病率呈逐年上升趋势,已成为严重影响人类健康的常见代谢性疾病之一。流行病学调查显示,全球患病率为0.1% ～ 10.0%3,其中我国痛风患病率为1%～3%,并呈逐年上升趋势,以男性发病人数居多,约为女性的15倍,平均年龄48.28岁,发病年龄日趋年轻化4。该病还可导致关节畸形、功能障碍,甚至累及肾脏,引发慢性肾病和肾功能不全,已成为冠心病、高血压、糖尿病等多种疾病的独立危险因子5。痛风性关节炎的现代医学治疗主要集中在急性期的抗炎镇痛和慢性期的降尿酸治疗,但长期使用这些药物可能对肝肾功能造成损害,并引发胃肠道不良反应、皮炎等问题6。因此,进一步探索痛风性关节炎的发病机制和治疗方法具有重要意义。

  Key words: Gouty arthritis; Hyperactivity syndrome; Ferroptosis; Etiological pathogenesis; Syndrome differentiation and treatment

  Submit time: 12 December 2025

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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