二羟基腺嘌呤可能是诱发痛风的“元凶”

A new purine metabolite,2,8-dihydroxyadenine,might involve urate sediment igniting gout

流行病学研究证明痛风与高尿酸血症存在极高的相关性,实验研究证明尿酸盐注射到关节腔能造成痛风发作,甚至在痛风石中找到了尿酸的存在;但《原发性痛风诊断和治疗指南》却提示痛风与血清尿酸水平不存在必然联系。面对这些疑问,本文梳理了嘌呤的代谢途径,尿酸在体液中的溶解度,继而提出与尿酸结构相似但溶解度更低的二羟基腺嘌呤(DHA)可能是导致痛风发作的“元凶”,并分析DHA致痛风的可能机制,为痛风的基础研究和临床诊治提供了新思路。

Epidemiological data showed that gout is highly correlated with hyperuricemia.Experimental results proved that urate sediment is able to result in gouty arthritis,and even that urate is the main component of tophi.However,Guidelines for the Diagnosis and Treatment of Primary Gout suggested that there could be no causal relationships between gout attack and hyperuricemia.In order to clarify the paradoxes,the article combed the purine metabolism pathways and the solubility of urate in body fluid,and then put forward that 2,8-dihydroxyadenine(DHA),a purine metabolite whose structure is similar to uric acid but with lower solubility,could be the immediate cause igniting gout attack.The mechanism of how DHA triggers gout was also discussed.Therefore,the article would give new clues to gout treatment and experimental researches.