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痛风性关节炎的发病机制受到尿酸钠晶体及其诱导的炎症过程的严重影响(Wise和Agudelo 1996)。肾脏尿酸盐排泄效率低下,导致尿酸盐结晶饱和点以上尿酸水平升高,是该病的主要决定因素。嘌呤分解代谢导致代谢副产物尿酸的形成。在大多数哺乳动物中,如高等灵长类动物、许多鸟类和一些爬行动物,尿酸氧化酶(uricase)将尿酸(相对不溶性)转化为尿囊素(高溶性),导致血清尿酸水平非常低。中新世乌里素基因的一系列平行突变导致乌里素功能失调,导致较高水平的不溶性尿酸积累,进而发展为痛风性关节炎(Liote和Ea 2006;Eggebeen 2007)。嘌呤的降解导致内源性产生的尿酸,通常占人体尿酸库的三分之二,其余的由饮食摄入。在每天形成的尿酸中,约70%通过肾脏排出,其余排出进入胆道,然后由结肠细菌尿酶转化为尿囊素。因此,在绝大多数痛风患者中,高尿酸血症的发生是由于肾脏尿酸清除率的降低。


Pathogenesis of gouty arthritis is critically influenced by sodium urate crystals and inflammatory processes they induce (Wise and Agudelo 1996). An inefficient renal urate excretion which leads to the elevated levels of uric acid above the saturation point for urate crystal formation is a major determinant of the disease. Purine catabolism leads to the formation of metabolic by-product, uric acid. In most mammals like higher primates, many birds and some reptiles, the urate oxidase (uricase) enzyme converts uric acid (relatively insoluble) to allantoin (highly soluble), leading to very low serum uric acid levels. A series of parallel mutations in the genes of uricase in the Miocene period results in the production of the dysfunctional form of uricase that leads to accumulation of relatively higher level of insoluble uric acid and subsequently the development of gouty arthritis (Liote and Ea 2006; Eggebeen 2007). Degradation of purines results in the endogenous production of uric acid that usually contributes about two-thirds of the body urate pool, the remainder being originated by dietry intake. Of the uric acid formed daily, about 70% is excreted through the kidney while the rest is eliminated into the biliary tract and then converted to allantoin by colonic bacterial uricase. Therefore, in the vast majority gouty patients, hyperuricaemia occurs from reduced efficiency of renal urate clearance .


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