促尿酸排泄疗法以及尿酸在血液和尿液中的溶解度

Uricosuric therapy and urate solubility in blood and urine.

作者信息

Gröbner W, Zöllner N

出版信息

Postgrad Med J. 1979;55 Suppl 3:26-31.

Abstract

In most patients with primary gout hyperuricaemia results from a renal defect in tubular uric acid secretion. An increased endogenous purine biosynthesis is observed in only 2% of all patients with gout. Secondary hyperuricaemai results either from an increased breakdown of endogenous nucleic acids as in polycythaemia or from a decreased renal excretion of uric acid due to drug treatment, renal insufficiency or metabolic disturbances. Hyperuricaemia may be defined either in statistical terms from epidemiological studies of normal and gouty populations or from physicochemical properties of urate. Monosodium urate and uric acid are soluble in water to the extent of 6.32 mmol/l and 0.39 mmol/l respectively. In human plasma saturation of monosodium urate occurs at a concentration of about 0.42 mmol/l. The solubility of uric acid and urate in urine is more complicated as it is affected by changes in pH and salt concentration. Uricosuric drugs decrease serum uric acid concentration by enhancing the renal excretion of uric acid. Effects and side effects of uricosuric therapy are discussed.

摘要

在大多数原发性痛风患者中，高尿酸血症是由肾小管尿酸分泌的肾脏缺陷引起的。在所有痛风患者中，仅2%观察到内源性嘌呤生物合成增加。继发性高尿酸血症要么是由于内源性核酸分解增加（如在红细胞增多症中），要么是由于药物治疗、肾功能不全或代谢紊乱导致尿酸肾排泄减少。高尿酸血症可以根据正常人群和痛风人群的流行病学研究的统计学定义，也可以根据尿酸盐的物理化学性质来定义。尿酸钠和尿酸在水中的溶解度分别为6.32 mmol/L和0.39 mmol/L。在人体血浆中，尿酸钠的饱和度在浓度约为0.42 mmol/L时出现。尿酸和尿酸盐在尿液中的溶解度更为复杂，因为它受pH值和盐浓度变化的影响。促尿酸排泄药物通过增强尿酸的肾排泄来降低血清尿酸浓度。讨论了促尿酸排泄疗法的作用和副作用。