Gröbner Wolfgang
Kreisklinik Wertingen.
Dtsch Med Wochenschr. 2015 Oct;140(21):1615-26. doi: 10.1055/s-0041-104420. Epub 2015 Oct 21.
In most cases (98-99 %) primary hyperuricemia is caused by impaired renal excretion of uric acid. Overproduction of uric acid is rare. Secondary hyperuricemia has to be differentiated from primary forms. Clinical manifestations of hyperuricemia are acute inflammatory arthritis, tenosynovitis, bursitis, chronic arthropathy and accumulation of urate crystals in the form of tophaceous deposits. In addition renal complications can occur. Pathophysiology and diagnosis of gout were described. Treatment of gout has two goals: Treatment of the acute gout attack, to terminate pain and disability and treatment of hyperuricemia by lifestyle modification and with urate lowering drugs. A serum uric acid value below 6 mg/dl (360 µmol/L) should be achieved.
在大多数情况下(98 - 99%),原发性高尿酸血症是由尿酸肾排泄受损引起的。尿酸生成过多的情况很少见。继发性高尿酸血症必须与原发性类型相鉴别。高尿酸血症的临床表现为急性炎症性关节炎、腱鞘炎、滑囊炎、慢性关节病以及痛风石沉积形式的尿酸盐结晶积聚。此外,还可能出现肾脏并发症。文中描述了痛风的病理生理学和诊断方法。痛风的治疗有两个目标:治疗急性痛风发作,以终止疼痛和功能障碍;通过生活方式改变和使用降尿酸药物治疗高尿酸血症。应使血清尿酸值低于6mg/dl(360µmol/L)。