Norby L, Flamenbaum W, Lentz R, Ramwell P
Lancet. 1976 Sep 18;2(7986):604-6. doi: 10.1016/s0140-6736(76)90669-3.
A young patient with Bartter's syndrome was treated for three months with 100 mg/kg/day of aspirin to inhibit prostaglandin synthesis. Clinical symptoms resolved and serum-potassium increased from 2-9 to 3-5 mmol/l. Urinary excretion and plasma concentration of prostaglandins E and F were significantly reduced during aspirin therapy. Plasma-renin activity declined from 85 to 20 ng/ml/h (normal 1-5-4 mg/ml/h) and hyperaldosteronism was corrected. These results suggest that overproduction of prostaglandins has a central role in the pathogenesis of Bartter's syndrome.
一名患有巴特综合征的年轻患者接受了为期三个月的阿司匹林治疗,剂量为100毫克/千克/天,以抑制前列腺素合成。临床症状得到缓解,血清钾从2.9毫摩尔/升升至3.5毫摩尔/升。在阿司匹林治疗期间,前列腺素E和F的尿排泄量及血浆浓度显著降低。血浆肾素活性从85纳克/毫升/小时降至20纳克/毫升/小时(正常范围为1.5 - 4纳克/毫升/小时),高醛固酮血症得到纠正。这些结果表明,前列腺素的过度产生在巴特综合征的发病机制中起核心作用。