血管紧张素转换酶抑制作为巴特综合征的治疗原则。

Angiotensin-converting enzyme inhibition as a therapeutic principle in Bartter's syndrome.

作者信息

Jest P, Pedersen K E, Klitgaard N A, Thomsen N, Kjaer K, Simonsen E

机构信息

Department of Clinical Chemistry, Odense University Hospital, Denmark.

出版信息

Eur J Clin Pharmacol. 1991;41(4):303-5. doi: 10.1007/BF00314956.

DOI:10.1007/BF00314956

PMID:1804643

Abstract

The effect of captopril has been investigated in four patients with Bartter's syndrome treated for 12 weeks. Baseline biochemistry showed normal serum aldosterone (mean 347 pmol.l-1) and a mean serum renin of 217 mU-l-1, and a considerable increase in serum renin during captopril treatment. Serum aldosterone decreased gradually during the study period to about half its initial value. The patients presented with a mean serum potassium of 2.5 mmol.l-1, which rose to 3.4 mmol.l-1 on captopril. Lymphocytes showed a substantial captopril-induced increase in intracellular sodium (from 15 to 22.5 mmol.l-1 on average), but no change in the potassium content. Captopril was well-tolerated. It may be an alternative to potassium-sparing diuretics for maintaining normal serum potassium levels in patients with Bartter's syndrome.

摘要

已对4例巴特综合征患者使用卡托普利进行了为期12周的治疗，并对其疗效进行了研究。基线生化检查显示血清醛固酮正常（平均347 pmol·l⁻¹），血清肾素平均为217 mU·l⁻¹，且在卡托普利治疗期间血清肾素显著升高。在研究期间，血清醛固酮逐渐下降至初始值的一半左右。患者的血清钾平均为2.5 mmol·l⁻¹，使用卡托普利后升至3.4 mmol·l⁻¹。淋巴细胞显示卡托普利可使细胞内钠大量增加（平均从15 mmol·l⁻¹增至22.5 mmol·l⁻¹），但钾含量无变化。卡托普利耐受性良好。对于维持巴特综合征患者的正常血清钾水平，它可能是保钾利尿剂的一种替代药物。