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锂诱导的肾性尿崩症患者对1-去氨基-8-D-精氨酸加压素的正常血流动力学和凝血反应。前列腺素合成抑制剂(吲哚美辛)的治疗结果。

Normal hemodynamic and coagulation responses to 1-deamino-8-D-arginine vasopressin in a case of lithium-induced nephrogenic diabetes insipidus. Results of treatment by a prostaglandin synthesis inhibitor (indomethacin).

作者信息

Hober C, Vantyghem M C, Racadot A, Cappoen J P, Lefebvre J

机构信息

Service d'Endocrinologie et Métabolismes, C.H.U. Lille, France.

出版信息

Horm Res. 1992;37(4-5):190-5. doi: 10.1159/000182308.

Abstract

The effect of 1-deamino-8-D-arginine vasopressin (DDAVP) on mean arterial pressure, pulse rate (PR), plasma renin activity (PRA), plasma factor VIIIc and von Willebrand factor were studied in a case of persistent lithium-induced nephrogenic diabetes insipidus (LINDI). 20% decrease in MAP, 22% increase in PR, 100% in PRA, and release of coagulation factors (2- to 3-fold) were noticed after infusion of 0.3 micrograms/kg DDAVP. Urinary prostaglandin (PG) E2 were enhanced. The treatment of this LINDI by PG synthesis inhibitor (PSI) combined with a low osmotic diet (LOD) led to a 51% fall in urine volume, 57% in free water clearance and 75% in sodium clearance. Urinary osmolality rose by 42% but remained low, probably in part because of the LOD. Urinary PGE2 was about one fifth of the initial high value. The results argue for (1) an end-organ resistance to DDAVP confined to the kidneys in LINDI and (2) an effectiveness of indomethacin combined with an LOD.

摘要

在一例持续性锂诱导的肾性尿崩症(LINDI)患者中,研究了1-去氨基-8-D-精氨酸血管加压素(DDAVP)对平均动脉压、脉搏率(PR)、血浆肾素活性(PRA)、血浆凝血因子Ⅷc和血管性血友病因子的影响。输注0.3微克/千克DDAVP后,平均动脉压下降20%,脉搏率增加22%,血浆肾素活性增加100%,凝血因子释放(增加2至3倍)。尿前列腺素(PG)E2增加。用前列腺素合成抑制剂(PSI)联合低渗饮食(LOD)治疗该LINDI患者,尿量下降51%,自由水清除率下降57%,钠清除率下降75%。尿渗透压上升42%,但仍较低,可能部分是由于低渗饮食所致。尿PGE2约为初始高值的五分之一。结果表明:(1)在LINDI中,终末器官对DDAVP存在仅限于肾脏的抵抗;(2)吲哚美辛联合低渗饮食有效。

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