Hensen J, Dolz M, Oelkers W
Endokrinologische Abteilung, Medizinische Klinik, Universitätsklinikum Steglitz, Freie Universität Berlin.
Med Klin (Munich). 1991 Dec 15;86(12):623-8.
Two pregnant women developed overt polyuria (up to 11 l/day) and polydipsia during their second and third trimesters of pregnancy. In one patient hydronephrosis was present. Both patients suffered from mild gestational diabetes mellitus. Plasma sodium was 145 and 162 mmol/l. Polyuria and urinary hypo-osmolality responded well to desmopressin acetate. After delivery, polyuria and polydipsia disappeared in one patient and significantly improved in the other. Infusion of hypertonic saline one and two weeks respectively after delivery led to plasma hyper-osmolality (294 mosmol/kg and 305 mosmol/kg) without detectable stimulation of arginine vasopressin (AVP). Anterior pituitary function was normal. No stimulation of AVP occurred following insulin-induced hypoglycemia. AVP plasma disappearance after i.v. pulse injection of 1 microgram AVP as well as AVP plasma concentration after continuous infusion of 10 ng AVP/min was studied two weeks after delivery in one patient. The results suggested markedly elevated degradation of AVP compared to control subjects, probably due to an increased vasopressin activity. Eight months after delivery, hypertonic saline infusion in one patient led to a plasma-osmolality of 312 mosmol/kg without stimulation of AVP. In the second patient, AVP was not detectable (less than 0.2 pg/ml) six months after delivery when plasma osmolality was 290 mosmol/kg. Our studies demonstrate that a subclinical compensated diabetes insipidus was preexistent in both patients. Exacerbation occurred due to an increased AVP-clearance and presumably due to the hemodynamic and hormonal alterations during pregnancy, including a mild gestational diabetes mellitus.
两名孕妇在妊娠中期和晚期出现明显的多尿（每日尿量达11升）和烦渴。其中一名患者存在肾积水。两名患者均患有轻度妊娠期糖尿病。血浆钠浓度分别为145和162 mmol/L。多尿和低渗尿对醋酸去氨加压素反应良好。分娩后，一名患者的多尿和烦渴消失，另一名患者则明显改善。分娩后分别在第1周和第2周输注高渗盐水导致血浆高渗（294 mosmol/kg和305 mosmol/kg），但未检测到精氨酸血管加压素（AVP）受刺激。垂体前叶功能正常。胰岛素诱导的低血糖未刺激AVP分泌。对其中一名患者在分娩后2周研究了静脉注射1微克AVP后血浆AVP的消失情况以及持续输注10 ng AVP/min后的血浆AVP浓度。结果表明与对照组相比，AVP降解明显增加，可能是由于血管加压素活性增加所致。分娩后八个月，对一名患者输注高渗盐水导致血浆渗透压达312 mosmol/kg，未刺激AVP分泌。在第二名患者中，分娩后六个月血浆渗透压为290 mosmol/kg时未检测到AVP（低于0.2 pg/ml）。我们的研究表明，两名患者均预先存在亚临床代偿性尿崩症。病情加重是由于AVP清除增加，可能还由于妊娠期间的血流动力学和激素变化，包括轻度妊娠期糖尿病。
