Acute Diabetes Insipidus Mediated by Vasopressinase After Placental Abruption

• Published in: The journal of clinical endocrinology and metabolism 2013-03, Vol.98 (3), p.881-886
• Main Authors: Wallia, Amisha, Bizhanova, Aigerim, Huang, Wenyu, Goldsmith, Susan L, Gossett, Dana R, Kopp, Peter
• Format: Article
• Language: English
• Subjects: Abruptio Placentae - blood; Abruptio Placentae - physiopathology; Acute Disease; Adult; Antidiuretic Agents - administration & dosage; Arginine Vasopressin - administration & dosage; Biological and medical sciences; Cesarean Section; Cystinyl Aminopeptidase - blood; Deamino Arginine Vasopressin - administration & dosage; Diabetes Insipidus - blood; Diabetes Insipidus - drug therapy; Diabetes Insipidus - etiology; Drug Resistance; Endocrinopathies; Feeding. Feeding behavior; Female; Fundamental and applied biological sciences. Psychology; HEK293 Cells; Humans; Hypothalamus. Hypophysis. Epiphysis (diseases); Medical sciences; Non tumoral diseases. Target tissue resistance. Benign neoplasms; Postpartum Period - blood; Postpartum Period - drug effects; Pregnancy; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Vertebrates: endocrinology
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jc.2012-3548

Context: Postpartum, diabetes insipidus (DI) can be part of Sheehan's syndrome or lymphocytic hypophysitis in combination with anterior pituitary hormone deficiencies. In contrast, acute onset of isolated DI in the postpartum period is unusual. Case Presentation: This patient presented at 33 weeks gestation with placental abruption, prompting a cesarean delivery of twins. Immediately after delivery, she developed severe DI. The DI could be controlled with the vasopressinase-resistant 1-deamino-8-D-arginine vasopressin (DDAVP), but not with arginine vasopressin (AVP), and it resolved within a few weeks. Objective: The aim of this study was to demonstrate that the postpartum DI in this patient was caused by the release of placental vasopressinase into the maternal bloodstream. Methods and Results: Cells were transiently transfected with the AVP receptor 2 (AVPR2) and treated with either AVP or DDAVP in the presence of the patient's serum collected postpartum or 10 weeks after delivery. The response to the different treatments was evaluated by measuring the activity of a cAMP-responsive firefly luciferase reporter construct. The in vitro studies demonstrate that the patient's postpartum serum disrupts activation of the AVPR2 by AVP, but not by the vasopressinase-resistant DDAVP. Conclusions: Placental abruption can rarely be associated with acute postpartum DI caused by release of placental vasopressinase into the bloodstream. This clinical entity must be considered in patients with placental abruption and when evaluating patients presenting with DI after delivery.