MOJ ISSN: 2475-5494 MOJWH

Women's Health
Case Report
Volume 5 Issue 6 - 2017
Gestational Diabetes Insipidus (Gdi) Associated with Pre-Eclampsia
Afsoon Razavi*, Muhammad Umair, Zehra Tekin and Issac Sachmechi
Department of medicine, Icahn School of Medicine at Mount Sinai/NYC Health+ Hospital/Queens, USA
Received: July 25, 2017 | Published: August 16, 2017
*Corresponding author: Afsoon Razavi, MD, Department of Medicine, Icahn School of Medicine at Mount Sinai/NYC Health + Hospital/Queens, Diabetes center, 4th floor, Suit P-432, Pavilion building, Queens hospital center, 82-68 164th street, Jamaica, New York, 11432, USA, Tel: +8183843165; Email:
Citation: Razavi A, Umair M, Tekin Z, Sachmechi I (2017) Gestational Diabetes Insipidus (GDI) Associated with Pre-Eclampsia. MOJ Womens Health 5(6): 00139. DOI: 10.15406/mojwh.2017.05.00139

Abstract

Gestational diabetes insipidus (GDI) is a rare complication of pregnancy, usually developing in the third trimester and remitting spontaneously 4-6 weeks post-partum. It is mainly caused by excessive vasopressinase activity, an enzyme expressed by placental trophoblasts which metabolizes arginine vasopressin (AVP). The treatment requires desmopressin. A 38 year old G3P0A2 women with no significant medical history was admitted to obstetrical service on 36th week of gestation due to significant malaise, anorexia, nausea, vomiting, polyuria, nocturia, and polydipsia, worsening in the 2 weeks prior to presentation. Physical examination demonstrated decreased skin turgor, hyperactive tendon reflexes and no pedal edema, and her blood pressure was 170/100 mmHg, heart rate 67 beats/min and weight 60kg (BMI 23.1kg/m2). Her laboratory results a month prior to admission showed normal basic metabolic panel and liver function tests. On admission she found to have urine osmolality112 mOsmol/kg (350-1000); serum osmolality 308mOsmol/kg (278-295); Urinalysis revealed specific gravity less than 1005 with proteinuria. serum sodium 151 mmol/L (135-145); potassium 4.1 mmol/L (3.5-5.0); Cl 128 mmol/L, urea 2.2 mmol/L (2.5-6.7), creatinine 1.4 mg/dL, Bilirubin 1.3 mg/dL, AST 1270 U/L, alkaline phosphatase, 717 U/L, uric acid 10.1 mg/dL and INR 1.1. Full blood count was within the normal reference range. Patient underwent into emergent C-section a few hours after admission due to fetal distress. Post operatively patient remained polyuric and polydipsic. She was given DDAVP as needed for two weeks. A fetus was delivered at the 36th week without major problems. Two weeks post-partum the patient stopped the DDAVP. At 4 weeks post-partum, her sodium, serum and urine osmolality were within the normal reference range, and she no longer suffered from polyuria, polydipsia or nocturia. She remains clinically well.

Keywords: Nocturia; Polydipsia; Polyuria; Apgar; Eclampsia; Pre-eclampsia

Abbreviations

GDI: Gestational Diabetes Insipidus; AVP: Arginine Vasopressin; ADH: Antidiuretic Hormone; DDAVP: Deamino-8-D-arginin Vasopressin; NICU: Neonatal Intensive Care Unit; G3P0A2: Gravid3 Para0 Abortion2; HELLP syndrome: Hemolysis, elevated Liver enzymes, Low Platelets

Introduction

Gestational DI occurs only during pregnancy and the postpartum period. During pregnancy, women produce vasopressinase in the placenta, which breaks down antidiuretic hormone (ADH). GDI is thought to occur with excessive production and or impaired clearance of vasopressinase. Most cases of GDI can be treated with desmopressin, deamino- 8-D-arginine vasopressin (DDAVP), but not vasopressin. Diabetes insipidus is also associated with some serious diseases of pregnancy, including pre-eclampsia, HELLP syndrome and acute fatty liver of pregnancy. These cause DI by impairing hepatic clearance of circulating vasopressinase [1]. It is important to consider these diseases if a woman presents with diabetes insipidus in pregnancy, because their treatments require delivery of the baby before the disease will improve. Failure to treat these diseases promptly can lead to maternal or perinatal mortality.

Case Presentation

A 38 year old G3P0A2 women with no significant medical history and uneventful prenatal course was admitted to obstetrical service on 36th week of singleton gestation due to significant malaise, anorexia, nausea, vomiting, polyuria (around 9l/day), nocturia, and polydipsia, worsening in the 2 weeks prior to presentation. Her past medical history was unremarkable, she denied alcohol intake or smoking, and she was not taking any medication. There was no family history of endocrinopathy or liver disease. Physical examination demonstrated decreased skin turgor, hyperactive tendon reflexes and no pedal edema, and her blood pressure was 170/100 mmHg, heart rate 67 beats/min and weight 60kg (BMI 23.1kg/m2). In view of elevated blood pressure she was suspected to have pre-eclampsia and given MgSO4. Her laboratory results a month prior to admission showed normal basic metabolic panel and liver function tests. On admission she found to have urine osmolality112 mOsmol/kg (350-1000); serum osmolality 308mOsmol/kg (278-295); Urinalysis revealed specific gravity less than 1005 with proteinuria. serum sodium 151 mmol/L (135-145); potassium 4.1 mmol/L (3.5-5.0); Cl 128 mmol/L, urea 2.2 mmol/L (2.5-6.7), creatinine 1.4 mg/dL, Bilirubin 1.3 mg/dL, AST 1270 U/L, alkaline phosphatase, 717 U/L, uric acid 10.1 mg/dL and INR 1.1. Full blood count was within the normal reference range.

The 24-h urine output prior to desmopressin was 9000 ml/24. Considering the risk of dehydration in pregnancy, a water deprivation test was not performed. Patient underwent into emergent C-section a few hours after admission due to fetal distress. Post operatively patient remained polyuric and polydipsic. She was given DDAVP as needed for two weeks in different routes of administration with a significant response. More than 50% decrease in urine output was noted, as well as an increase in urine specific gravity. A male fetus with a 1-min Apgar score of 9 was delivered at the 36th week; he was transferred to NICU due to premature birth. Two weeks post-partum the patient stopped her DDAVP. At 4 weeks post-partum, her sodium, serum and urine osmolality were within the normal reference range, and she no longer suffered from polyuria, polydipsia or nocturia. She remains clinically well.

Discussion

Gestational DI is a rare complication of pregnancy occurring in two to four out of 100, 000 pregnancies [2,3]. It usually develops at the end of second or third trimester of pregnancy and remits spontaneously 4-6 weeks after delivery [3,4]. Symptoms include hypotonic polyuria, polydipsia, fatigue, weight loss, decreased skin turgor and nausea, which usually develop over a few days, and may worsen in the subsequent days or weeks if this condition is not properly identified and treated [1,5]. Its pathophysiology is thought to result from increased degradation of arginine vasopressin (AVP) by a placental enzyme called vasopressinase. Vasopressinase is a cysteine aminopepdase of molecular weight 330 kDa, and is produced by the placental trophoblasts during pregnancy [6]. Throughout pregnancy, vasopressinase levels increase by 100,000 fold while placental mass grows, Serum concentrations can be detected as early as the 7th week of gestation, reaching the maximum around the 40th week, and are usually undetectable around the 6th week postpartum [7]. Being synthesized from the placenta, higher enzyme concentrations were observed in twin and triple pregnancies. After placental expulsion during delivery enzyme levels decrease rapidly, but remains elevated in the blood for couple of weeks postpartum.

There are substantial physiologic changes that occur during pregnancy to increase intravascular volume, including reduction of set point for serum osmolality for AVP hormone secretion and increased thirst in response to lower serum concentrations. In most of the pregnancies increased secretion of AVP by four fold maintains water balance despite increased degradation by vasopressinase, while pregnancy may unmask pre-existing Central or Nephrogenic Diabetes Insipidus, or lead to GDI which is more commonly seen in multiple gestations due to increased vasopressinase production from trophoblastic mass or with syndromes of hepatic dysfunction (e.g., HELLP syndrome, pre-eclampsia and eclampsia) due to impaired metabolism of vasopressinase by liver [8]. Affected individuals can be treated with DDAVP which is the vasopressinase resistant, synthetic form of AVP.

References

  1. Kalelioglu I, Kubat Uzum A, Yildirim A, Ozkan T, Gungor F, et al. (2007) Transient gestational diabetes insipidus diagnosed in successive pregnancies: review of pathophysiology. Pituitary 10(1): 87-93.
  2. Ananthakrishnan S (2009) Diabetes insipidus in pregnancy: etiology, evaluation, and management. Endocr Pract 15(4): 377–382.
  3. Wallia A, Bizhanova A, Huang W, Goldsmith SL, Gossett DR (2013) Acute diabetes insipidus mediated by vasopressinase a er placental abrupon. J Clin Endocrinol Metab 98(3): 881-886.
  4. Bellastella A, Bizzarro A, Colella C, Bellastella G, Sinisi A, et al. (2012) Subclinical diabetes insipidus. Best Pracce & Research. Clinical Endocrinology & Metabolism 26(4): 471-483.
  5. Gambito R, Chan M, Sheta M, Ramirez-Arao P, Gurm H, et al. (2012) Gestational diabetes insipidus associated with HELLP syndrome: a case report. Case Rep Nephrol 2012: 640365.
  6. Gordge MP, Williams DJ, Huggett NJ, Payne NN, Neild GH (1995) Loss of biological activity of arginine vasopressin during its degradation by vasopressinase from pregnancy serum. Clin Endocrinol (Oxf) 42(1): 51-58.
  7. Davison JM, Sheills EA, Barron WM, Robinson AG, Lindheimer MD (1989) Changes in the metabolic clearance of vasopressin and in plasma vasopressinase throughout human pregnancy. J Clin Invest 83(4): 1313-1318.
  8. Krege JH, Katz VL (1990) A proposed relationship between vasopressinase altered vasopressin and preeclampsia. Med Hypotheses 31(4): 283-287.
Scholar Awards

At MedCrave we believe that knowledge should be shared. We also believe that   Read more...

Paper of the Year

In regard to the novelty and excellence of the manuscript MedCrave Group (MCG)   Read more...

Financial Support

MedCrave loves to recognize all the outstanding services delivered in the realms   Read more...

Sponsors

MedCrave accelerates the advancement of scientific research by convening   Read more...

MedCrave Reprints

MedCrave Group is ardent to provide article reprints at an instant affordable Read more...

© 2014-2017 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at http://medcraveonline.com
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy