Critical Care Medicine-Endocrine Disorders>>>>>Pituitary
Question 4#

A 26-year-old, previously healthy, G1P0 female at 36 weeks gestational age comes to the emergency department due to polyuria, nocturia, and polydipsia. Her pulse is 78 beats/min, blood pressure 102/63 mm Hg, and weight 53 kg (BMI 22.6 kg/m2 ). Physical examination is normal except for decreased skin turgor and dry mucous membranes. Laboratory data reveal:

Serum ADH is 0.5 pg/mL (normal 1-5 pg/mL). MRI of her brain demonstrates no acute findings.

Which of the following statements best explains her symptoms?

A. Kidney disease affecting renal sensitivity to ADH
B. Ischemic insult decreasing release of ADH
C. Placental trophoblasts producing excessive vasopressinase
D. Autoimmune destruction of the pituitary

Correct Answer is C


Correct Answer: C

Gestational DI is a rare complication of pregnancy, occurring in about 1 in 30,000 pregnancies. It usually develops at the end of the second or third trimester of pregnancy and will resolve spontaneously 4 to 6 weeks after delivery. The pathophysiology of gestational DI is different from both central and nephrogenic DI; rather than a deficiency in ADH secretion or decreased ADH receptor sensitivity, gestational DI involves excessive vasopressinase activity. Vasopressinase is an enzyme expressed by placental trophoblasts during pregnancy, and it metabolizes ADH. The level of activity is proportional to the placental weight, explaining its higher activity in the third trimester or in multiple pregnancies. Vasopressinase is metabolized by the liver, and thus pregnant women with liver dysfunction, such as hemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome, acute fatty liver of pregnancy, hepatitis, and cirrhosis, have higher concentrations.

Patients with gestational DI should be treated with desmopressin, which is not metabolized by vasopressinase. Fluid restriction is not recommended in gestational DI as it can lead to significant dehydration and complications such as oligohydramnios and intrauterine growth restriction.


  1. Marques P, Gunawardana K, Grossman A. Transient diabetes insipidus in pregnancy. Endocrinol Diabetes Metab Case Rep. 2015;2015:150078.
  2. Rodrigo N, Hocking S. Transient diabetes insipidus in a post-partum woman with pre-eclampsia associated with residual placental vasopressinase activity. Endocrinol Diabetes Metab Case Rep. 2018;2018:18-52.