“an Atypical Presentation of Adrenal Insufficiency in Pregnancy As Recurrent Abdominal Pain”

Presentation Number: SAT-0764
Date of Presentation: June 21st, 2014

Muhammad A Mahmood*1 and Christine Irene Oakley2
1Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, 2Joan C. Edwards School of Medicine Marshall university, Huntington, WV


Objective: To describe an unusual case of adrenal insufficiency (AI) in pregnancy.

Clinical Case: A 26 year-old G1P0 female with microprolactinoma, currently off medical therapy, presented at 32 weeks gestation with sudden onset sharp right upper quadrant (RUQ) pain associated with malaise and vomiting. She was afebrile and normotensive, with mild RUQ tenderness. Laboratory evaluation was unremarkable except leukocytosis. Abdominal ultrasonography was normal. CT scan of abdomen showed a 4.2 x 3.1 cm right adrenal mass likely representing hemorrhage and normal left adrenal. Endocrinology was consulted. Patient recalled that her father underwent adrenalectomy for unknown reason.  Plasma metanephrines and normetanephrines were normal. MRI two days later demonstrated stability of adrenal mass and changes consistent with hemorrhage. Her hematocrit was stable. She was discharged, but readmitted four days later with recurrence of abdominal pain more so on left, associated with nausea and fatigue. Vitals were stable and laboratory evaluation unremarkable. Repeat MRI showed stability of right adrenal mass. A morning serum cortisol was 7.2ug/dL (>21ug/dL normal in 3rd trimester). Cosyntropin (250ug) stimulation showed baseline cortisol of 7.5ug/dL, 8.2ug/dL at 30 minutes, and 7.7ug/dL at 60 minutes indicative of AI. Serum ACTH was 286.4pg/mL (normal:7.2-63.3pg/mL). Twenty-one hydroxylase antibodies were ordered, but specimen lost. The patient started hydrocortisone 20mg in the morning and 10mg in the afternoon leading to resolution of her symptoms. She delivered a healthy baby at 37 weeks gestation via elective Cesarean section. She was lost to endocrine follow-up. 

Discussion/Conclusion: With a reported incidence of 1/3,000 (1), the diagnosis of AI in pregnancy should be entertained in those with significant malaise and emesis beyond the 1st trimester, or in those with symptoms of weight loss, salt craving, orthostatic hypotension, hypoglycemia, or electrolyte abnormalities. Primary AI manifests when more than 90% of each adrenal gland is destroyed (2) making primary AI from adrenal hemorrhage unlikely in our case, and autoimmune disease more likely.  As cortisol binding globulin levels rise in pregnancy, levels of serum cortisol should be higher, leading to higher diagnostic cutoffs (3). Recognition of AI is vital to prevent maternal adrenal crisis, IUGR and fetal demise (3).


Nothing to Disclose: MAM, CIO