Isolated Intact Ovarian Axis and Brugada Phenocopy in Postpartum Hypopituitarism with a Review of TSH Analysis

Program: Abstracts - Orals, Poster Previews, and Posters
Session: SAT 444-462-Hypopituitarism, Apoplexy, and other Pituitary Syndromes
Saturday, March 7, 2015: 1:00 PM-3:00 PM
Hall D-F, Neuroendocrinology (San Diego Convention Center)

Poster Board SAT-445
Yasmin Khan, MD and Diana Barb, MD
University of Florida, Gainesville, FL

The natural progression in the development of postpartum hypopituitarism is classically seen as a sequential loss of trophic hormones, with failure to lactate and amenorrhea being the earliest and most frequently observed clinical manifestation. We present a rare case of postpartum panhypopituitarism with preserved gonadal function, and review the interpretation of TSH levels and possible association with Brugada-type EKG pattern in this clinical setting.


A 23 year old female was hospitalized for recurrent pneumonia and longstanding fatigue.  Interestingly, she reported a history of Brugada syndrome with presyncope episodes and tachycardia. Her symptoms began after an uncomplicated spontaneous vaginal delivery 15 months prior.  She was unable to lactate, however had resumed regular menses and was started on Depo-Provera for contraception.  At the time of evaluation, she was actively menstruating and received her last Depo-Provera injection over 3 months prior. She endorsed malaise, cold intolerance, constipation and a 50 pound unintentional weight loss. She denied treatment with systemic or inhaled steroids, headaches or vision changes. On exam, she had low-grade fever, mild hypotension without tachycardia and no visual field deficits. EKG demonstrated a type 3 Brugada pattern. BMP showed mild hyponatremia and hypokalemia. CBC demonstrated mild anemia.

Further tests showed a low cortisol (<0.5 mcg/dL, n AM 7-22, PM 3-9) and mildly elevated TSH (5.6 mIU/L, n 0.27-4.2). Repeat paired AM cortisol and ACTH were decreased at 0.6 mcg/dL and 5 pg/ml (n 6-58), respectively. ACTH stimulation test confirmed adrenal insufficiency with a cortisol of 2.7 mcg/dL at 60 minutes.  She had significantly decreased FT4 (0.4 ng/dL, n 0.93-1.7), TT3 (51 ng/dL, n 80-200), IGF-1 (74 ng/mL, n 87-368) and prolactin (0.3 ng/mL, n 4.8-23.3) levels.  Gonadal axis was consistent with the follicular phase (LH 2.6 mIU/ml, n 2.4-12.6; FSH 5.4 mIU/ml, n 3.5-12.5; estradiol 67, n 13-166). MRI showed pituitary atrophy on a background of partial empty sella. Panhypopituitarism with preserved gonadal function was diagnosed, likely secondary to postpartum apoplexy. Transbronchial biopsy showed eosinophillic pneumonia. Her symptoms resolved after steroid and thyroid replacement.


While partial pituitary necrosis with preservation of some hormones have been described, there are very few reported cases of postpartum hypopituitarism with preserved ovarian axis in the literature to date. Intact menses in this condition can therefore be a misleading symptom. Paradoxically elevated TSH in pituitary disorders can also occasionally occur as an exaggerated response to TRH, but with secretion of biologically inactive isoforms. Lastly, Brugada phenocopy may be relevant in our patient with two reported cases of EKG normalization after treatment of adrenal crisis and hypothyroidism.

Nothing to Disclose: YK, DB

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