Endocrine Abstracts

Introduction: Postpartum necrosis of the anterior pituitary gland is well-described, but antepartum pituitary insufficiency (API) is reported only in a few women with type 1 diabetes (T1D). API has an abrupt onset and may have fatal outcome.

Case report: A 36-year-old woman with T1D and laser-treated retinopathy became pregnant after repeated IVF. In gestational week (GW) 10, she used insulin 34–42 U/day, HbA1c was 6.2% and cortisol (0800 h) was 664 nmol/l. In GW 34, she was hospitalized with intense headache and vomiting. On admission, plasma glucose was 2.6 mmol/l. Neurological examination, CSF and cerebral MRI, were normal. She had no sign of preeclampsia. Insulin doses were reduced. At 0800 h. cortisol was 144 nmol/l, ACTH <1.1 pmol/l, prolactin 285 mU/l, GH 1.5 mU/l, indicating pituitary failure. She was treated with i.v. glucose and hydrocortisone. An emergency Caesarean section was performed, without excessive haemorrhage. She was nomotensive. The newborn’s weight was 2610 g and Apgar score 9 (1 min). Three days postpartum (PP) pituitary MRI was normal. She was unable to breastfeed. Two months PP, insulin tolerance test (ITT) showed subnormal cortisol and ACTH responses (436 nmol/l and 2.8 pmol/l, respectively). Despite substantial reduction in insulin dose and low-dose cortisol replacement, she experienced frequent hypoglycaemias without warning. Repeated MRI at three months PP revealed reduced contrast uptake in the pituitary consistent with necrosis. ITT after 2 years showed subnormal responses of both cortisol (peak 468 nmol/l) and GH (peak 4.5 mU/l). GH replacement improved her hypoglycaemia awareness and her general well-being.

Conclusion: The hypertrophied pituitary of late pregnancy may be vulnerable to infarction and necrosis. We speculate whether repeated ovarian stimulation together with microvascular diabetic complications may have increased the vulnerability to thromboembolism and subsequent pituitary infarction in this woman with API.