A 30-year-old woman with long standing type 1 diabetes presented with recurrent severe hypoglycaemia. One month earlier she had given birth to her first child. Before pregnancy her HbA1c had been 7.8 to 9.2 percent (RR 3.1 to 5.0 percent) but improved by the third trimester to 6.8 percent. Before pregnancy her total daily insulin dose was 50 units and by the third trimester it had only increased by 25 percent to 60 units. The pregnancy and birth were uneventful with no hypoglycaemia or post-partum bleeding although she failed lactate and has not menstruated. Despite a significant reduction in insulin dosage she suffered recurrent severe hypoglycaemia and at presentation was taking a total of 6 units a day. She denied headaches or visual disturbance. Renal and liver function were normal and endomysial antibodies were negative. Baseline pituitary function tests were unremarkable including ACTH 29 nanograms per litre (RR 0 to 47) other than a low IGF-1 of 6.0 nanomoles per litre (RR 13 to 50). An insulin stress test demonstrated a sub-optimal response to hypoglycaemia with a peak cortisol of 305 nanomoles per litre and peak growth hormone of 3.9 milliunits per litre. After commencing hydrocortisone (20mg 8am, 10mg 5pm) her blood glucose levels started to rise necessitating an increase in her insulin approaching pre-partum doses.
We believe that lymphocytic hypophysitis is the most likely diagnosis (MRI awaited) due to its predilection for women in the post-partum period and its relationship with other autoimmune diseases. This case of hypophysitis is dominated by ACTH deficiency but even with the commencement of hydrocortisone her insulin requirements have yet to return to pre-partum levels. We surmise this is due to her, as yet, untreated growth hormone deficiency.
22 - 24 Mar 2004
British Endocrine Societies