Endocrine Abstracts

A 27-years old man admitted unconscious due to severe hypoglycemia of 18 mg/dl with right-sided hemiparesis and hypotension. There was a several months history of tiredness and weight loss. Past medical history was remarkable for traumatic brain injury after unexplained syncope, primary hypothyroidism and an episode of hypoglycemia of 2 mmol/l with total improvement after iv infusion of glucose(five months previously). There was no history of drug or alcohol intake. He was on levothyroxine replacement therapy at the dosage of 75 mcg. He appeared lean (weight 58 kg, height 185 cm). There was no abnormal skin or mucosal pigmentation and secondary sexual characteristics were normal. His laboratory findings of TSH 20.35 μIU/l (0.2–4.2), free T4 3.7 ng/L (8.0–17.0), cortisol 2 ug/l (45–260) and plasma ACTH 1.7 ng/l (7.2–63.3) were consistent with adrenal insufficiency and uncompensated hypothyroidism. Abdominal CT-scan showed normal adrenal glands and cholelithiasis. During MRI of the brain pathology of the hypothalamus-pituitary region was excluded. He showed quick improvement after iv infusion of glucose and hydrocortisone with complete resolution of right-sided hemiparesis in two weeks. One month after he re-admitted for evaluation the hypothalamic-pituitary-adrenal axis. Basal morning hormone levels suggested secondary adrenal deficiency without other significant changes in pituitary and islet-cells function: cortisol <28 nmol/l (119–618), ACTH <1.1 pmol/l (0–10.2), TSH 15.5 μIU/l (0.4–4.0), free T4 18.6 pmol/l (11.5–23.2), insulin 11.6 mIU/l (5.0–25.0), C-peptid 0.73 nmol/l (0.5–2.5), LH 3.6 IU/l (0.6–12.0), FSH 7.28 IU/l (1.0–12.0), total testosterone 10.4 nmol/l (3–12), GH 0.4 μIU/l (0.16–13.0), IGF1 238 ng/ml (117–329), prolactin 548.6 mcIU/ml (40–390). After insulin-induced hypoglycemia there was an absence of cortisol and ACTH increase – cortisol remained <27.6 nmol/l (119–618) and ACTH <1.1 pmol/l (0–10.2) at the glucose level of 20 mg/dl on the 50th minute. There were no growth hormone changes of clinical significance in the test. These results confirmed isolated ACTH deficiency whereas hyperinsulinism and other causes of hypoglycemia and syncope were excluded. Patient discharged on hydrocortisone 25 mg and levothyroxine 100 mcg per day. During a year follow-up there were no episodes of hypoglycemia and fatigue.

Conclusion: This case shows the importance of timely investigation of episodes of hypoglycemia of unclear origin in patients with existent autoimmune disorders to exclude secondary adrenal insufficiency.