Adrenal dysfunction was not identified as a cause of hypoglycaemia in any of them. are rather non-specific, they may well be mistaken as those occurring from other disorders in patients suffering from severe co-morbidities. We encountered a rare case of a chronic haemodialysis patient with type 2 diabetes, alcoholic cirrhosis and pancreatitis, presenting as hypoglycaemic coma due to severe adrenal failure caused by ACTH deficiency. == Case report == A 62-year-old man was admitted in emergency in the early morning because he could not be awakened. His type 2 diabetes had been treated with insulin for 18 years. He had started haemodialysis for diabetic nephropathy 3 years previously and had been receiving regular haemodialysis three times a week. He also suffered from hypertension, alcoholic cirrhosis and chronic pancreatitis. During the last 15 months, with progressive appetite loss and fatigue, HbA1chad become lower with smaller amounts of insulin. Seven weeks previously, he had experienced hypoglycaemia and was treated with intravenous (iv) glucose. Insulin dosing was 4 U NovoRapidtwice a day at that time, which had been stopped since then. Upon arrival, the level of consciousness was Glasgow coma scale 14 (E4V4M6) without focal neurological deficit. He appeared malnourished (body mass index 16 kg/m2) without skin pigmentation. His body temperature was 33. 1C (on a warm June day), blood pressure (BP) 146/78 mm Hg, pulse rate 66/min, respiration rate 14/min, arterial pH 7. 383 and O2saturation 100% (with room air). The general laboratory data (Table 1) were compatible with the known morbidities of chronic renal failure, liver cirrhosis and chronic pancreatitis, except for hypoglycaemia and a lowered HbA1cfor a patient with diabetes. Ten grams of glucose was administered iv and, 30 min FLJ12894 later, capillary blood glucose (BG) was 5. 7 mmol/L, and he was fully conscious. However , he again became drowsy 1 h later when the BG was 2 . 8 mmol/L. He was admitted for further evaluation. == Table 1 . == Laboratory data AST, aspartate aminotransferase; ALT, alanine aminotransferase; LDH, lactate dehydrogenase; GTP, glutamyl transpeptidase. aThe patient was receiving 7500 U Epogenper week. bCortisol and ACTH were determined before breakfast on Day 2; other endocrine data were obtained at 1000 h on Day 7 when capillary blood glucose was 6. 2 mmol/L; cortisol was undetectable by radioimmunoassay (Immunotech) with the detection limit being 5. 5 nmol/L. The reference range for the endocrine data is indicated in the parentheses. Factitious, alcoholic and drug-induced hypoglycaemia were excluded by history. This was securely confirmed by information from his wife. The computerized tomography scan revealed no tumour in the abdomen. Cortisol was undetectable with a very low ACTH level (Table 1), which established 7-Methylguanosine a diagnosis of adrenal failure due to ACTH deficiency. Plasma renin activity and aldosterone level were within the normal range. Mild secondary hypogonadism and hyperprolactinaemia were also present (Table 1). The magnetic resonance imaging revealed no hypothalamic or pituitary 7-Methylguanosine abnormality, and serum antipituitary antibody [2] was negative. He was receiving 5 mg of amlodipine, and BP was 132 16/67 9 mm Hg (mean SD, n= 17) during Days 18. Upon diagnosing adrenal failure, 25 mg of oral hydrocortisone (10 mg, 10 mg and 5 mg after each meal, respectively) was 7-Methylguanosine started on Day 9, which promptly restored appetite and well-being. BP was 151 18/83 14 mm Hg (n= 15) during Days 916 with 5 mg of amlodipine, which was modestly higher than the values recorded before the treatment with hydrocortisone (P = 0. 005 for 7-Methylguanosine systolic BP and P < 0. 001 for diastolic BP, MannWhitneyU-test). Hypoglycaemia did not recur, and insulin was resumed on Day 11, because BG (mean SD from the premeal and the midnight values) for the preceding 2 days was 11. 8 2 . 2 mmol/L (n= 7) with 1800 kcal diet. == Discussion == In this patient, adrenal failure was due to ACTH deficiency, not due to Addisons 7-Methylguanosine disease, hence there was no skin pigmentation. Loss of appetite, general fatigue, malnutrition and previous hypoglycaemic events had been considered to be due alcoholic binge drinking, liver cirrhosis, chronic pancreatitis, renal failure or a combination thereof. Anaemia was not marked because he had been appropriately treated with erythropoietin. Above all, he was receiving an antihypertensive agent, amlodipine and hypertensive. This is very.