Endocrine Abstracts

A 32 year old female presented with recurrent episodes of severe hypoglycaemia. Type 1 diabetes had been diagnosed 10 years earlier and she had undergone subtotal colectomy/ileostomy 20 months earlier for chronic diarrhoea. Histology suggestive of eosinophilic colitis. High stoma output (>4 litres per 24 hours) was causing stomal incontinence with disruption of normal lifestyle. Treatment with combinations of loperamide, codeine, omeprazole and octreotide were ineffective. Examination revealed dehydration, sinus tachycardia 120 beats per minute and blood pressure 100/60 mmHg. Investigations confirmed AKI and metabolic acidosis: sodium 125 mmol/L, potassium 4.9 mmol/L, urea 28 mmol/L, creatinine 248 μmol/L, pH 7.25, bicarbonate 9.6 mmol/L, glucose 3.4 mmol/L, ketones 1.1. mmol/L and cortisol 714 nmol/L. The latter was not available to the admitting team who administered IV fluids plus hydrocortisone to cover possible adrenal suppression secondary to previous glucocorticoid treatment, with rapid correction of both AKI and metabolic acidosis. Further investigations revealed 09:00 hours cortisol 52 nmol/L and ACTH 8.9 ng/L. It was ascertained that morphine sulphate 10mg po was administered 6 hours prior to these investigations suggesting opiate induced hypoadrenalism. 09:00 hours cortisol 394 nmol/L and ACTH 65.6 ng/L off opiates. Pituitary function, PRA and aldosterone levels were normal. A cortisol level of 39 nmol/L coincidental with a blood glucose of 1 mmol/L was recorded on treatment with loperamide 8 mg tds. Treatment with high dose loperamide (14, 16, 32 and 16 mg daily) reduced stoma output to <1 litre/24 hours but resulted in cortisol levels of 32-68 nmol/L and ACTH 1.8-3.0 nmg/L on day profiles. Hydrocortisone at replacement doses was therefore commenced with dramatic improvement in her quality of life and resolution of hypoglycaemic episodes.