Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 15 P57

Southend Hospital, Westcliff on Sea, UK.


A 79-year-old lady presented with a 6 months history of confusion and slurred speech and was found to have recurrent spontaneous hypoglycaemia (plasma glucose 1.3, 1.8 and 2.6 mmol/l). Pituitary and adrenal function were normal, and raised insulin (102 pmol/l) and C-peptide (630 pmol/l) levels confirmed the diagnosis of insulinoma, which was identified as a solitary 2 cm mass in the head of pancreas. Treatment with diazoxide 100–150 mg tds led to normalisation of glucose levels. She then became unwell with vomiting and pyrexia, was found to have septicaemia due to Proteus mirabilis infection which was treated with co-amoxiclav. When ill she became markedly hyperglycaemic (glucose 17–22 mmol/l); diazoxide was stopped, but the hyperglycaemia progressed to ketoacidosis (glucose 18–25 mmol/l, urinary ketones 3+, pH 7.35, base excess −6.7 mmol/l indicating a compensated metabolic acidosis). She was treated with intravenous insulin (40 units per day) and IV fluids, and recovered over 5 days. Hypoglycaemia recurred prior to resection of the insulinoma; insulin immunohistochemistry was positive, and there was no evidence of tumour necrosis. Following surgery the fasting plasma glucose was 6 mmol/l.

This patient presented with hypoglycaemia due to an insulinoma but developed marked hyperglycaemia and ketoacidosis when she became unwell. It is unlikely that the hyperglycaemia was due to diazoxide as it persisted and progressed several days after stopping diazoxide (half-life 28 h). It is recognised that autonomous insulin secretion leads to suppression of insulin production from normal beta cells.

This case demonstrates that autonomous insulin secretion from an insulinoma may be insufficient to maintain normal glucose levels when acute illness increases insulin resistance, and that hyperglycaemic ketoacidosis may develop as a result. We conclude that, paradoxically, insulinoma can produce hyperglycaemia in severe illness, because the autonomous insulin production is insufficient for the stress-induced rise in insulin requirements.

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