Endocrine Abstracts

A 69-year-old man presented in a life threatening hypoglycaemic coma which following resuscitation required continuous intravenous dextrose to maintain euglycaemia. Random blood sugar was confirmed at 0.7 mmol/l. Past medical history included a large (19×14.5 cm) recurrent malignant fibrous tumour of the pleura which was resected in 1989 but recurred in 2006. At that time the tumour was thought not to be responsive to chemotherapy and radiotherapy and debulking surgery was deferred as the patient was asymptomatic. Renal, liver and thyroid function was normal. HbA1c was 5%. Synacthen test was normal. During a hypoglycaemic episode plasma levels of insulin (<1.0 pmol/l) and C-peptide (<1.0 pmol/l) were undetectable. IGF I and IGF II were 8.8 nmol/l and 76.7 nmol/l respectively resulting in an elevated IGF II/IGF I ratio of 8.7 (normal 3:1). Levels of big IGF II are awaited. Corticosteroid therapy (Prednisolone 40 mg daily) established euglycaemia. Attempts to reduce corticosteroid therapy resulted in hypoglycaemia. Debulking surgery is now being considered.

The findings were consistent with the diagnosis of non-islet cell tumour hypoglycaemia (NICTH) which was first reported by Doege and Potter in 1930. IGF II levels are elevated as is the ratio of IGF II–IGF I. IGF II is thought to bind and activate insulin receptors inducing hypoglycaemia. The form of IGF II secreted by non islet cell tumours implicated in hypoglycaemia has been widely reported as being of a larger molecular weight. Big IGF II demonstrates decreased binding to its serum binding proteins which may allow it to have a different activity profile at a given serum level compared to the usual form IGF II.

NICTH is a rare but important cause of hypoglycaemia complicating malignancy. This case illustrates that NICTH can be associated with hypoglycaemic coma and highlights the role for corticosteroids when more definitive treatment is being considered.