ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2004) 7 P156

Metastatic glucagonoma transforming to an insulinoma

A Byard, S Rangan, A Dixon, K Kos, M Edavalath, HN Buch & BM Singh

The Diabetes Centre, New Cross Hospitals, The Royal Wolverhampton NHS Trust, Wolverhampton, UK.

Neuroendocrine tumours are uncommon and often present difficult therapeutic challenges. They may be composed of different cell types and are often multihormonal. We present the case of a 75 year-old man diagnosed to have a glucagonoma in 1995. He was deemed unfit for curative surgery and was managed medically including insulin therapy for control of hyperglycaemia. Over the next 7 years the patient became progressive more symptomatic due to increase in tumour size and hepatic metastases and he received five cycles of chemotherapy (carboplatin and etoposide) for palliation. 2 months later, the patient experienced several episodes of symptomatic hypoglycaemia, which persisted despite withdrawal of insulin. Biochemical assessment during one episode of hypoglycaemia (plasma glucose = 2.0 mmol/L) showed inappropriately elevated insulin, C-peptide and pro-insulin levels (values), and negative sulphonylurea screen confirming endogenous hyperinsulinaemia. Hypoglycaemia responded partially to octreotide and currently patient's hypoglycaemic symptoms are well controlled on monthly long acting octreotide although his overall condition is deteriorating due to increasing tumour load.

This patient presents an unusual scenario where a neuroendocrine tumour initially presented as a glucagonoma and subsequently the predominant hormone secretion changed to that of insulin. As this change was temporally associated with chemotherapy we postulate that following chemotherapy, one cell type was more successfully reduced as compared to others, resulting in a new predominance of the cell type, which secreted insulin

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