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Distinct mechanisms of hypoglycaemia in patients with somatostatin-secreting neuroendocrine tumours

Peter Wiesli, Vojtech Pavlicek, Michael Brändle, Thomas Pfammatter, Aurel Perren & Christoph Schmid

abstract

Introduction
Somatostatin-secreting neuroendocrine tumours may present with diabetes, cholelithiasis and steatorrhoea. In addition, hypoglycaemia has been associated with somatostatinomas. However, the mechanism of hypoglycaemia in patients with somatostatinomas has not been well characterized.

Methods
We describe two patients with recurrent neuroglycopenic episodes caused by somatostatin-secreting neuroendocrine tumours in the liver, detected by abdominal CTs and whole-body octreotide scintigraphy scans and confirmed by biopsy.

Results
Pancreatic islet hyperplasia and co-secretion of insulin (in addition to somatostatin) from tumour cells, respectively, have been characterized as completely distinct mechanisms of hypoglycaemia at both the functional and morphological levels in these two patients.

Conclusions
Hypoglycaemia may be caused by different mechanisms in patients with somatostatinomas.
   
citation Wiesli P, Pavlicek V, Brändle M, Pfammatter T, Perren A, Schmid C. Distinct mechanisms of hypoglycaemia in patients with somatostatin-secreting neuroendocrine tumours. Endocrinol Diabetes Metab 2019; 2:e00083.
   
type journal paper/review (English)
date of publishing 27-06-2019
journal title Endocrinol Diabetes Metab (2/4)
ISSN electronic 2398-9238
pages e00083
PubMed 31592116
DOI 10.1002/edm2.83