Malignant Somatostatinoma Presenting with Diabetic Ketoacidosis and Inhibitory Syndrome: Pathophysiologic Considerations

Theodoraki, Aikaterini; Khoo, Bernard; Hamda, Arif; Grillo, Frederica; Meyer, Tim; Bouloux, Pierre

doi:10.4158/ep10109.cr

Cited by 8 publications

(2 citation statements)

References 15 publications

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“…However, it is unclear whether the differential inhibition of insulin and diabetogenic hormones can explain the usual mild degree of hyperglycaemia and the rarity of ketoacidosis in patients with somatostatinoma. An "inhibitory syndrome" was reported in a malignant somatostatinoma, characterized by mild nonketonic hyperglycaemia, hyperchlorhydria, cholelithiasis, steatorrhoea, and weight loss [83]. In these tumours, the absence of ketoacidosis is thought to arise from the somatostatin-induced simultaneous suppression of the secretion of both insulin and glucagon.…”

Section: Somatostatinomamentioning

confidence: 99%

Diabetes and pancreatic neuroendocrine tumours: Which interplays, if any?

Gallo

Ruggeri

Muscogiuri³

et al. 2018

Cancer Treatment Reviews

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Pancreatic neuroendocrine tumours (PanNETs) represent an uncommon type of pancreatic neoplasm, whose incidence is increasing worldwide. As per exocrine pancreatic cancer, a relationship seems to exist between PanNETs and glycaemic alterations. Diabetes mellitus (DM) or impaired glucose tolerance often occurs in PanNET patients as a consequence of hormonal hypersecretion by the tumour, specifically affecting glucose metabolism, or due to tumour mass effects. On the other hand, pre-existing DM may represent a risk factor for developing PanNETs and is likely to worsen the prognosis of such patients. Moreover, the surgical and/or pharmacological treatment of the tumour itself may impair glucose tolerance, as well as antidiabetic therapies may impact tumour behaviour and patients outcome. Differently from exocrine pancreatic tumours, few data are available for PanNETs as yet on this issue. In the present review, the bidirectional association between glycaemic disorders and PanNETs has been extensively examined, since the co-existence of both diseases in the same individual represents a further challenge for the clinical management of PanNETs.

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Section: Somatostatinomamentioning

confidence: 99%

Diabetes and pancreatic neuroendocrine tumours: Which interplays, if any?

Gallo

Ruggeri

Muscogiuri³

et al. 2018

Cancer Treatment Reviews

View full text Add to dashboard Cite

show abstract

“…This should not, however, account for increased insulin and C-peptide secretion. Alternate effects of omeprazole on somatostatin or other antral peptides might alter glucagon or insulin secretion [18, 19] and may explain the observed effects on insulin or C-peptide secretion. In fact, a combination of effects might result in our observations.…”

Section: Discussionmentioning

confidence: 99%

Improved Diabetes Control and Pancreatic Function in a Type 2 Diabetic after Omeprazole Administration

Mefford¹,

Mefford²,

Burris³

2012

Case Reports in Endocrinology

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A 43-year-old man with type 2 diabetes, opposed to insulin use and poorly responsive to oral agents added sequentially over 6 years, was placed on 40 mg omeprazole twice daily. A linear decline in daily fasting blood glucose was observed over the first two-month treatment, and his hemoglobin A1c was reduced from 11.9% to 8.2%, then sustained at 8.1% after four months. Glucose, insulin, and C-peptide response to a 2-hour glucose tolerance test were consistently improved across this time period, and calculated beta-cell mass increased by 67%. We believe these responses are consistent with activation or neogenesis of pancreatic beta cells, possibly through a gastrin-mediated mechanism.

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Somatostatin-Producing Tumor

Komminoth

2015

Pancreatic Neuroendocrine Neoplasms

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Malignant Somatostatinoma Presenting with Diabetic Ketoacidosis and Inhibitory Syndrome: Pathophysiologic Considerations

Cited by 8 publications

References 15 publications

Diabetes and pancreatic neuroendocrine tumours: Which interplays, if any?

Diabetes and pancreatic neuroendocrine tumours: Which interplays, if any?

Improved Diabetes Control and Pancreatic Function in a Type 2 Diabetic after Omeprazole Administration

Somatostatin-Producing Tumor

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