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Diabetic ketoacidosis in acromegaly: a case study—somatostatin analogs adverse event or disease complication?

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ARTICLE DOWNLOAD

Diabetic ketoacidosis in acromegaly: a case study—somatostatin analogs adverse event or disease complication?

10$

Nunzia Prencipe, Fabio Bioletto, Chiara Bona, Filippo Gatti & Silvia Grottoli 

Introduction

Glucose alterations (diabetes mellitus/impaired glucose tolerance) occur in up to 56% of patients with acromegaly, due to insulin resistance caused by chronic exposure to high levels of growth hormone (GH). Indeed, chronic GH excess impairs insulin sensitivity, increases gluconeogenesis, reduces glucose uptake in adipose tissue and muscle and can alter pancreatic β cells function [1]. Diabetic ketoacidosis (DKA) has been described as a rare complication of acromegaly, resulting from a combination of insulin resistance and relative insulin deficiency. In addition, available therapies for acromegaly differently impact on glucose tolerance: in particular somatostatin analogs (SSA) can alter glucose homeostasis by reducing pancreatic insulin and glucagon secretion. Pasireotide, compared to first-generation SSA (octreotide and lanreotide), causes a greater glucose homeostasis impairment, due to its higher inhibition of incretins production and different affinity profile for somatostatin receptors (SSTRs) on pancreatic islet cells, as it shows higher affinity for SSTR5 (which is more expressed on insulin-producing beta-cells) and lower affinity for SSTR2 (which is more expressed on glucagon-producing alpha-cells) Fig. 1 [2]. However, to date, no clear cases of pasireotide-induced DKA have been described.

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Year 2020
Language English
Format PDF
DOI 10.1007/s00592-019-01437-z