2020
DOI: 10.1002/ccr3.3017
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A case of insulinoma effectively treated with low‐dose diazoxide

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Cited by 7 publications
(5 citation statements)
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“…18 Diazoxide, a non-diuretic benzothiadiazine, increases plasma glucose levels by activating the opening of pancreatic ß-cell potassium channels, inhibiting insulin secretion via agonism of alpha-adrenergic receptors on pancreatic ß-cells and increasing hepatic gluconeogenesis. 19,20 For this dog to require exogenous insulin, the normal pancreatic ß-cells and the neoplastic insulinoma cells must have stopped producing and secreting insulin. This case likely experienced non-neoplastic ß-cell atrophy exacerbated by medicationinduced insulin resistance.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…18 Diazoxide, a non-diuretic benzothiadiazine, increases plasma glucose levels by activating the opening of pancreatic ß-cell potassium channels, inhibiting insulin secretion via agonism of alpha-adrenergic receptors on pancreatic ß-cells and increasing hepatic gluconeogenesis. 19,20 For this dog to require exogenous insulin, the normal pancreatic ß-cells and the neoplastic insulinoma cells must have stopped producing and secreting insulin. This case likely experienced non-neoplastic ß-cell atrophy exacerbated by medicationinduced insulin resistance.…”
Section: Discussionmentioning
confidence: 99%
“…In summary, glucocorticoid glucose regulation is achieved by promoting hepatic gluconeogenesis, decreased glucose uptake and utilisation from skeletal muscle and adipose tissue, and regulation of glycogen metabolism to increase hepatic storage 18 . Diazoxide, a non‐diuretic benzothiadiazine, increases plasma glucose levels by activating the opening of pancreatic ß‐cell potassium channels, inhibiting insulin secretion via agonism of alpha‐adrenergic receptors on pancreatic ß‐cells and increasing hepatic gluconeogenesis 19,20 . For this dog to require exogenous insulin, the normal pancreatic ß‐cells and the neoplastic insulinoma cells must have stopped producing and secreting insulin.…”
Section: Discussionmentioning
confidence: 99%
“…12 It also can be used safely and effectively, on a long term basis, when it cannot be localized or removed surgically and SSA represent a good alternative, specially used in patients who cannot undergo surgical intervention and when diazoxide is not recommended due to adverse effects or inefficacy. 12,[16][17][18] In cases of malignant insulinoma, SSA can also be considered first-line treatment because of their antiproliferative effect. Everolimus can be used for refractory hypoglycaemia and glucocorticoids are only used when better pharmacological options were not available.…”
Section: Discussionmentioning
confidence: 99%
“…Este es considerado como el medicamento inicial de elección para el tratamiento sintomático; en la mayoría de los pacientes ha sido usado por una corta duración, mientras se estudia la localización del tumor (73). Esta benzotiadiazina antihipertensiva actúa al inhibir la liberación de insulina mediante la apertura de los canales de potasio dependientes de ATP de las células beta pancreáticos (74), de esta forma promueve la glucogenólisis y aumenta la producción hepática de glucosa, con una efectividad de 47-50 %, administrada en 3-8 mg/kg/día en 2-3 dosis. Sus efectos secundarios son edema periférico (generalmente se añade un diurético), hirsutismo, trombocitopenia e insuficiencia renal (73).…”
Section: Diazóxidounclassified