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Clin Nephrol
November 2011
Division of Nephrology, Hypertension and Endocrinology, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Disopyramide, an antiarrhythmic drug, has been reported to cause hypoglycemia; however, its mechanism of action remains unclear. Pre-existing factors that increase the concentration of the drug in the blood increase the risk of hypoglycemia. Furthermore, other factors can also increase the risk of hypoglycemia even when disopyramide levels are in the therapeutic range.
View Article and Find Full Text PDFDiabet Med
January 2009
Diabetes and Metabolic Disease Research Centre, Hidaka Hospital, Gunma, Japan.
Background: Disopyramide, an antiarrhythmia drug, has been reported to cause hypoglycaemia. Pre-existing factors that increase the concentration of the drug in the blood increase the risk of hypoglycaemia. Furthermore, other factors can also increase the risk of hypoglycaemia even when disopyramide levels are in the therapeutic range.
View Article and Find Full Text PDFAm J Physiol
August 1993
Department of Physiology, Faculty of Medicine, Kyoto University, Japan.
An antiarrhythmic agent, disopyramide, was found to enhance the insulin secretory capacity of Wistar rat pancreatic islets with a half-maximal concentration of 23.3 microM. Employing a patch-clamp technique, disopyramide was found to inhibit ATP-sensitive K+ (KATP) channel activity in rat pancreatic beta-cells in primary culture without altering the unitary conductance.
View Article and Find Full Text PDFAnn Pharmacother
April 1992
University of Southern California, San Diego.
Objective: To report a case of disopyramide-induced hypoglycemia and to discuss the observed inadequate adrenergic response in this patient. Risk factors, possible etiologies, and preventive measures are also discussed.
Data Sources: References from case reports and review articles as identified by MEDLINE.
Metabolism
February 1989
Department of Internal Medicine (II), School of Medicine, Kanazawa University, Japan.
The mechanism of disopyramide-induced hypoglycemia, a life-threatening complication in the antiarrhythmic drug treatment, is still controversial. To elucidate this, we have evaluated plasma insulin (IRI) and glucagon (IRG) responses in the pancreatic vein (PV) of the in situ pancreas as well as responses of plasma IRI, IRG, and glucose in the femoral artery (FA) to disopyramide phosphate administration in anesthetized dogs. First, infusion of disopyramide at a dose of 50 mg for ten minutes directly into the pancreatic artery, but not the vehicle, increased significantly plasma IRI concentration in the PV (P less than .
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