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Mechanism of disopyramide‐induced hypoglycaemia in a patient with Type 2 diabetes
Author(s) -
Negishi M.,
Shimomura K.,
Proks P.,
Mori M.,
Shimomura Y.
Publication year - 2009
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2008.02619.x
Subject(s) - disopyramide , medicine , glimepiride , diabetes mellitus , pharmacology , hypoglycemia , endocrinology , type 2 diabetes
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. It has been proposed that disopyramide‐induced hypoglycaemia is caused by inhibition of the pancreatic B‐cell K ATP channels. Case report We report a case of severe disopyramide‐induced hypoglycaemia in a 62‐year‐old woman with Type 2 diabetes taking low‐dose glimepiride treatment. She had not experienced hypoglycaemia prior to the start of disopyramide therapy. No further hypoglycaemic episodes occurred following withdrawal of disopyramide therapy. Functional study Current recordings of K ATP channels expressed in Xenopus oocytes showed that at their estimated therapeutic concentrations, disopyramide and glimepiride inhibited K ATP channels by about 50–60%. However, when both drugs were applied together, K ATP channels were almost completely closed (~95%). Such dramatic inhibition of K ATP channels is sufficient to cause B‐cell membrane depolarization and stimulate insulin secretion. Conclusions Disopyramide therapy is not recommended for patients treated with K ATP channel inhibitors.