Comparative Tolerability of Sulphonylureas in Diabetes Mellitus
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Drug Safety 2000 Apr; 22 (4): 313-320 0114-5916/00/0004-0313/$20.00/0 © Adis International Limited. All rights reserved.
Comparative Tolerability of Sulphonylureas in Diabetes Mellitus Andrew D. B. Harrower Department of Medicine and Bracco House Diabetes Centre, Monklands Hospital, Airdrie, Lanarkshire, Scotland
Contents Abstract . . . . . . . . . . . . . . . . . . 1. Hypoglycaemia . . . . . . . . . . . . . . 2. Nonspecific Adverse Effects . . . . . . . 3. Specific Adverse Effects . . . . . . . . . . 3.1 Hyponatraemia . . . . . . . . . . . . 3.2 Flushing After Alcohol Consumption 4. Secondary Failure . . . . . . . . . . . . . 5. Ischaemic Heart Disease . . . . . . . . . 6. Effects on the Sulphonylurea Receptor . 7. Conclusions . . . . . . . . . . . . . . . . .
Abstract
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The sulphonylurea drugs have been the mainstay of oral treatment for patients with diabetes mellitus since they were introduced. In general, they are well tolerated, with a low incidence of adverse effects, although there are some differences between the drugs in the incidence of hypoglycaemia. Over the years, the drugs causing the most problems with hypoglycaemia have been chlorpropamide and glibenclamide (glyburide), although this is a potential problem with all sulphonylureas because of their action on the pancreatic β cell, stimulating insulin release. Other specific problems have been reported with chlorpropamide that occur only rarely, if at all, with other sulphonylureas. Hyponatraemia secondary to inappropriate antidiuretic hormone activity, and increased flushing following the ingestion of alcohol, have been well described. The progressive β cell failure with time results in eventual loss of efficacy, as these agents depend on a functioning β cell and are ineffective in the absence of insulin-producing capacity. Differences in this secondary failure rate have been reported, with chlorpropamide and gliclazide having lower failure rates than glibenclamide or glipizide. The reasons for this are unclear, but the more abnormal pattern of insulin release produced by glibenclamide may be partly responsible and, indeed, may explain the increased risk of hypoglycaemia with this agent. Previously reported increased mortality associated with tolbutamide therapy has not been substantiated, and more recent data have shown no incr
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