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Barry L. Carter, Michael E. Ernst, Thiazide-Induced Hyperglycemia: Can It Be Prevented?, American Journal of Hypertension, Volume 22, Issue 5, May 2009, Page 473, https://doi.org/10.1038/ajh.2009.48
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Thiazide-type diuretics are a cornerstone of antihypertensive therapy but the development of new onset diabetes following the administration of thiazides has generated extensive controversy. There has been a call for research in the prevention of thiazide-induced hyperglycemia by the National Heart, Lung and Blood Institute.1 Individualized therapy to improve therapeutic response or reduce harm is the “holy grail” of applied pharmacotherapy. In this regard, identification of patients at higher risk for thiazide-induced hyperglycemia could lead to safer use of these agents.
Bozkurt and colleagues have increased our understanding of this area with a nested case–control genetic study in patients taking thiazides.2 They report increased risk of diabetes with several polymorphisms, especially carriers of the ACE4656 GG genotype. The effect was only significant with higher dosages of thiazides, lending credibility to the findings. They used a defined daily dose equivalent of 25 mg for both hydrochlorthiazide and chlorthalidone. However, as the authors note, chlorthalidone is twice as potent as hydrochlorothiazide so one might suspect that the effect would be greater with chlorthalidone. In fact, the authors found an adjusted odds ratio of 1.79 with chlorthalidone and 1.56 with hydrochlorothiazide, further supporting a dose-related effect. The fact that the risk for diabetes was much greater with the angiotensin-converting enzyme (ACE) GG genotype may help explain why studies have found heterogeneity in the development of diabetes.
