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Glucose metabolism and calcium antagonists
1Medizinische Poliklinik, University of Bern, Switzerland.
Insights
Calcium channel blockers do not significantly impact glucose metabolism in hypertensive patients, whether diabetic or not. Long-term studies show no adverse effects on blood sugar control, making them a safe treatment option.
Area of Science:
- Cardiology
- Endocrinology
- Pharmacology
Background:
- Hypertension, diabetes mellitus, and glucose intolerance are key risk factors for cardiovascular disease.
- Antihypertensive medications should not negatively affect glucose homeostasis in any patient population.
Purpose of the Study:
- To evaluate the impact of calcium antagonists on glucose metabolism in hypertensive patients.
- To determine if calcium antagonists pose a risk to carbohydrate homeostasis in diabetic and non-diabetic individuals.
Main Methods:
- Review of over 100 short-term and long-term clinical trials involving calcium antagonists.
- Analysis of studies measuring glucose metabolism and glycated hemoglobin levels.
- In vitro pancreas perfusion experiments to assess insulin output.
Main Results:
- Most trials indicate calcium antagonists do not impair glucose metabolism at standard antihypertensive doses.
- Acute studies with high doses or glucose challenges yielded controversial results.
- 13 long-term trials (up to 5 years) showed no change in glycated hemoglobin.
Conclusions:
- Available data suggest calcium antagonists do not clinically relevantly alter glucose handling in non-diabetic or diabetic patients.
- Concerns regarding adverse effects on carbohydrate homeostasis are not justified.
- Benefits of calcium antagonists for hypertension can be utilized without fear of worsening glucose control.
Abstract:
High blood pressure, but also diabetes mellitus and even glucose intolerance are well known risk factors for premature cardiovascular morbidity and mortality. To counteract these sequelae, it is obvious that drug treatment of hypertension should not adversely affect the glucose homeostasis in nondiabetic as well as in diabetic patients. Therefore, the findings that calcium antagonists could dose-dependently throttle the insulin output after addition of glucose in pancreas perfusion experiments in vitro were of considerable concern. Within the last years, most of more than 100 short-term and long-term trials in diabetic and non-diabetic patients were able to show that different calcium antagonists at their "usual" antihypertensive dosages did not impair the glucose metabolism, whereas results of acute studies, especially with higher doses and after a glucose challenge, were more controversial. However, in all of the 13 long-term follow-up trials (up to 5 years) with determinations of the glycated hemoglobin published to date, this most relevant parameter remained unchanged. Thus, currently available data indicate that calcium antagonists do not alter glucose handling at a clinically relevant degree, both in non-diabetic or diabetic patients, so that it is not justified to withhold the benefits of these medications from hypertensives out of fear to introduce a deterioration in their carbohydrate homeostasis.