The effect of thiazide therapy on glucose, insulin and cholesterol metabolism and of glucose on potassium: Results of a cross-sectional study in patients from the Hypertension Detection and Follow-up Program
Department of Medicine, University of Mississippi Medical Center, Jackson 39216-5405.Journal of Human Hypertension (Impact Factor: 2.7). 11/1990; 4(5):491-500.
Fasting and one hour post-glucose load blood samples were obtained from 497 participants in the Hypertension Detection and Follow-up Program (HDFP), 79.8% of whom were on antihypertensive therapy at the time of their five-year examination. Major findings include a positive correlation between glucose/insulin ratio and serum potassium (P = 0.0014) and a weaker negative correlation between fasting insulin and serum potassium (P = 0.004). These data are compatible with a primary effect of hypokalaemia producing insulin 'resistance'. In addition, the glucose load was followed by a mean reduction in serum potassium of 0.135 +/- 0.525 meq/l (P less than 0.001). Twenty percent of participants experienced a drop of more than 0.5 meq/l. Cholesterol was associated with the fasting glucose/insulin ratio (P less than 0.032). The results are compatible with the hypothesis that prevention of hypokalaemia may prevent certain metabolic effects attributed to thiazide.
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ABSTRACT: Treatment with thiazide diuretics causes impaired glucose tolerance, biochemical diabetes, and insulin resistance. The effect of diuretics on glucose tolerance is clearly dose-related. Spironolactone does not impair glucose tolerance, even at high dosage, but differences among other diuretics could be due to comparisons at doses that are not equal. Diuretic-induced changes in glucose metabolism are not conclusively related to altered potassium homeostasis, and impaired glucose tolerance occurs even when relatively low doses of thiazide are combined with potassium-sparing agents. The effects of diuretics on glucose homeostasis are in large part and probably entirely reversible. These disturbances of glucose metabolism have been detected only by detailed biochemical testing, and their clinical relevance is uncertain. In established diabetes, diuretics have a rapid and substantial adverse effect on metabolic control. In nondiabetic subjects, diuretics rarely cause or trigger a serious hyperosmolar nonketotic diabetic syndrome. Otherwise, it is not known whether the metabolic changes cause clinical diabetes or lead to microvascular complications in the long term. Evidence from large outcome trials suggests that biochemical diabetes, glucose intolerance, and insulin resistance do not increase the risk of coronary heart disease in treated hypertensive patients. Diuretics should be avoided in patients with diabetes unless their use is essential. Otherwise, a low dose of thiazide remains as excellent choice for first-line antihypertensive therapy. Dihydropyridine calcium antagonists, diltiazem, and verapamil appear to have no important effects on glucose homeostasis. There is very limited evidence that selective alpha-antagonists increase insulin sensitivity. The importance of metabolic differences between drug classes will be established only by comparative outcome trials with coronary events as the end point.
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ABSTRACT: A multicenter, randomized, double-blind, parallel-group trial was conducted to compare the effects of long-term treatment with lisinopril versus hydrochlorothiazide plus amiloride on lipids, glucose, uric acid, and electrolytes in patients with mild to moderate essential hypertension. After 6 months of treatment with hydrochlorothiazide 50 to 100 mg plus amiloride 5 to 10 mg or lisinopril 10 to 20 mg given once daily, the patients receiving the diuretics showed an increase in triglycerides, very-low-density lipoproteins, and apolipoproteins A and B, while the patients receiving lisinopril had only minimal changes in these parameters and an increase in high-density lipoproteins. Serum uric acid levels rose significantly in the group receiving diuretics but did not change in the lisinopril group. The antihypertensive effect was similar for both drug regimens. These data show that the long-acting angiotensin converting enzyme inhibitor lisinopril did not induce any metabolic effects and should be preferred, as a first choice, to antihypertensive drugs such as diuretics, which may cause lipid and uric acid metabolism disorders.
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