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.
ABSTRACT 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: 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.Current Therapeutic Research 09/1992; 52(3):397-405. DOI:10.1016/S0011-393X(05)80414-X · 0.45 Impact Factor
- Progress in Cardiovascular Diseases 07/1993; 36(1):1-38. DOI:10.1016/0033-0620(93)90020-E · 2.44 Impact Factor
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ABSTRACT: Whether non-potassium-sparing diuretics (NPSD) increase the risk of sudden cardiac death in hypertensive patients has been vigorously debated. Diuretic-induced potassium or magnesium depletion leading to cardiac arrhythmias has been suggested as the underlying mechanism. A clear dose-response relationship between NPSD and the reduction in serum K+ exists. Data regarding serum Mg++ and intracellular K+ and Mg++ are too limited to allow conclusions. NPSD seem to increase the risk of ventricular arrhythmias among hypertensive patients with clinical evidence of heart disease, but the number of studies is small. The findings among patients without evidence of heart disease are less conclusive. The interpretation of the studies on electrolyte changes and arrhythmias following diuretic therapy is obscured by the fact that only a minority of studies included a randomly allocated placebo-treated control group. The large hypertension trials provide the strongest evidence that NPSD for hypertension may induce sudden death. Although blood pressure lowering may be expected to reduce the incidence of sudden cardiac death, the incidence in the NPSD group is similar to or even higher than that in the control group in 9 of 10 trials. We conclude that the beneficial effect of NPSD therapy for hypertension is partly offset by an excess risk of sudden death. Thus, alternative drugs, notably potassium-sparing diuretics or beta-blockers, could be preferred as antihypertensive drugs of first choice, although the efficacy of beta-blockers in older patients has recently been challenged.Drugs 06/1994; 47(5):711-33. DOI:10.2165/00003495-199447050-00002 · 4.13 Impact Factor