Effect of diuretics on the plasma lipid profile

Weidmann, P.; De Courten, M.; Ferrari, P. (1992). Effect of diuretics on the plasma lipid profile. European Heart Journal, 13(Suppl G), pp. 61-67. Oxford University Press 10.1093/eurheartj/13.suppl_G.61

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Hypertension, dyslipidaemia, glucose intolerance (associated with insulin resistance and compensatory hyperinsulinaemia) and other abnormalities are complementary coronary risk factors which often occur in association. A familial trait for essential hypertension seems to coexist commonly with defects in carbohydrate and lipoprotein metabolism which can be detected before the appearance of hypertension. Diabetes mellitus as well as obesity promotes the development of hypertension and dyslipidaemia. Moreover, certain drugs used for antihypertensive therapy can further modify lipoprotein and glucose metabolism.

Thiazides in high dosage and loop-diuretics can increase serum low-density-lipoprotein cholesterol (LDL-C) and/or verv-LDL-C and the total C/high-density lipoprotein cholesterol (HDL-C) ratio, while HDL-C is largely unchanged; triglycerides (Tg) are also often elevated. Premenopausal women may beprotected from this side effect. Whether diureticinduced dyslipidaemia is dose-dependent and low thiazide doses (i.e. hydrochlorothiazide ≤12·5 mg daily) are less active, awaits clarification. The diuretic-antihypertensive agent, indapamide, given at a dose of 2·5 mg. day−1, seems to exert no relevant effect on serum lipoprotein or glucose metabolism. The potassium-sparing diuretic, spironolactone, also may be largely neutral with regard to lipids. Moreover, potassium sparing diuretics may possibly counteract, at least in part, a dyslipidaemic influence of potassium-loosing diuretics in medium dose.

Drug-induced dyslipidaemia, as well as glucose intolerance, represent potentially adverse influences. In the hypertensive population, effective blood pressure control with traditional drug therapy based on thiazide-type diuretics in high dosage led to a distinct decrease in cerebrovascular morbidity and mortality, but a lesser decrease in coronary events. The prognostic relevance of drug-induced metabolic changes such as dyslipidaemia, altered insulin sensitivity, and glucose intolerance awaits further clarification. It is of clinical interest that several of the generally available antihypertensive drugs seem to be metabolically ‘neutral’ or sometimes perhaps even potentially beneficial with regard to the lipoprotein and glucose metabolism.

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