[Drug-induced hyperglycemia as a possible cardiovascular risk factor].

Several drugs are known to increase cardiovascular risk by altering the metabolism of glucose cholesterol and triglycerides. Several groups of drugs are described and theories about their metabolic effects are discussed. First diuretics such as thiazide diazoxide and loop diuretics are mentioned; different studies suggest that the induction of hyperglycemia is not directly related with the diuretic effect. Possible reasons could be induced hypo-insulinemia potassium depletion reflex catacholamines. Then estrogens and progestin are discussed. Although there are different beliefs regarding estrogens it is generally accepted that progestins have caused hyperglycemia even if to different degrees: levonorgestrel seems to be the most active. There is also a direct correlation with the duration of therapy. Even the low-dose triphasic oral contraceptives seem to be related to decreased glucose tolerance with prolonged use. Mechanisms indicated as responsible for these effects include steroid metabolism growth hormone effects and reduction of peripheral insulin receptors. A study indicates that after 10 years of continued oral contraceptive use the risk of myocardial infraction is 2.5 times that of the control. Natural and synthetic steroids are then analyzed; they enhance gluconeogenesis and decreasing cellular glucose intake in some peripheral tissues. Several studies discussing these mechanisms are quoted. Finally a brief review is given of beta-blockers clonidine prazosines phenitoine aspirin indomethacin neuroleptic and epinephrine.