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Abstract
Introduction: Increased level of lipoprotein(a) (Lp(a)) constitutes an emerging, independent risk factor for coronary artery disease. Recently, it has been recommended to lower increased (> 50 mg/dl) Lp(a) concentration. Most lipid lowering agents – except niacin – have little or no effect whereas sex hormones significantly reduce Lp(a) level. The effect of sex hormones on Lp(a) level is related to the setting, the drug, the dose and the way of administration. Androgen esters, oral estrogens, alone or in combination with progestogens, and tibolone constantly decrease Lp(a) level, especially in postmenopausal women.
Areas covered: This paper reviews the pathophysiology, structure and metabolism of Lp(a). Clinical studies evaluating, in various settings, the effect of exogenous administration of androgens, estrogens – alone or in combination with progestogens – selective receptor estrogen modulators (SERMs), aromatase inhibitors (AIs) and tibolone on Lp(a) level are analyzed.
Expert opinion: The results obtained for SERMs are conflicting whereas AIs do not seem to reduce Lp(a) concentration. The effect of hormonal therapy on lipids is complex, depending on drugs and way of administration. Moreover, both androgens and estrogen could determine, in specific settings, severe adverse effects. These drugs are not currently recommended either for treatment of dyslipidemias with increased Lp(a) level or for the prevention of cardiovascular disease.
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