Danazol and plasma lipoprotein metabolism
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Danazol's effects on hepatic lipase, LDL receptor function, and lecithin:cholesterol acyl-transferase activity may influence lipoprotein metabolism, while also decreasing fibrinogen, lipoprotein (a), and promoting fibrinolysis, thereby inhibiting thrombosis.
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Abstract
The potential long-term impact of danazol on coronary risk hinges on its effect on lipoprotein metabolism rather than its influence on total plasma lipids. Danazol may exert a regulatory influence on three key processes in lipoprotein metabolism: hepatic lipase activity; low-density lipoprotein receptor function; and lecithin:cholesterol acyl-transferase activity. Danazol decreases plasma fibrinogen and lipoprotein (a) levels, promotes fibrinolysis and causes a rise in plasminogen. Such changes are beneficial as they inhibit the process of thrombosis. Androgenic properties of danazol produce effects of plasma lipids and lipoproteins which oppose estrogen-induced changes. The usual recipients of danazol therapy are premenopausal females, in whom the absolute risk of ischemic heart disease is low. If the drug were shown to increase ischemic heart disease risk, detrimental factors must be weighted against its considerable and proven clinical benefits.
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Cites (3)
- Profound alterations of the lipoprotein metabolism during danazol treatment in premenopausal women 1984
- Cholesterol fractions and apolipoproteins during endometriosis treatment by a gonadotrophin releasing hormone (GnRH) agonist implant or by danazol 1991
- Lipoprotein Lp(a) levels are reduced by danazol, an anabolic steroid 1992
Cited by (3)
References (17)
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Cited by (3)
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