M Whitehead1. 1. King's Healthcare Trust, King's College Hospital, London, United Kingdom.
Abstract
OBJECTIVE: To consider whether the addition of a progestin or an androgen to estrogen replacement therapy (ERT) will modify the effects of the estrogen upon arterial disease risk. DESIGN: Review of selected literature. SETTING: Population studies, clinical trials, and laboratory investigations. PATIENTS: Postmenopausal women. INTERVENTIONS: Exogenous progestin or androgen in hormone replacement regimens. MAIN OUTCOME MEASURES: Lipids and lipoproteins, carbohydrate metabolism, prostaglandin and thromboxane metabolism, fibrinolysis and coagulation, fat distribution, and arterial tone. RESULTS: The favorable lipid and lipoprotein changes induced by estrogens are modified by progestin and androgen addition. Some of these modifications are potentially adverse (progestin lowering of high-density lipoprotein-2 cholesterol) but some are potentially beneficial (progestin lowering of triglycerides). Recent studies suggest that progestins may not reverse the estrogen-induced reduction in low-density lipoprotein cholesterol. The scant data upon the effects of androgens on lipid and lipoproteins suggest that the addition of T to the estrogen may block the rise in high-density lipoprotein cholesterol seen in women receiving estrogen alone. Because of a lack of appropriate data, it is this author's opinion that the clinical effects of progestin or T addition to ERT cannot be predicted at this time. Further studies are urgently needed to clarify how progestin or T addition modify estrogen effects upon carbohydrate, prostaglandin and thromboxane metabolism, upon fibrinolysis and coagulation, and upon arterial tone.
OBJECTIVE: To consider whether the addition of a progestin or an androgen to estrogen replacement therapy (ERT) will modify the effects of the estrogen upon arterial disease risk. DESIGN: Review of selected literature. SETTING: Population studies, clinical trials, and laboratory investigations. PATIENTS: Postmenopausal women. INTERVENTIONS: Exogenous progestin or androgen in hormone replacement regimens. MAIN OUTCOME MEASURES: Lipids and lipoproteins, carbohydrate metabolism, prostaglandin and thromboxane metabolism, fibrinolysis and coagulation, fat distribution, and arterial tone. RESULTS: The favorable lipid and lipoprotein changes induced by estrogens are modified by progestin and androgen addition. Some of these modifications are potentially adverse (progestin lowering of high-density lipoprotein-2 cholesterol) but some are potentially beneficial (progestin lowering of triglycerides). Recent studies suggest that progestins may not reverse the estrogen-induced reduction in low-density lipoprotein cholesterol. The scant data upon the effects of androgens on lipid and lipoproteins suggest that the addition of T to the estrogen may block the rise in high-density lipoprotein cholesterol seen in women receiving estrogen alone. Because of a lack of appropriate data, it is this author's opinion that the clinical effects of progestin or T addition to ERT cannot be predicted at this time. Further studies are urgently needed to clarify how progestin or T addition modify estrogen effects upon carbohydrate, prostaglandin and thromboxane metabolism, upon fibrinolysis and coagulation, and upon arterial tone.