Abstract
Agonists of the estrogen receptor include estrogens and selective estrogen receptor
modulators (SERMs). Both types of compounds increase the risk for thrombosis in the
arterial and the venous tree. The magnitude of the effect is influenced by potency,
which depends on the type of compound and the dose. The particulars of the process
change in each territory. Atherosclerosis, which creates local inflammatory conditions,
may favor thrombogenesis in arteries. A direct effect of estrogen agonists is also
well endorsed at both arteries, as suggested from data with high-estrogenic contraceptives,
and veins. Dose reduction has been proved to be an effective strategy, but there is
debate on whether additional benefit may be attained beyond a certain threshold. Hormone
therapy and SERMs exhibit a lower potency estrogenic profile, but are mainly used
by older women, who have a baseline increased thrombogenic risk. When used as sole
agents, estrogens substantially reduce the increased risk (venous thrombosis) or may
even be neutral (coronary disease). SERMs exhibit a neutral profile for coronary disease
and possibly for stroke but not for venous thrombosis.
Keywords
contraceptive - estrogen - hormone therapy - SERM - thrombosis
