Method of using dehydroepiandrosterone and dehydroepiandrosterone-sulfate as inhibitors of thrombuxane production and platelet aggregation

摘要

Treating human beings with pharmacological quantities of DHEA results in their blood having increased serum DHEA and DHEA-S and lower rates of platelet aggregation. Reducing the rate of platelet aggregation can significantly reduce the incidence of morbidity and mortality from vascular events such as myocardial infarction and stroke, as well as reduce the occurrence of restenosis following vascular interventions. The concentration of DHEA and DHEA-S in the blood and the pre-incubation time of DHEA and DHEA-S with the blood will affect its impact on platelet aggregation. Hence, prior treatment of patients who are at risk with DHEA may produce the most beneficial affects. In addition, treatment of blood with DHEA-S reduces thromboxane production. Thromboxane is produced after platelets are subjected to many different types of agonists and is responsible for recruiting other platelets to aggregate and form a thrombus; therefore, blocking the production of thromboxane will reduce or prevent platelet aggregation.