Studies on the mechanism of action of oral contraceptives with regard to fibrinolytic variables

Article Abstract:

There is an association between blood clot formation (thrombosis) and oral contraceptive use in women over the age of 35, especially those who smoke. Although reduced estrogen formulas have decreased the risk of thromboembolic disease, the risk still exists. Changes in blood clotting factors cause clots to form, dislodge and travel to block the flow of blood through the vessels. The defect is thought to involve the fibrinolytic system, which breaks up small blood clots. Oral contraceptives seem to promote changes that affect some of the proteins required during the normal process of fibrinolysis. However, some studies examining the effect of oral contraceptives on these proteins point to an increase in fibrinolytic activity, rather than a decrease as would be expected with cardiovascular disease. A model was created that used cultured endothelial cells derived from the lining inside human blood vessels to see the effect of sex hormones on the various components of the fibrinolytic system. Fibrinolytic activity is more dependent upon how much tissue plasminogen activator (t-PA) is circulating in the blood than the concentration of t-PA inhibitor. A decrease in t-PA should cause a decrease in fibrinolytic activity and thus an increase in undissolved clots. Indeed, oral contraceptives users have decreased levels of t-PA, despite a concomitant increase in t-PA inhibitor. Examination of the gene expression of t-PA indicates that there are hormone-dependent elements, particularly estrogen and progesterone, in the coding of the genes for t-PA, t-PA inhibitor and other variables involved in the fibrinolytic system. The amount of t-PA is also mediated by the number of hormone receptors, places on the surfaces of some cells that have a particular affinity for sex steroids. When endothelial cells were exposed to sex steroids in the laboratory, sex steroid hormone receptors were not found. Receptors for estrogen and androgens (male hormones), but not progesterone, were found on the surfaces of the cells derived from the liver, where plasminogen inhibitor is synthesized. Neither liver nor endothelial cells showed a change in t-PA or t-PA inhibitor production when they were exposed to sex steroids for three days. There is no evidence, on the basis of this model, that the sex hormones contained in oral contraceptives formulas affect the production of t-PA or t-PA inhibitor. It is possible that oral contraceptives increase the clearance of the proteins involved in fibrinolysis by increasing the number of cell receptors for a binding molecule that is under hormonal control. (Consumer Summary produced by Reliance Medical Information, Inc.)

Tissue plasminogen activator

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Effects of monophasic low-dose oral contraceptives on fibrin formation and resolution in young women

Article Abstract:

Use of monophasic, low-dose oral contraceptives does not appear to significantly alter the regulation of blood coagulation and fibrinolysis in healthy women. The coagulation and fibrinolysis systems control blood clotting, and their proper balance and their interaction with estrogen may play a role in preventing thromboembolism. Thromboembolism is the obstruction of a blood vessel by a blood clot. Of 34 healthy women who took low-dose estrogen oral contraceptives, 15 took a combination of ethinyl estradiol and desogestrel, and 19 took a combination of ethinyl estradiol and gestodene. There were no significant changes in the activation or balance of the coagulation and fibrinolytic systems in either group before and after initiating oral contraceptive use.

Blood clotting, Blood coagulation

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Effects of hormone replacement therapy on hemostatic cardiovascular risk factors

Article Abstract:

Hormone replacement therapy appears to lower certain cardiovascular risk factors. Researchers measured several different risk factors in blood samples from 90 postmenopausal women, 60 of whom took continuous or cyclic hormone replacement therapy. Hormone replacement therapy caused reductions in blood levels of fibrinogen, tissue-type plasminogen activator, plasminogen activator inhibitor-1 and lipoprotein(a). Elevated levels of these proteins are a risk factor for heart disease. This could explain how hormone replacement therapy lowers a woman's risk for heart disease.

Cardiovascular diseases, Risk factors, Hormone therapy

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