[Hormonal contraceptive therapy and thromboembolic disease]
- PMID: 7038816
[Hormonal contraceptive therapy and thromboembolic disease]
Abstract
A group of 55 patients with rheumatoid arthritis (RA) and 25 healthy persons is studied. In peripheral blood, the number of E rosettes is similar in both groups but in patients with RA who are not on steroid therapy, these is a decreased number of the absolute value of T lymphocytes. There is a positive correlation between quantitative cellular immunity and different biologic and clinical parameters.
PIP: Through a careful review of the published literature this document presents the most recent knowledge on the action of estrogens on the mechanism of blood coagulation. It now seems clear that oral contraceptives (OCs) cause an increase in the activity of platelet factor 3, and also an increase in platelet aggregation; at the same time coagulation is activated through decreased levels of antighrombin 3, resulting in a concentration of soluble fibrin fragments. Alteration of fibrinolysis is very possible, although the literature is contradictory on this point. Estrogens can also cause thrombotic accidents by alteration of the vascular walls, and by alteration of the lipid metabolism. According to different authors, the risk of thrombotic accident in OC users is greater than in nonusers. The risk greatly increases in smokers. It is possible that thrombotic risk can be decreased with the use of OCs with a lower estrogen content.