PIP: A relationship between use of oral contraceptives and thromboembolic disease has been suspected for years. Recent experimental studies indicate that venous thromboses can be triggered by the interaction of stasis and coagulation activation, also called hypercoagulability. Stasis is promoted by widening of the veins, a change known from pregnancy, although it is not clear whether this can be definitively related to estrogen or progestagen release. In addition, estrogens cause an increase in fibrinogen neosynthesis and increased whole blood viscosity. At low flow rates this causes early occurrence of erythrocyte aggregates. Although an increase in coagulation factors observed by many authors among oral contraceptive users cannot be unequivocally equated to an increased thromboembolic risk, detection of activated coagulation factors is a sensitive indicator of coagulation activation. Thus it was shown by the level of circulating fibrin in plasma that varied coagulation activation occurred in users of 30 and 50 micrograms ethinyl estradiol. In this study of a 3 stage contraceptive (0.5 mg norethisterone, 0.035 mg ethinyl estradiol; 0.75 mg norethisterone, 0.035 mg ethinyl estradiol; 1 mg norethisterone, 0.35 mg ethinyl estradiol) with 22 patients, no significant change in fibrinogen level was found. The same applied to other hypercoagulability parameters fibrinopeptide A and antithrombin III. The constant blood level of early fibrinolysis product F-CB3 also indicated absence of relevant thrombin induced coagulation activation. This is apparently linked to low estrogen dose.