During a 28-year period the incidence of thrombosis and pulmonary embolism (TE) in pregnancy remained practically equal (0.7%), the incidence of puerperal TE was higher (2.3%) but decreased during the last 7 years. Puerperal TE was influenced by age, mode of delivery, hypertension and prophylactic anticoagulant therapy. TE during pregnancy was not noticeably correlated with age and hypertension. TE during pregnancy and in the puerperium are closely related diseases, but their epidemiological characteristics are apparently distinct. Both are associated with a high rate of preterm deliveries and a high perinatal mortality rate.

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Antithrombin III (AT III) is the main physiological inhibitor of blood coagulation. In a prospective study, plasma AT III was determined in 653 women during pregnancy, using an automated amidolytic technique. A control value 8 weeks after delivery was obtained in 192 of the women. In women with pregnancy-induced or aggravated hypertension a significant decrease in AT III levels was observed compared with normotensive controls of the same period of gestation and compared with the patients’ own control values 6–8 weeks after delivery. No AT III depression occurred in patients with chronic hypertension during pregnancy. Patients with pregnancy hypertension and proteinuria had lower AT III levels than those without proteinuria, whose AT III levels were also depressed. Lowest AT III levels were seen in 2 eclamptic patients and in patients with severe preeclampsia, whose pregnancies were terminated for fetal distress while the infants were still preterm. Monitoring AT III levels is of value in preeclampsia.

Plasma antithrombin III (AT III) was determined in four groups of subjects, by employing an automated chromogenic technique. In 25 women, discontinuing oral contraceptives led to a 9% elevation of AT III, while in 13 women AT III levels fell by 9% after starting with the pill. In 77 normotensive pregnant patients AT III levels were normal during the third trimester and did not differ from control values 6-8 weeks after delivery. Women taking the pill at that time did not have lower AT III levels than those who did not. Furthermore, AT III levels in 414 oral contraceptive users were the same as in 572 controls, when random samples were taken during pill cycle and menstrual cycle. It is concluded that although synthetic estrogens do cause a decrease in AT III levels, this decrease is probably the result of estrogen-induced hemodilution, which may also occur during the normal menstrual cycle. If low dose pills are thrombogenic, mass screening for AT III deficiency will not identify those at risk, with the exception of the rare cases of hereditary AT III deficiency.