ABSTRACT
Factor XII (FXII) is an important protease that plays a major role in the initiation of the intrinsic pathway of blood coagulation. Although congenital FXII deficiency is not associated with a clinical bleeding tendency, it can be identified on a routine coagulation test, such as a prolonged activated partial thromboplastin time. This deficiency is a rare autosomal recessive disorder. It is still unclear whether FXII deficiency causes any disorders during pregnancy. Recurrent miscarriages and placental abruption were reported in cases with FXII deficiency. We successfully treated a woman whose pregnancy was complicated by congenital FXII deficiency. We report her clinical courses of gestation, delivery, and puerperium and discuss the role of maternal FXII associated with pregnancy. In our case, courses of gestation and delivery were normal. Postpartum uterine bleeding was, however, prolonged due to a subinvolution of the puerperal uterus. Our results indicate that, except for postpartum uterine contraction, FXII does not play a major role in gestation and delivery. We suggest that FXII deficiency is not associated with recurrent miscarriage and that normal gestation and vaginal delivery are possible even in cases with congenital FXII deficiency. We assert that the possible correlation of FXII deficiency with recurrent miscarriage merits reevaluation.
KEYWORD
Factor XII deficiency - miscarriage - kinin formation - postpartum bleeding - uterine contraction
