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
