Women with IBD are exposed to several haemostatic challenges during various stages of pregnancy. In the first trimester bleeding can occur following spontaneous miscarriage, invasive prenatal diagnostic procedures, and termination of pregnancy. Close collaboration between haematologists and obstetricians is important to determine whether haemostatic cover is indicated to reduce excessive or prolonged bleeding that can occur during these events. Bleeding that occurs after the 24th week of gestation and prior to delivery

is less common and termed antepartum haemorrhage (APH). APH occurs in 3–5% of all pregnancies and is a leading cause of perinatal and maternal morbidity worldwide. APH selleck occurs from bleeding at the placental site, lesions

of the cervix or vagina and occasionally foetal origin. Among the most important causes, that has potential to result in major haemorrhage, include placenta previa (31%) and placental abruption (22%) [21]. Women with coagulation disorders pose special clinical challenge in pregnancy and during delivery. In the literature, scarce data on the bleeding risk Galunisertib in the first trimester are reported for the women with rare bleeding disorders (RBDs) [22]. There are case reports and case series documenting the increased risk of miscarriage in women with some IBD, particularly among women with fibrinogen and FXIII deficiency [23]. An increased risk of APH, particularly placental abruption, has been observed in women with FXIII and fibrinogen deficiencies [24]. Retroplacental haematoma and preterm delivery are also reported in women with FX deficiency [25]. Discordant data are reported for APH in women with von Willebrand disease (VWD) [26, 27]. The involvement of fibrinogen and FXIII in maintaining placental integrity has been analysed in mouse model. Hypofibrinogenemic and experimental afibrinogenemic mice exhibited similar features of bleeding tendency and miscarriage [28]. Pregnant

mice homozygous for a deletion of the Fg-γ chain, which results in a total fibrinogen deficiency state, aborted the foetus at the equivalent gestational stage seen in humans. Fibrinogen deficiency does not appear to alter embryonic development, but formation of the placenta and yolk sac is significantly compromised. The loss of embryo in afibrinogenemic Casein kinase 1 mice is because of an exacerbation of the haemorrhage that normally occurs during the critical stage of maternal and foetal vascular development, when the blastocyst is invading the maternal decidua. Severe uterine bleeding events have been reported in animal models, specifically in FXIII-A as well as FXIII-B subunit-deficient mice [29, 30]. In these studies, a strain of FXIII-A knockout mice showed a severe bleeding tendency similar to human FXIII deficiency. Homozygous FXIII-A female knockout mice were capable of becoming pregnant, but most of them died from severe uterine bleeding.