Hereditary factor VII deficiency in pregnancy: Peripartum treatment with factor VII concentrate

Robertson, L. E.; Wasserstrum, Nathan; Bañez, Eugenio I.; Vásquez, María Alejandra; Sears, David

doi:10.1002/ajh.2830400108

Cited by 39 publications

(45 citation statements)

References 12 publications

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“…This observation is consistent with the fact that women with congenital deficiencies in Factor VII, fibrinogen, and Factor XIII exhibit severe postpartum hemorrhage (36)(37)(38). There have been no reports of congenital deficiencies in TF, but we speculate that reduced TF expression in the uterine epithelium may be associated with hemorrhagic complications in humans during childbirth.…”

Section: Discussionsupporting

confidence: 88%

Tissue factor is required for uterine hemostasis and maintenance of the placental labyrinth during gestation

Erlich

Parry

Fearns

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

115

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We employed a novel mouse line that expresses low levels of human tissue factor (TF) in the absence of murine TF to analyze the role of TF in gestation. Low-TF female mice had a 14-18% incidence of fatal postpartum uterine hemorrhage, suggesting that TF plays an important role in uterine hemostasis. Low-TF female mice mated with low-TF male mice had a 42% incidence of fatal midgestational hemorrhage (n ‫؍‬ 41), whereas no fatal midgestational hemorrhages were observed in low-TF female mice mated with wild-type male mice (n ‫؍‬ 43). Placentas of low-TF embryos from both low-TF and normal (؉͞؊) TF females were abnormal and contained numerous maternal blood pools in the labyrinth. Placentas of TF null embryos surviving beyond embryonic day 10.5 exhibited similar defects. The mouse maternal-embryonic placental barrier consists of four cellular layers (layers I, II, and III and endothelial cells), where layer I lines the maternal lacunae. Comparison of TF-deficient placentas with control placentas by immunohistochemical and ultrastructural analyses revealed thinning of layer I and a reduction in the number of cellular contacts of layer I trophoblasts spanning the maternal blood space between adjacent trabeculae. These structural changes in low-TF and TF null placentas result in enlarged maternal lacunae, as determined by morphometric analysis, and placental hemorrhage, which leads to midgestational death of low-TF female mice. This study demonstrated that TF is required for uterine hemostasis and revealed an unexpected role of TF in the maintenance of the placental labyrinth.

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Section: Discussionsupporting

confidence: 88%

Tissue factor is required for uterine hemostasis and maintenance of the placental labyrinth during gestation

Erlich

Parry

Fearns

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

115

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“…The rarity of these two disorders may fully justify the finding. Instead, there are at least 21 additional cases of pregnancies and deliveries in homozygous FVII deficiency patients [27,28,29,30,31,32,33,34,35,36,37,38,39]. This is probably due to the fact that the defect is not as rare as FII or FX deficiency.…”

Section: Discussionmentioning

confidence: 99%

Pregnancy and Oral Contraceptives in Congenital Bleeding Disorders of the Vitamin K- Dependent Coagulation Factors

Girolami

Randi²,

Ruzzon³

et al. 2006

Acta Haematol

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Pregnancies and deliveries represent important hemostatic challenges for congenital coagulation disorders. The same is true for the assumption of oral contraceptives. Available information mainly deals with von Willebrand’s disease, factor XI (FXI) deficiency and carriers of hemophilia A. Data concerning patients with congenital prothrombin complex factor deficiencies are very scanty. In the present study, data of a total of 27 women are presented, 11 patients with homozygous or double heterozygous deficiencies of FII, FVII and FX, together with 16 cases of hemophilia B carriers. The patients with FII, FVII or FX defects had a total of 14 pregnancies and often needed transfusion therapy. Proper management resulted in a decrease in postpartum bleeding and satisfactory fetal outcome. Elective cesarean delivery seems indicated only in recent years. Carriers of hemophilia B had a total of 19 pregnancies but showed no bleeding and needed no substitutive therapy. Searching the literature, we discovered only 9 additional patients with prothrombin deficiency or FX deficiency, having a total of 16 pregnancies. On the contrary, there were at least 17 additional patients with FVII deficiency, with a total of 21 pregnancies. The management of the diseases has been variable, but in substantial agreement with the personal observations. Oral contraceptive therapy was administered in some of our patients and in a few additional cases described in the literature. Medication was always well tolerated and patients who took it for a long period of time showed a decrease in menometrorrhagia and an improvement in hematocrit levels. This led to a decrease in transfusional needs and to improved general conditions.

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“…These observations are consistent with the fact that women with congenital deficiencies in FVII, fibrinogen, and FXIII exhibit spontaneous abortion, abruption, and postpartum hemorrhage. [93][94][95] …”

Section: Role Of Tf In the Uterusmentioning

confidence: 99%

Role of Tissue Factor in Hemostasis, Thrombosis, and Vascular Development

Mackman¹

2004

ATVB

566

460

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Hereditary factor VII deficiency in pregnancy: Peripartum treatment with factor VII concentrate

Cited by 39 publications

References 12 publications

Tissue factor is required for uterine hemostasis and maintenance of the placental labyrinth during gestation

Tissue factor is required for uterine hemostasis and maintenance of the placental labyrinth during gestation

Pregnancy and Oral Contraceptives in Congenital Bleeding Disorders of the Vitamin K- Dependent Coagulation Factors

Role of Tissue Factor in Hemostasis, Thrombosis, and Vascular Development

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