7 research outputs found

    VTE and anticoagulation in menstruating women

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    Women of childbearing potential have a high prevalence of venous thromboembolism (VTE) due to high estrogen states, such as pregnancy and the use of estrogen-containing contraceptives. Abnormal uterine bleeding (AUB) affects up to two-thirds of menstruating women on anticoagulation (AC), and can severely impair a woman\u27s quality of life. Rates of heavy menstrual bleeding (HMB) and other forms of AUB including inter-menstrual and postmenopausal bleeding are consistently underreported in the original clinical trials utilizing AC. VTE can occur at any time in a woman\u27s life, and the aim of this review article is to discuss the current landscape of literature on AUB for women on AC, VTE and AC in women of child bearing potential, planning for pregnancy while on AC, VTE during pregnancy, and considerations for VTE risk in postmenopausal women. This survey of the current literature may offer data for providers to consider while making clinical decisions on the duration of and appropriate choice of anticoagulation

    Factor VIII: Long-established role in haemophilia A and emerging evidence beyond haemostasis

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    Abstract Factor VIII protein (FVIII) as a coagulation replacement factor has for decades been used as the standard of care for management of people with haemophilia A. It is effective for treatment of bleeding events, as prophylaxis to prevent bleeding events and preserve joint function, and to support surgery in people with haemophilia A. Despite long experience in treating haemophilia A, we are only beginning to understand the functions of FVIII beyond its established role as a coenzyme to factor IXa to expedite thrombin generation through the intrinsic pathway of coagulation. Here, we review the current role of FVIII coagulant (FVIII:C) in haemophilia A management and emerging evidence for the role of FVIII across multiple systems, including the cardiovascular system, angiogenesis and maintenance of bone health. For instance, supraphysiological FVIII levels are a risk factor for venous thromboembolism. von Willebrand factor (VWF), which forms a non-covalent complex with circulating FVIII, is an established marker and regulator of angiogenesis. In a mouse model of haemophilia, treatment with FVIII decreased expression of receptor activator of nuclear factor kappa-Î’ ligand (RANKL), a marker for bone turnover. Longitudinal follow-up data in people with haemophilia A are needed to confirm and extend these observations
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