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Spontaneous ovarian bleeding in patients with congenital coagulopathy: Case series and review of the literature

Von Willebrand’s disease is a hereditary bleeding disorder caused by a deficiency or defect of von Willebrand factor (VWF), which is synthesised by endothelial cells and megakaryocytes and circulates in plasma as a high molecular weight glycoprotein. The gene for VWF is carried on chromosome 12 and there are three recognised subtypes of VWD. Types 1 and 3 are associated with a quantitative deficiency of VWF, with a qualitative deficiency in type 2. Type 1 and type 2 VWD occur more commonly and account for 60 – 70% of cases. In VWD, the platelet count is usually normal but there is a prolonged bleeding time, prolonged activated partial thromboplastin time (APTT), reduced factor VIII clotting activity, reduced levels of VWF and reduced ristocetin-induced platelet aggregation. VWF plays a major role in the early phases of homeostasis by promoting platelet and vessel wall and platelet – platelet interactions under shear conditions. VWF is also the carrier of coagulation factor VIII in plasma. If trauma occurs or surgery is scheduled, cryoprecipitate, desmopressin (DDAVP) or fresh plasma may be needed to raise the levels of VWF and factor VIII levels (Frederici 1998, Frederici and Mannucci 2002). Bernard – Soulier syndrome describes a congenital disorder of platelet function. In this condition, there is absence of glycoprotein-1B and therefore platelets lack receptors to adhere to the walls of blood vessels. Affected women are generally well but tend to bruise easily and usually have heavy periods that would generally respond to medical treatment such as tranexamic acid, danazol or the oral contraceptive pill.