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von Willebrand disease (vWD) is a hereditary bleeding disorder characterized by impaired blood clotting due to deficiencies in von Willebrand factor (vWF), a glycoprotein essential for platelet adhesion and coagulation. The condition is classified into three primary types—Type 1, Type 2, and Type 3—each varying in severity and genetic basis.

Type 1 vWD, the most common form, accounts for approximately 70% of cases and is marked by a quantitative deficiency of vWF. Symptoms typically include mild to moderate bleeding, such as prolonged nosebleeds, excessive menstrual bleeding, or easy bruising. Diagnosis often relies on laboratory tests measuring vWF levels, ristocetin cofactor activity, and factor VIII levels.

Type 2 vWD encompasses several subtypes (2A, 2B, 2M, and 2N) distinguished by qualitative abnormalities in vWF structure or function. These variants may present with more pronounced bleeding tendencies, particularly in mucocutaneous areas. Genetic mutations affecting the vWF gene (*VWF*) on chromosome 12 are responsible for these variations.

Type 3 vWD is the rarest and most severe form, characterized by near-complete absence of vWF. Individuals with this subtype often experience severe bleeding episodes, including life-threatening hemorrhages, and typically require lifelong treatment with vWF-containing therapies.

Management of vWD depends on the type and severity of symptoms. Mild cases may only require supportive measures, while moderate to severe cases may necessitate desmopressin (DDAVP) for Type 1 and Type 2 subtypes or recombinant vWF/factor VIII concentrates for Type 3. Genetic counseling is recommended for affected families to assess inheritance patterns and recurrence risks.

Early diagnosis and tailored treatment can significantly improve quality of life for individuals with vWD, allowing them to manage symptoms effectively while minimizing complications. Research continues to advance understanding of the disease, potentially leading to more targeted therapies in the future.