Platelet-type von Willebrand disease (PT-VWD) is a rare autosomal dominant bleeding disorder with a defect in platelet glycoprotein Ib α (GP1bα), the receptor for the adhesive glycoprotein von Willebrand factor (VWF). The inter action between the two proteins is crucial to primary hemostasis and the formation of a platelet plug at the site of vascular injury. While this interaction does not take place in normal situations, the disease is typically character ized by an enhanced responsiveness of platelets, due to gain-of-function mutations in the platelet GP1BA gene resulting in clearance of the hemostatically active VWF multimers as well as platelets, with subsequent mucocutaneous bleeding [1]. Despite the typically encountered mildto-moderate bleeding, the PT-VWD bleeding phenotype can be life threatening in stressful conditions such as infection, pregnancy and surgeries. This necessitates correct diagnosis and management. Unlike its nonidentical twin, type 2B VWD, PT-VWD is less frequent, commonly undiagnosed, often misdiagnosed and ideally treated with platelet concentrate rather than VWF preparations, as is the case in type 2B VWD [2].