We performed a nationwide cross‐sectional study in patients with VWD in the Netherlands; the “Willebrand in the Netherlands” (WiN) study (de Wee et al, 2010 , 2012 ). Patients with VWD were recruited between October 2007 and October 2009. The inclusion criteria were haemorrhagic symptoms or a family history of VWD, and historically lowest VWF antigen (VWF:Ag) and/or VWF ristocetin cofactor activity (VWF:RCo) ≤0·30 iu/ml and/or FVIII coagulant activity levels (FVIII:C) ≤0·40 iu/ml (for type 2N VWD). Patients were excluded if they had other haemostatic disorders. Blood and saliva samples were obtained at study inclusion.
For the current analyses, we excluded patients with type 3 VWD (defined as VWF levels <0·05 iu/ml and VWF propeptide (VWFpp) <0·05 iu/ml), because by definition there will be no increase of VWF levels in these patients (Sanders et al,2015a ). Furthermore, we excluded patients younger than 16 years old, patients with missing data on comorbidities, patients without centrally measured VWF levels or with centrally measured VWF levels during pregnancy, or desmopressin medication or clotting factor concentrate infusion 72 h prior to blood sampling. The study was performed according to the Declaration of Helsinki and approved by the Medical Ethical Committees of all participating centres. Informed consent was signed by all patients.
For the current analyses, we excluded patients with type 3 VWD (defined as VWF levels <0·05 iu/ml and VWF propeptide (VWFpp) <0·05 iu/ml), because by definition there will be no increase of VWF levels in these patients (Sanders et al,