Abstract
Background and aimsNon‐O blood type (BT) is a risk factor for thromboses, which has been attributed to its effects on von Willebrand factor (VWF)/factor VIII (FVIII) levels. Although high VWF/FVIII may be risk factors for portal vein thrombosis (PVT) in patients with advanced chronic liver disease (ACLD), the impact of BT on PVT is unknown. We aimed to assess (I) whether non‐O‐BT is a risk factor for PVT and (II) whether non‐O‐BT impacts VWF/factor VIII in patients with ACLD.MethodsRetrospective analysis comprising two cohorts: (I) “US” including all adult liver transplantations in the US in the MELD era and (II) “Vienna” comprising patients with a hepatic venous pressure gradient (HVPG) ≥6 mmHg.Results(I) The “US cohort” included 84 947 patients (non‐O: 55.43%). The prevalence of PVT at the time of listing (4.37% vs 4.56%; P = .1762) and at liver transplantation (9.56% vs 9.33%; P = .2546) was similar in patients with O‐ and non‐O‐BT. (II) 411 patients were included in the “Vienna cohort” (non‐O: 64%). Mean HVPG was 18(9) mmHg and 90% had an HVPG ≥10 mmHg. Patients with non‐O‐BT had slightly increased VWF levels (318(164)% vs 309(176)%; P = .048; increase of 23.8%‐23.9% in adjusted analyses), but this difference was driven by patients with less advanced disease. However, non‐O‐BT explained only 1% of the variation in VWF and had no effect on FVIII.ConclusionsAlthough non‐O‐BT impacts VWF in patients with early stage ACLD, its contribution to VWF variation is considerably smaller than in the general population. Moreover, non‐O‐BT had no impact on FVIII. These findings may explain the absence of an association between non‐O‐BT and PVT in patients with advanced cirrhosis.
Highlights
As a consequence of abnormal routine coagulation tests and thrombocytopenia, cirrhosis has long been considered an acquired bleeding disorder.[1]
Data were obtained through the Organ Procurement and Transplantation Network (OPTN) and the data set supplied by the United Network for Organ Sharing (UNOS)
In the “US cohort,” portal vein thrombosis was evaluated at the time of listing as well as at the time of liver transplantation
Summary
As a consequence of abnormal routine coagulation tests and thrombocytopenia, cirrhosis has long been considered an acquired bleeding disorder.[1] the liver plays a central role in coagulation and plasma levels of most procoagulant factors are significantly reduced in patients with cirrhosis These changes are balanced by decreased levels of anticoagulant proteins[2] and highly elevated levels of the platelet adhesive protein von Willebrand factor (VWF).[3] patients with cirrhosis are nowadays considered to have a rebalanced haemostatic equilibrium.[4] when compared to liver-healthy subjects, this equilibrium seems to be instable and tips in one direction, which may lead to bleeding or thrombosis.[5,6] while clinically relevant non-portal hypertensive bleeding is rare, the prevalence/incidence of portal vein thrombosis (PVT) in patients with advanced cirrhosis is considerably high.[7] PVT is a clinically relevant complication in patients with cirrhosis,[7] especially in the liver transplant waiting list setting. These findings may explain the absence of an association between non-O-BT and PVT in patients with advanced cirrhosis
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