The management of portal vein thrombosis (original) (raw)

European Journal of Gastroenterology & Hepatology, 2019

Abstract

A frequent, often life-threatening, complication of cirrhosis is portal vein thrombosis; for its treatment, Valentin et al. [1] reviewed transjugular intrahepatic portosystemic shunt; however, its cost compared with anticoagulation is staggering. Moreover, a five times increase in deaths due to acute myocardial infarction and ischemic stroke among patients with liver cirrhosis has been reported [2,3]. These events highlight the existence of other, often neglected causes, of thrombosis in cirrhotic patients. One such possible cause that could be easily and cost-effectively detected and cured, if searched for, is the infection by pathogenic strains of Helicobacter pylori particularly those strains expressing the cytotoxin-associated antigen A protein that has been found with high prevalence in patients with cirrhosis [4], myocardial infarction [5], and ischemic stroke [6]. This bacterium is known to mimic human antigens and induce autoimmunity against endothelial cells [7], cause the antiphospholipid syndrome [8] and autoimmune thrombotic thrombocythemia that are ameliorated after the infection is eradicated [8,9]. Furthermore, a neutrophilic-activating protein is secreted by H.pylori, which causes neutrophilic infiltration of the vascular wall and activates neutrophils stimulating the production of reactive oxygen species, and inflammation. Neutrophilic-activating protein also stimulates the production of tissue factor and plasminogen activator inhibitor-2 by mononuclear cells [10]. These latter effects are procoagulant and antifibrinolytic thus affecting the coagulation-fibrinolysis balance toward fibrin deposition and coagulation [10]. Patients infected by H. pylori circulate aggregates of platelets and neutrophils [11]: neutrophilic infiltration of vascular walls may lead to venous thrombosis [12]. We suggest that all patients with cirrhosis ought to be tested for the presence of pathogenic strains of H. pylori and to cure those who are positive. This simple action will decrease the risk of gastric and duodenal ulcer, and possibly also portal vein thrombosis and other ischemic illnesses in cirrhosis patients.

Antonio Ponzetto hasn't uploaded this paper.

Let Antonio know you want this paper to be uploaded.

Ask for this paper to be uploaded.