Portal vein thrombosis in cirrhosis: Why a well-known complication is still matter of debate

Abstract

Portal vein thrombosis (PVT) represents a well-known complication during the natural course of liver cirrhosis (LC), ranging from asymptomatic cases to life-threating conditions related to portal hypertension and hepatic decompensation. Portal flow stasis, complex acquired hypercoagulable disorders and exogenous factors leading to endothelial dysfunction have emerged as key factors for PVT development. However, PVT occurrence remains unpredictable and many issues regarding its natural history, prognostic significance and treatment are still elusive. In particular although spontaneous resolution or disease stability occur in most cases of PVT, factors predisposing to disease progression or recurrence after spontaneous recanalization are not clarified as yet. Moreover, PVT impact on LC outcome is still debated, as PVT may represent itself a consequence of liver fibrosis and hepatic dysfunction progression. Anticoagulation and transjugular intrahepatic portosystemic shunt are considered safe and effective in this setting and are recommended in selected cases, even if the safer therapeutic option and the optimal therapy duration are still unknown. Nevertheless, their impact on mortality rates should be addressed more extensively. In this review we present the most debated questions regarding PVT, whose answers should come from prospective cohort studies and large sample-size randomized trials.

Nontumoral Portal Vein Thrombosis: A Challenging Consequence of Liver Cirrhosis

“…11 The indication, contraindication, and currently available therapeutic agents are summarized in Supplementary Table 3. [1][2][3]11,25,46,[79][80][81][82][83][84][85][86][87][88][89][90][91][92][93] Anticoagulation Anticoagulation is the primary management of acute PVT, with supporting evidence of high efficacy and a favorable safety profile ( Table 1). The objective is to achieve recanalization of the portal vein and prevent the extension of the thrombus to decrease the notorious consequences of portal hypertension and mesenteric ischemia and allow conventional end-to-end portal vein anastomosis to be technically possible in transplant candidates.…”

Efficacy and Safety of Nadroparin Calcium-Warfarin Sequential Anticoagulation in Portal Vein Thrombosis in Cirrhotic Patients: A Randomized Controlled Trial

“…Based on the current available data, the incidence of PVT in cirrhotic patients is higher than that in noncirrhotic population, varying from 10% to 15% ( 1 ). PVT aggravates the complications of portal hypertension ( 2 , 3 ), and occlusive PVT decreases the post-transplantation survival rate ( 4 , 5 ).…”

Direct Oral Anticoagulants in Patients with Liver Disease in the Era of Non-Alcoholic Fatty Liver Disease Global Epidemic: A Narrative Review

“…Histopathological studies on cirrhotic livers have shown that micro-thrombotic occlusion of small intrahepatic veins and sinusoids, secondary to hepatic necroinflammation, frequently occurs; this event is followed by progressive venous obstruction and enhanced fibrogenesis through a process called parenchymal extinction, which may eventually lead to liver dysfunction, worsening of portal hypertension and PVT [ 58 – 60 ]. A pathogenic model of NASH progression has been proposed based on lipotoxic necrotic damage, leading to direct inflammatory injury of hepatic veins and, finally, venous obstruction with secondary collapse, fibrous septation and cirrhosis [ 61 ].…”