Portal vein thrombosis in liver cirrhosis

Abstract

Portal vein thrombosis (PVT) is observed in 10-20% of patients with liver cirrhosis, which is responsible for 20% of all PVT cases. The main pathogenic factor of PVT in cirrhosis is the obstacle to portal flow, but acquired and inherited clotting abnormalities may play a role. The formation of collateral veins allows many patients to remain asymptomatic and prevents the onset of clinical complications also in patients with totally occlusive PVT. Gastrointestinal bleeding, thrombosis of superior mesenteric vein and refractory ascites are typical manifestations of PVT. Instrumental diagnosis can be obtained by colour-doppler ultrasonography. Future studies should verify whether asymptomatic PVT worsens liver failure, or if its life-threatening complications reduce survival in patients with cirrhosis. Moreover, randomized controlled trials should clarify the potential effectiveness of anticoagulant therapy in the treatment of PVT.

JAK2V617F Mutation in Patients with Splanchnic Vein Thrombosis

“…Among the acquired factors associated with splanchnic vein thromboses, there are systemic conditions such as MPNs, oral contraceptive use and chronic inflammatory diseases, and abdominal causes such as cirrhosis, other chronic liver diseases, local inflammation, trauma, surgical injury to the portal venous system, and tumors of abdominal organs [33]. MPNs and cirrhosis are the leading causes in the developed world [4,34,35]. However, the diagnosis of MPN in this context is often problematic, and the availability of the JAK2V617F as a diagnostic tool could be particularly useful in these patients.…”

Diagnostic value of the JAK2 V617F mutation for latent chronic myeloproliferative disorders in patients with budd-chiari syndrome and/or portal vein thrombosis

“…Liver cirrhosis is among the most common acquired risk factors for PVT, responsible for approximately 20% of all PVT cases (1). The high prevalence of PVT in patients with cirrhosis (10%-20%) has been attributed to a decrease in portal blood flow and the presence of periportal lymphangitis and fibrosis (2).…”

“…The high prevalence of PVT in patients with cirrhosis (10%-20%) has been attributed to a decrease in portal blood flow and the presence of periportal lymphangitis and fibrosis (2). Moreover, acquired and inherited clotting abnormalities may play a role in the pathogenesis of PVT (1). The F2 G20210A mutation is more common in PVT patients with liver cirrhosis than the C677>T substitution mutation of the methylenetetrahydrofolate reductase (MTHFR) gene (a mutation causing increased plasma levels of homocysteine, a thrombotic factor) or FVL mutation (3-7).…”

Does the right inferior phrenic artery has a supplying role in liver cirrhosis without HCC?: 64-slice CT evaluation

“…In response to PVT, portoportal and portosystemic collateral veins develop within a few days to compensate for the decreased portal blood flow (6,7). The portal cavernoma is a typical feature of chronic PVT, which consists of a network of collateral vessel around the portal vein.…”