Dr Mangia and colleagues compared frequencies of 3 common prothrombotic mutations.
Thrombotic factors considered by the team were factor V Leiden, the G20210A mutation of the prothrombin gene, and homozygosity for C677T methylenetetrahydrofolate reductase.
The researchers included 219 cirrhotic patients, 43 with and 176 without portal vein thrombosis.
|Combination of the 2 acquired factors increases the risk for portal vein thrombosis|
|European Journal of Gasroenterology and Hepatology|
Variables related to portal vein thrombosis included prothrombin levels, platelet count, Child-Pugh classification, and previous abdominal surgery.
The researchers also assessed the number of decompensation events, size of varices, red markers on varices, and sclerotherapy.
The research team followed up all patients for a mean period of 18 months.
The team detected prothrombotic mutations in 30% of the cirrhotic patients, at equal frequency in patients with or without portal vein thrombosis.
Using univariate analysis, the researchers showed that portal vein thrombosis was associated with Child-Pugh classes B and C, and signs of liver decompensation.
The team also showed that portal vein thrombosis was associated with large varices with red markings, sclerotherapy, and abdominal surgery.
The team noted after multivariate analysis, that portal vein thrombosis was associated with sclerotherapy and previous surgery.
The researchers observed that combination of the 2 acquired factors increased risk for portal vein thrombosis, whereas combination of local with genetic defects did not.
The team reported that only 1 patient with genetic thrombophilia and without portal vein thrombosis at inclusion developed the complication during follow-up.
The 1 patient who developed complications, concomitantly developed hepatocellular carcinoma.
Dr Mangia concludes, “In cirrhotic patients prothrombotic mutations by themselves are not causative of portal vein thrombosis.”
“Sclerotherapy and previous abdominal surgery favour the development of two-thirds of cases of portal vein thrombosis; in the remaining cases the pathogenesis remains elusive.”