1–1.4), this study did not recommend that routine testing for the MTHFR C677T polymorphism should be incorporated into any clinical thrombophilia assessment. Recently, a larger meta-analysis, including 27 studies regarding the association of homocysteine with venous thrombosis and 53 studies regarding the association of MTHFR 677TT genotype with venous thrombosis, revealed that hyperhomocysteinemia carried a 27–60% higher risk of venous thrombosis, and the MTHFR 677TT genotype was associated with a 20% higher risk of venous thrombosis compared with the MTHFR 677CC genotype.[58] Accordingly, the homozygous MTHFR mutation should be considered as the causality of venous thromboembolism. It

may be reasonable Fostamatinib cost that these results were extrapolated to the venous thrombosis at unusual sites, such as the portal and hepatic vein. On the basis of the currently available evidence, our study did support

the positive association between hyperhomocysteinemia and BCS or non-cirrhotic PVT. Therefore, the routine testing of the plasma homocysteine levels may be necessary in both BCS and non-cirrhotic PVT patients. However, the limited data just showed a statistically significantly higher prevalence of homozygous MTHFR C677T mutation in BCS patients, www.selleckchem.com/products/Rapamycin.html rather than non-cirrhotic PVT patients. Maybe a firm conclusion regarding the risk of PVT in non-cirrhotic patients carrying homozygous 上海皓元 MTHFR C677T mutation could be achieved in studies with a larger sample size. On the other hand, it has been increasingly recognized that cirrhotic patients have a high risk of developing venous thromboembolism.[59-61] Increased levels of factor VIII and decreased levels of protein C could be a potential cause for this phenomenon.[62, 63] In addition, it may be explained by a higher prevalence of hyperhomocysteinemia and MTHFR C677T polymorphism in cirrhotic patients than in healthy controls.[64, 65] Our meta-analysis further suggested the contribution of homozygous MTHFR C677T mutation to the development of PVT in liver cirrhosis. It may be attributed to the

concomitant low levels of folate and increased levels of homocysteine in these patients.[66] However, our study did not find any significant association between hyperhomocysteinemia and PVT in cirrhotic patients. This unexpected finding could be explained by the two following points. First, only two studies compared the prevalence of hyperhomocysteinemia between cirrhotic patients with and without PVT, and their results were completely inconsistent. Second, as we closely analyzed the studies comparing the plasma homocysteine levels between cirrhotic patients with and without PVT, two of three included studies showed a significantly higher homocysteine level in cirrhotic patients with PVT than in those without PVT, and only one of them showed a similar homocysteine level between the two groups.