First, three meta-analyses confirmed that a high prevalence of JAK2 V617F mutation was observed in BCS and PVT patients, and routine screening for JAK2 V617F mutation was useful to diagnose the latent myeloproliferative neoplasms.[51-53] One of them further demonstrated that polycythemia

vera was clearly more common in BCS than in PVT.[53] Second, one meta-analysis confirmed that the prevalence of factor V Leiden mutation and factor II G202010A mutation were significantly higher in PVT patients with and without liver diseases than in controls.[54] Third, one recent meta-analysis demonstrated that the prevalence of inherited antithrombin, protein C and protein S deficiencies were significantly higher in non-cirrhotic patients with PVT than in healthy controls.[55] But the limited evidence did not show any association between these inherited deficiencies and BCS. Additionally, another meta-analysis did not support the relationship between antithrombin, Dabrafenib order protein C and protein S concentrations and the development of PVT in liver cirrhosis.[56] Generally, the results of these meta-analyses are helpful to determine the potential etiology of BCS and PVT and to establish the clinical necessity of screening for thrombotic risk factors in such patients.

However, to the best of our knowledge, no Enzalutamide cell line systematic review and meta-analysis has been conducted to explore selleck chemicals the role of MTHFR C667T mutation and homocysteine in BCS and

PVT patients. Our study showed the major following findings: (i) the prevalence of homozygous MTHFR C677T mutation was significantly higher in BCS patients than in healthy controls; (ii) the prevalence of homozygous MTHFR C677T mutation was higher in non-cirrhotic PVT patients than in healthy controls, but the difference was not statistically significant; (iii) BCS or non-cirrhotic PVT patients had a significantly higher prevalence of hyperhomocysteinemia and plasma homocysteine level than healthy controls, which potentially suggested that hyperhomocysteinemia may be a risk factor of BCS and non-cirrhotic PVT; and (iv) compared with those without PVT, cirrhotic patients with PVT had a significantly higher prevalence of homozygous MTHFR mutation, but a similar prevalence of heterozygous MTHFR C667T mutation, which indicated that MTHFR C667T mutation in a homozygous trait may contribute to the pathogenesis of PVT in liver cirrhosis. An early meta-analysis of nine studies demonstrated a significantly increased risk of venous thromboembolism in patients with elevated plasma homocysteine levels.[7] Subsequently, their meta-analysis of 31 studies showed a statistically significant difference in the prevalence of MTHFR 677TT genotype between patients with venous thromboembolism and controls.[57] However, considering that the trend towards an increasing risk of venous thromboembolism in such patients was weak (OR = 1.