Hyperhomocysteinemia and MTHFR C677T polymorphism in patients with portal vein thrombosis complicating liver cirrhosis

- Hyperhomocysteinemia (HHcy) was suggested as independent risk factor for deep vein thrombosis.
- Liver cirrhosis is associated with sulphur aminoacid metabolism impairment and HHcy.
- Patients with PVT complicating liver cirrhosis have high frequency of HHcy.
- Patients with liver cirrhosis complicated by HCC and TVP have often HHcy.
- They resulted carriers for MTHFRC677T TT polymorphism, a possible risk factor for cancer.

BackgroundPortal vein thrombosis (PVT) is serious complication of liver cirrhosis (LC), especially in the presence of hepatocellular carcinoma (HCC). The liver plays a key role in homocysteine (Hcy) metabolism: mild hyperhomocysteinemia (HHcy) has been described in LC. HHcy is a risk factor for deep vein thrombosis. Methylen-tetrahydrofolate-reductase (MTHFR) C677T polymorphism is the commonest determinant of mild HHcy and has been involved also in cancer development.AimTo investigate a possible relation between HHcy, MTHFR status, HCC and PVT in patients affected by LC.Materials and methods100 patients affected by LC, 38 with (PVT group, 24 with HCC) and 62 without PVT (LC group, 14 with HCC) sex-, age-, liver disease stage and etiology-matched were assessed for thrombophilia, smoking status, plasma Hcy, MTHFRC677T polymorphism and homocysteine-related vitamin status.ResultsA higher prevalence of HCC, HHcy and MTHFR TT status was observed in PVT group. No significant difference in vitamin status was observed between groups. Patients with HCC showed significantly higher plasma Hcy and higher prevalence of HHcy than patients without HCC. They had also higher prevalence of MTHFR TT status. In patients with TT status (n = 11) and HCC, 10 had HHcy e 9 had PVT.ConclusionsMild HHcy is associated to LC may have a role in PVT development and assessment of plasma Hcy may be suggested in patients with LC (especially if complicated by HCC). Association between HCC and MTHFR TT status is intriguing, due the postulated role for this polymorphism in cancer: it may represent a possible link between HCC and PVT.