Karaciğer hastalıklarında (siroz veya hepatit) homosistein ve selenyum düzeyleri

Background/aim: The liver has a crucial role in homocysteine synthesis and metabolism. Important changes in homocysteine metabolism occur when hepatic deficiency exists. Selenium levels have also been reported as being decreased in liver damage. Furthermore, many changes take place in the liver when selenium deficiency occurs, and the role in pathogenesis is being investigated. We aimed to search the changes in homocysteine and selenium levels in liver damage and determine the probable influencing factors. Materials and methods: Twenty-two chronic hepatitis (m:11, f:11, average age: 43.90±15.02), 28 cirrhotic patients (m:25, f:3, average age: 42.50±16.00) and 20 healthy subjects (m:12, f:8, average age: 36.65±8.29) were included in the study. Etiology was hepatitis B in 36, hepatitis C in 7, hepatitis B + D in 3 and Wilson disease in 1 patient. Three patients had cryptogenic cirrhosis. Homocysteine level was measured by fluorescent detector using high performance liquid chromatography (HPLC); selenium level in graphite mode by atomic absorption; AST, ALT, GGT and albumin by Abotte Aeroset autoanalyzer with photometric method; and vitamin B12 and folate levels by ELECYSIS E170 using chemiluminescence method; methylene tetrahydrofolate reductase (MTHFR) gene analysis in DNA of whole blood samples was done. Results: There was no significant difference between the three groups with respect to age. Both chronic hepatitis and cirrhotic groups had higher homocysteine levels than those of the control group (p=0.001). There was no difference in homocysteine levels between chronic hepatitis and cirrhotic groups. On the other hand, there was no difference between chronic hepatitis and control groups with respect to vitamin B12 levels. Vitamin B12 level was higher in the cirrhotic group than in controls and the difference was statistically significant. There was no difference between any of the groups in respect to folate levels. MTHFR gene mutation was similar in both patient and control groups. Selenium level was found to be lower in both patient groups than in the control group (p=0.001). Conclusion: Our results showed that hyperhomocysteinemia in chronic hepatitis and cirrhosis is not related to deficiency in folate and vitamin B12 and MTHFR gene mutation. It is seen that other enzymes involved in homocysteine metabolism might play a part in this process. It is noteworthy that selenium deficiency exists in both chronic hepatitis and liver cirrhosis.