Tumour necrosis factor alpha polymorphisms are not involved in the development of steatosis in chronic hepatitis C

AIMTo determine whether the different tumour necrosis factor alpha (TNF-α) promoter gene polymorphisms are involved in the development of steatosis in chronic hepatitis C. PATIENTS AND METHODSOne hundred and thirty patients (89 men and 41 women; mean age 42.5 ± 12.3 years) with chronic hepatitis C were included. Insulin resistance was measured according to the Homeostasis model assessment (HOMA IR). Serum leptin levels were also obtained and the body mass index and fat mass were calculated. Liver biopsy was carried out in all the patients, and steatosis was measured as one of four stages (0 to 3)stage 0, no steatosis; stage 1, < 25% of hepatocytes with steatosis; stage 2, 25–50%; and stage 3, > 50%. DNA samples were obtained in order to describe the polymorphisms at the TNF-α promoter gene position. RESULTSFifty-nine of the 130 (45.38%) patients had different degrees of steatosis, while 71/130 (54.62%) were not steatosic. Six of the 59 (10.2%) patients with steatosis presented mutations at the −238 position of the TNF-α promoter region, while 5/71 (7.0%) patients without steatosis also showed mutations at this position (P = NS). Seventeen of the 59 (28.8%) steatosic patients showed a mutation at the −308 position, while 16/71 (22.5%) without steatosis also had this mutation (P = NS). Insulin resistance, beta cells reserve, insulin and leptin levels showed no differences between patients with or without mutations at the promoter region of the TNF-α gene. CONCLUSIONSTNF-α mutations do not seem to play any role in the development of steatosis in chronic hepatitis C.