الفهرس 
INTRODUCTION
Pathogenesis of fibrosis in different liver diseasesOnly 14 pages are availabe for public view
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Abstract
In the last few years many studies were interested with the link between serum leptin level and hepatic steatosis and /or fibrosis. Some found a correlation and some did not found such link. This started a new argument about role of leptin in hepatic steatosis and fibrosis, also if leptin can be used as a marker for steatosis or fibrosis. This study was conducted on thirty one of chronic hepatitis C virus infected patients. Those patients were collected from the out patient clinic of the Gastroenterology center of Mansoura University. Patients were 22 males and 9 females with mean age of 45 years (from 30 yr to 58 yr). They were diagnosed according to detection of Anti HCV antibodies in their serum. Also HCV RNA was detected quantitatively in their serum. Patients were compared by a control group (8 males & 4 females) with mean age of 28 years ranging from 21 yr to 40 yr. They were collected too from the same centre. Patients were divided into two groups according to Metavir score after examination of liver biopsy. The first group includes patients from F0 to F2; the second group includes patients from F3 and F4. Patient history and epidemiological data were collected. Also patients were examined clinically. Body mass index was calculated according to weight and height. The following investigations were done: Liver function testes. Renal function testes. Lipid profile. Complete blood picture. Serum leptin levels were assayed in all patients and control groups. Results : A strong positive correlation was found between serum leptin level and BMI. So leptin levels were corrected according to body mass index, to exclude the effect of increased body fat mass in determining leptin level. Serum leptin level in patients was higher than in control group, also the same difference was still present after leptin correction. Serum leptin level was positively correlated to the degree of steatosis. Also this correlation was found after leptin correction to body mass index. But there was no correlation between serum leptin level and lipid profile, also there was no significant difference in lipid profile between patients and normal control or between the two groups of the study. A non significant correlation was found between leptin and the degree of fibrosis. Conclusion: The increased leptin level in patients with chronic hepatitis C than normal control indicates a link between leptin and chronic hepatitis C. The positive correlation between leptin and steatosis means either that leptin may be a direct causative factor in the development of steatosis or steatosis and HCV infection may activate hepatic stellate cells to excrete more leptin. The first concept was strengthened by the similar lipid profile in patients and control. The current study found that leptin was correlated to steatosis but not fibrosis. Recommendations: In chronic hepatitis C, our main concern relates to slowing progression of liver damage, either through sustained viral eradication or possibly continued therapy. In this regard we need to better define the role of potentially modifiable host factors such as steatosis. The functional significance of leptin mediated hepatic fibro genesis also needs to be characterized in term of fibrosis progression in chronic HCV infection. Prospective longitudinal studies may provide further information in this regard.