الفهرس 
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Abstract
Nonalcoholic fatty liver disease (NAFLD) includes a wide range of liver clinicpathological conditions, starting from pure fatty steatosis (fatty infiltration in more than 5% of hepatocytes) which is a benign condition up to nonalcoholic steatohepatitis (NASH), which may develop to cirrhosis, liver failure and hepatocellular carcinoma (Noureddin et al., 2015).NAFLD has become by far the commonest chronic liver disease (CLD) in the United States, accounting for a steadily increasing percentage of CLD cases over the last quarter century. NAFLD accounted for 46.8% of CLD cases from 1988 to 1994; 62.8% from 1994 to 2004 and 75.1% from 2005 to 2008 (Younossi et al., 2011).
Visfatin was identified first as PreB cell Colony Enhancing Factor (PBEF). Recently, PBEF was identified by Fukuhara et al, as visfatin a novel adipokine (Fukuhara A et al., 2005).Visfatin is inflammatory cytokine that is produced and released by the adipose tissue derived macrophages. It promotes B-cell maturation, inhibits neutrophil apoptosis, enhances activation of leukocytes, synthesis of adhesion molecules and production of proinflammatory cytokines (DahL T et al., 2011). Visfatin is also suggested to be expressed in hepatocytes and inhibit apoptosis of hepatocytes in vitro, downregulation of visfatin in advanced inflammatory processes as NASH suggests a hepatoprotective role for visfatin(Jia SH et al., 2004).
The role of Visfatin in non-alcoholic fatty liver disease is unclear. Circulating serum visfatin levels in NAFLD patients were found to be higher than in healthy control subjects (Jarrar MH et al., 2008).Visfatin is inflammatory cytokine that is produced and released by the adipose tissue derived macrophages. It promotes B-cell maturation, inhibits neutrophil apoptosis, enhances activation of leukocytes, synthesis of adhesion molecules and production of proinflammatory cytokines (DahL T et al., 2011). Visfatin is also suggested to be expressed in hepatocytes and inhibit apoptosis of hepatocytes in vitro. Downregulation of visfatin in advanced inflammatory processes suggests a hepatoprotective role for visfatin(Jia SH et al., 2004).
The aim of the study was to evaluate serum visfatin level as a novel non-invasive marker for non-alcoholic fatty liver disease (NAFLD) and its role in progression to non-alcoholic steatohepatitis (NASH). To fulfill this aim, the present study was carried on 60 patients with NAFLD and 30 cntrol healthy subjects.
All subjects of the study will be subjected to History taking, clinical examination, calculation of body mass index, laboratory investigations including complete blood picture, liver function tests (AST, ALT, serum albumin, serum bilirubin and prothrombin time), fasting and 2hours postprandial blood glucose level, fasting blood insulin, insulin resistance by HOMA-IR, kidney function tests (serum creatinine and blood urea), lipid profile including (fasting triglycerides, cholesterol levels, LDL and HDL) , HBsAg, anti HCV AB, ANA and serum visfatin, calculation of NAFLD fibrosis score and ultrasound imaging.
The following results were obtained:
The present study showed that the circulating visfatin levels were significantly increased in subjects with NAFLD when compared to healthy controls. In addition, visfatin levels decreased markedly when NASH was diagnosed. However, it was still significantly higher than in healthy subjects.
In the present study in group I (NAFLD with normal ALT) there was positive correlation between visfatin and BMI, fasting blood sugar, HOMA-IR and NAFLD fibrosis score. While there was no correlation with transaminases and lipid profile.
But in group II (NAFLD with high ALT) there was no correlation between visfatin and anthropometric data, blood glucose level, HOMA-IR, transaminases, while There was negative correlation between visfatin and NAFLD fibrosis score.