الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of pathological conditions, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis, in the absence of excessive alcohol consumption. NAFLD increases the risk of end-stage liver disease, and induced liver failure is one of the most important reasons for liver transplantation. It is also strongly associated with overweight/obesity, insulin resistance (IR), type 2 DM.
NAFLD is closely associated with features of the metabolic syndrome and is regarded as the hepatic manifestation of the syndrome. The amount of intrahepatic fat closely correlates with serum liver enzyme levels and the number of metabolic syndrome features, the underlying mechanisms linking NAFLD with IR, type 2DM and poor glycemic control may originate from the development of an expanded and inflamed visceral adipose tissue mass, where IR causes intrahepatic triglyceride accumulation or vice versa.
Visceral adipose tissue-derived serine proteinase inhibitor (vaspin) was identified from visceral adipose tissues of OLETF (Otsuka Long- Evans Tokushima Fatty) rats, the increased vaspin expression may be an intrinsic compensatory mechanism in adipose tissue as a response to decreased insulin sensitivity or impairment of glucose metabolism. Serum vaspin levels significantly correlated with body mass index (BMI) and IR in obese type 2 diabetic patients as well as, it decreased by weight reduction and lifestyle modification in obese adults.
Our study aimed to assess the serum vaspin level in patients with NAFLD and NASH. Also, to assess the relationship between serum vaspin level and different laboratory, metabolic and anthropometric parameters.
Our study was a descriptive cross sectional survey conducted on 50 age and sex matched subjects, recruited from the outpatient clinic of the Internal Medicine Department, Alexandria Main University Hospital. They were divided into: group I: 20 patients with NAFLD and BMI more than 30 kg/m2; group II are 20 patients with NASH and BMI more than 30 kg/m2; and group III: 10 healthy subjects with BMI ranged from 18.5 to 24.9 kg/m2 as a control group. We excluded patients with diabetes mellitus, hypertension, renal failure, and/or manifest heart diseases such as cardiac failure, coronary arterial disease and arrhythmia, hepatic failure, history of alcohol intake, virus hepatitis, certain drugs (as amiodarone, tamoxifen and methotrexate), metabolic abnormalities (as galactosemia, glycogen storage diseases, homocystinuria, and tyrosinemia), or other health problems (as celiac sprue and wilson’s disease).
All of our 50 subjects included in the three groups signed an informed consent, and underwent full history taking, blood pressure, body weight and waist circumference measurements and BMI was calculated. Fasting blood sugar, HOMA–IR was calculated, lipid profile, AST, ALT with AST/ALT ratio, serum vaspin level measured by ELISA then abdominal ultrasonography was made for all 50 Patients. All results were tabulated and all measured parameters were correlated with serum vaspin level in patients with NAFLD and NASH.