الفهرس 
NONALCOHOLIC FATTY LIVER DISEASEOnly 14 pages are availabe for public view
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Abstract
Over the past few years there has been an expansion in studying and reporting various cases of NAFLD, propably secondary to the worldwide epidemic of obesity and type 2 DM.
NAFLD encompasses a spectrum of histopathology ranging from simple steatosis at the most clinically benign end of the spectrum to cirrhosis at the opposite extreme where most liver related morbidity and mortality occur while NASH is believed to be an intermediate lesion characterized by hepatocyte injury, death and inflammation and more liability of progressive fibrosis.
With all the progress that has occurred in studying various aspects of NAFLD, liver biopsy evaluation has retained an essential role in the clinical diagnosis and in assessing the prognosis with no factor that determine the disease progression had been established. However the frequent absence of manifestations of liver disease, the reluctance in performing liver biopsy in other wise apparently healthy individuals with fatty liver along with possible limitations of liver biopsy like probable complications and sampling errors; increase the need for non-invasive predictors of hepatic damage.
Adipokines are associated with various metabolic disorders including insulin resistance, obesity, and dyslipidemia. Metabolic disorders have also been reported to be associated with nonalcoholic fatty liver disease (NAFLD).
Several adipocytokines have been implicated in the pathogenesis non-alcoholic fatty liver disease (NAFLD).
In our study we aimed to identify various clinical and/or biochemical factors that may be associated with increased serum resistin level in patients with NAFLD and to correlate it with different laboratory profiles as liver function tests, blood glucose level, lipid profile, C- reactive protein and different grades of hepatic steatosis graded by abdominal ultrasound.
This study included 60 patients divided into three equal groups as following:
-Group 1: 20 obese and non obese patients diagnosed as nonalcoholic steatohepatitis with chronic elevation of transaminase levels (1.5 times the upper normal value for three months or longer) and the presence of ultrasound signs of liver steatosis with body mass index range (20-35 kg/m²).
-Group 2: 20 obese patients with body mass index above (30 kg/m²) without ultrasound signs of liver steatosis and normal transaminase levels.
-Group 3: 20 subjects as a control group without ultrasound signs of liver steatosis and normal transaminase levels, with body mass index range (20-30 kg/m²).
-All the patients were subjected to the following:
1- Full history taking and thorough clinical examination.
2- Body mass index BMI=weight(kg)/height²(m²).
3- Abdominal ultrasound.
4- Laboratory tests:
a- Complete blood picture.
b- Fasting and two hour post prandial blood glucose levels.
c-Liver function tests including alanine amino transferase(alt), aspartate aminotransferase(ast), alkaline phospahatase, gamma glutamyl Tran peptidase (GGT), total and direct bilirubin, serum albumin, and prothrombin time.
e- Autoantibodies of autoimmune hepatitis( Antinuclear Ab, Anti smooth muscle Ab, Anti liver-kidney microsomal Ab and Anti mitochondrial Ab).
f- kidney function tests : blood urea and serum creatinine.
g- Total cholesterol, high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL) and triglyecerides.
h- C-reactive protein.
I-Serum resistin level by ELISA.
J- statistical analysis of clinical, laboratory and ultrasound findings.