الفهرس 
HISTORY OF HCVOnly 14 pages are availabe for public view
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Abstract
E
ighty patients with chronic hepatitis HCV-related had been enrolled in this study, they divided into two groups, and were chosen from out-patient clinic in Ain Shams Specialized Hospital and Ain Shams University Hospital. Sixty patients in group I, with chronic active hepatitis (liver enzymes elevated more than two folds) HCV-related, with normal BMI and s.cholesterol. They were 44 males and 16 females, their age ranged from 21-50 years. Twenty patients in group II, with chronic non active hepatitis (mildly elevated liver enzymes)HCV-related, with increased BMI and normal or elevated s.cholesterol. They were 14 males and 6 females, their age ranged from 23-57 years.
To evaluate the significance of low density lipoprotein containing hepatitis C virus RNA in patients with chronic active hepatitis C infection, and compare the results with that of serum viral load, and necroinflammatory index in liver biopsy.
All patients were consecutively examined, none had been previously treated with interferon. Diagnosis of chronic active HCV infection was based on abnormal serum aminotansferases level of more than 6 months’ duration, and positive testing for serum anti-HCV markers and HCV-RNA. Liver biopsy was performed following clinical indication in all patients. Patients with cirrhosis (by histology, laboratory evidence of liver failure, and/or ultrasound-proven portal hypertension) hepatocellular carcinoma or any other cause for liver disease other than chronic hepatitis C, including hemochromatosis, alpha-1 antitrypsin deficiency, co-infection with HBV, Wilson’s disease, autoimmune hepatitis, alcoholic liver disease, recent or old schistosomiasis, and drug-related liver disease were excluded. Patients with positive testing for HIV or diabetes mellitus were also excluded. Those who received treatment for any other chronic medical illness were not eligible for this trial.
All patients underwent through chemical profile (Liver functions: serum bilirubin, ALT (alanin transaminase), AST (aspartate transaminase), alkaline phosphatase, serum albumin, alfa fetoprotein, and prothrombin time. Fasting plasma glucose, serum lipid pattern (total cholesterol, HDL, LDL, VLDL, and triglycerides), CBC, serum uric acid, serum creatinin, and blood urea), HCV Ab, HCV genotyping, serum HCV RNA, HCV RNA in LDL, liver biopsy, abdominal ultrasound, and BMI.
All patients were genotype 4, had normal CBC, s. albumin, s. bilirubin, prothrombin concentration, alkaline phosphatase, fasting blood sugar, AFP, s. uric acid, s. creatinin, and blood urea. BMI < 25 kg/m(2) in group I, and ranged from 25.2 to 34.2 kg/m(2). Normal s. cholesterol in group I and ranged from 143 to 240 mmol/dl in group II. Abdominal ultrasound revealed coarse liver, with no splenomegaly.
In our study group, HCV RNA was found in low density lipoprotein and represented 12.29% to 96.71% of total plasma HCV RNA. In the control group, HCV RNA was found in low density lipoprotein and represented 10.57% to 93.43% of total plasma HCV RNA.
In our study group, no correlation was found between HCV RNA in LDL, and HCV RNA serum level, fibrosis score, necroinflammatory index, liver enzymes or steatosis.
This explained by: hepatitis C virus RNA circulates in the blood of persistently infected patients in lipoviroparticles (LVP), which are heterogeneous in density and associated with host lipoproteins and antibodies. The variability and liability of these virus-host complexes on fractionation has hindered our understanding of the structure of LVP and determination of the physiochemical properities of the HCV virion.
Although classical hepatitis C virus (HCV) virions have been reported by some investigators, their role in the HCV life cycle has not been clearly identified. The detailed morphological analysis of authentic HCV particles is missing.
In our study group, there were no correlation between serum HCV RNA level and the grade of liver necroinflammatory activity and the stage of fibrosis.
However, other reports concluded that patients with chronic hepatitis without cirrhosis, the serum HCV RNA levels reflected the grade of liver necroinflammatory activity and the stage of fibrosis.
In our study group, there was no correlation between serum HCV RNA level and degree of steatosis.
In our study, there was no significant statistical difference between the two groups (group I with elevated enzymes more than 2 folds, and group II with mildly elevated enzymes) as regards serum HCV RNA level.
In our patients, there was no correlation between serum HCV RNA level and mean ALT/AST.
However, other reports found a statistically significant correlation between HCV RNA and aminotransferase levels.
In our study group, steatosis was present in only 21.66%, mild steatosis was present in 16.66%, moderate steatosis was present in 5%. This explained by: all patients in group I had BMI <24kg/m2, with no history of diabetes mellitus, or hyperlipidemia, and steatosis in HCV genotype 4 is mainly due to metabolic factors.
In our study group, there was no correlation between the degree of steatosis and mean ALT/AST. This is explained by: patients with only high grade of steatosis shows higher serum levels of ALT. Non of our studied patients had sever steatosis.
In our study group, there was a highly significant correlation between the degree steatosis and fibrosis score.
In our study group, there was no correlation between the degree of steatosis and necroinflammatory index score.
In our patients, there was no correlation between mean ALT/AST value and necro-inflammatory index score and fibrosis score.
However, other reports concluded that there were a statistically significant correlation between histological activity index (HAI) and both AST and ALT levels. The fibrosis score was significantly associated with AST and ALT values.
In our study, there was a highly significant statistical difference between group I and II as regards steatosis score. This is explained by: hepatic steatosis was associated with increased BMI (all patients in group II had elevated BMI, while in group I, BMI was normal in all patients).
In group II, s. cholesterol was elevated in 4 patients (20%). This is may be due to increased BMI, as HCV is usually associated with clinically significant lower cholesterol level.