الفهرس 
HEPATITIS C V IRUSOnly 14 pages are availabe for public view
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Abstract
HCV is a major cause of viral hepatitis leading to chronic liver disease and liver failure. With an estimated prevalence of 3% in the world population (around 170 million infected individuals worldwide), HCV heavily burdens public health. Even though the incidence of new infections is declining, at least in industrialized countries where they are restricted to intravenous drug users, morbidity and mortality associated with HCV infection are expected to increase over the next decade.
Steatosis is a benign and reversible condition. However, in a few cases, Steatosis is associated inflammation and hepatocyte changes, and is then defined as steatohepatitis. Steatosis can also be a co-factor in many chronic liver diseases that can lead to fibrosis, cirrhosis and rapid progreassion of the course of the disease.
The gold standard for diagnosis of hepatic steatosis is liver biopsy which is an invasive method with some limitations. Recently, controlled attenuation parameter (CAP) has been introduced to detect and quantify hepatic steatosis. CAP measures the ultrasonic attenuation in the liver tissue depending on the viscosity [fat] of the medium [liver] and the distance of propagation of the ultrasonic signals into the liver. NAFLD was defined by CAP values ≥ 216 dB/m.
Direct acting antivirals (DAAs) are a new era in treating HCV and associated with high sustained virologic response (SVR), i.e. undetectable HCV RNA 12 weeks (SVR12) or 24 weeks (SVR24) after the end of therapy.
The aim of this study to use the fibroscan as non invasive modality for study the impact of hepatic steatosis on SVR in HCV infected patients receiving DAA therapy.
This prospective observational study was conducted on 40 patients diagnosed as HCV with NAFLD based on positive anti-HCV antibody, positive HCV viremia, abdominal ultrasonography, serum liver enzymes, body mass index (BMI).
All patients assessed by TE with CAP to detect and quantify hepatic steatosis (CAP cut off value ≥ 216 dB/m) and also assessed by non invasive scores (APRI score, FIB-4 score, HSI score).
All included patients were subjected to full history taking, thorough clinical examination, full laboratory investigations including: complete blood count, liver profile tests, kidney function tests, lipid profile, abdominal ultrasonography. After start of antiviral treatment, patients were seen every 4 weeks until the end of therapy and 12 weeks after the end of therapy to assess SVR-12.
Statistical analysis of the presenting data show:
1-The treatment responses rates:
The overall SVR (n=36) was 90% and was not impacted by presence of hepatic steatosis. TE with CAP can be used as non invasive method for assessment of hepatic steatosis.
2-The predictors treatment responses/failure:
The comparison between SVR and Non-SVR patients through the baseline parameters showed that patients who failed to treatment had significantly higher bilirubin, BMI and ALT. Furthermore, liver function parameters was improved significantly in majority of cases.
3-The Impact of treatment on biochemical profile:
The Impact of treatment regimens on the liver enzymes indices; transaminases was significantly declines during and after complete treatment. On the other hand, serum albumin level was significantly decreased. Regarding the complete blood count indices we found the HB% level was significantly changed with transient declining during the treatment periods. The WBCs count, PLT count were not significantly changed.