الفهرس 
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Abstract
HCV is a blood borne pandemic disease, causes liver decompansation and HCC. HCVAb and HCV-RNA RT-PCR are mandatory for diagnosis and beginning the antiviral therapy while, liver biopsy is useful in assessing the severity of the disease. HCV genotype and pretreatment viral load are the main pretreatment predictors for achieving SVR but not predictors for chronicity of infection. SVR rate is lower in genotypes 1 and 4 than genotypes 2 and 3. Pegylation of IFNα and addition of RBV increases SVR. Currently approved antiviral therapy for HCV is PEG-IFNα plus RBV for 48 weeks in genotypes 1 and 4, and for 24 weeks for genotypes 2 and 3. However, RVR and EVR can modify the treatment duration. In genotypes 2 and 3 who achieve RVR, treatment duration could be reduced to 16, 14 or 12 weeks with no effect on SVR. Also, in genotypes 1 and 4 who achieve RVR, treatment duration could be reduced to 24 weeks. However, in patients who fail to achieve RVR and had detectable HCV-RNA at week 12 but had ≥2 log reduction of pretreatment viral load and cleard HCV-RNA at week 24, extended treatment duration is recommended for 72 weeks. Current antiviral therapy has many side effects which affect adherence to therapy thus reduce SVR. So, close monitoring of the patients receiving this regimen is recommended. Psychatric illness and depression frequently affect these patients and their families which might need antidepressant therapy. However, preemptive anti-depressant therapy is not recommended unless the patients show signs of severe psychosis. The use of hematopiotic stimulating growth factors can avoid repeated interruptions of therapy due to anemia, thrombocytopenia or neutropenia thus increasing adherence to the therapy and SVR. Thyroid functions should be investigated before and during treatment especially in endemic areas. Any TD should be treated according to its nature while antiviral therapy is continued. Patients with normal aminotransferases are candidates for therapy since they might have ongoing liver fibrosis evidenced by liver biopsy. They have the same SVR rate when compared with patients with elevated liver enzymes. Patients with compensated liver cirrhosis are candidates for antiviral therapy and may benefit from it, especially who achieve SVR. On the other hand, antiviral therapy in patients with decompansated liver cirrhosis may progress their liver disease, worsen their liver functions and fasten their progression to HCC. So, it is preserved only for LT candidates to avoid HCV recurrance after LT, which increases morbidity and mortality. Liver retransplantation for HCV recurrence has poor outcomes. African-Americans have higher incidence of HCV infection (mostly genotype 1) than Caucasians and have lesser SVR rate even with the same adherence to the therapy. They also have early baseline neutropenia which might affect the treatment. However, they have the same recommendations for treatment as Caucasians. HCV infection causes many renal diseases especially MPGN type 1 caused mostly by type II MC. Treating patients in early stages may preserve renal function and delay the need for HD and RT. Using RBV combination with IFN shold be preserved for patients with creatinine clearance ≥50 ml/min/1.73 m2. IFN therapy seems to worsen renal function after RT and causes graft rejection. HCV infection especially genotype 3 carries higher risk of IR and hepatic staetosis which in turn help progression of liver diseases. Steatosis and IR decreases SVR rate. On the other hand, achieving SVR decreases hepatic steatosis and improves IR. Insulin sensitizers are used to decrease IR thus increasing SVR. HBV/HCV co-infection is not uncommon, especially within areas of high prevalence of HBV. Dual infections present unique management challenges given the complex interaction of HBV and HCV, and the probability for developing more severe liver disease. HCV usually suppresses HBV, but any scenario could happen. Treatment options mostly include PEG-IFNα with or without lamivudine or RBV. Treatment decisions should be made based on the determination of the dominant hepatitis virus. Caution must be exercised in treating coinfected patients, as flares of the untreated virus may occur.