- HCV treatment offers the possibility of eradicating HCV within a defined treatment period. This is potentially advantageous for the subsequent management of the patient with HIV, and every co-infected patient should therefore be considered for treatment when the benefits of therapy outweigh the risks. This also needs to be seen in the context of faster liver fibrosis progression in HIV/HCV co-infection and with better HCV treatment outcome with improved management in these patients.
- Information on liver fibrosis staging is important for making therapeutic decisions in co-infected patients. However, a liver biopsy is not mandatory for considering treatment of chronic HCV. Current therapy is particularly recommended in patients with a high likelihood of achieving sustained virological response (SVR): genotypes 2 or 3 and patients infected with genotype 1 if the viral load is low (<400.000 IU/ml). More recently, insulin resistance (which can be determined using the homeostasis model assessment of insulin resistance HOMA IR) has been repeatedly reported as a negative predictor of achievement of SVR and therefore may also be considered during pretreatment evaluation and, if possible, should be effectively managed before treating HCV infection.
- In case of the availability of a liver biopsy or FibroScan demonstrating lower stages of liver fibrosis (F0-1), regardless of HCV genotype, treatment can be deferred. In these cases, fibrosis assessment should be carried out at frequent intervals to monitor for fibrosis progression. A liver disease stage assessment is especially important to perform in patients with a low chance of SVR.
- The combination of Peg-INF alpha and ribavirin (RBV) is the treatment of choice for HCV infection. The standard dose for Peg-INF 2a is 180 μg once weekly, and for Peg-INF 2b it is 1.5 μg/kg bodyweight once weekly. An initial weight adapted dose of RBV of 1000 (wt # 75kg) -1200 (wt > 75kg) mg/day (administered bid) is recommended for all HCV genotypes in the HIV setting.
- The primary aim of anti-HCV treatment is sustained virological response defined as undetectable serum HCV-RNA 24 weeks after the end of therapy, evaluated using sensitive molecular tests.
- If chronic hepatitis C is detected early in the course of HIV infection (before the initiation of HAART is necessary), treatment for chronic HCV is advised. However, if a co-infected patient has significant immunodeficiency (CD4 count < 350 cells/μl), the CD4 count should be improved using HAART prior to commencing anti-HCV treatment. Patients with a CD4 relative percentage >25% are more likely to achieve SVR than lower CD4 percentage.
- If an early virological response (decline of at least 2 log10 reduction in HCV-RNA at week 12 compared to baseline) is not achieved, treatment should be stopped (figure 3).
- During Peg-INF plus ribavirin therapy, ddI is contraindicated in patients with cirrhosis and should be avoided in patients with less severe liver disease. D4T and AZT should also be avoided if possible. The role of abacavir is uncertain at this point but cohort data suggests lower SVR results in patients receiving abacavir containing HAART. Data investigating RBV plasma levels have shown that the interaction between abacavir and ribavirin may be negligible if weight based ribavirin is used.
- In patients with acute HCV infection, HCV therapy is recommended if HCV-RNA is confirmed positive (1 week apart) by week 12 post HCV transmission, as SVR rates following treatment of acute HCV-infection are higher than for treatment of chronic HCV. Most experts recommend therapy for 24 weeks with Peg-INF and ribavirin; however the duration of therapy and use of ribavirin is currently under discussion. HCV-RNA levels at week 4 and 12 may help to guide treatment duration.
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