- Category: HIV/HCV Coinfection
- Published on Friday, 24 February 2012 00:00
- Written by Liz Highleyman
Interferon-based treatment for chronic hepatitis C helps slow liver disease progression among HIV/HCV coinfected patients as it does for people with hepatitis C alone, according to study findings reported in the January 2012 Journal of Hepatology.
Over years or decades, chronic hepatitis C virus (HCV) infection can lead to advanced liver damage including cirrhosis (scarring) and hepatocellular carcinoma, a form of primary liver cancer.
Research has shown that successful treatment using pegylated interferon (Pegasys or PegIntron) plus ribavirin can slow, halt, or even reverse liver fibrosis, but this has not been as well studied in HIV positive people. On average, HIV/HCV coinfected people experience more rapid liver disease progression and do not respond as well to interferon-based therapy; HCV-related liver disease is a leading cause of death among people with HIV.
In the present study, Patrick Ingiliz and Yves Benhamou from Pitié-Salpêtrière Hospital in Paris and colleagues retrospectively evaluated liver disease progression using information from a French hospital database.
The analysis included 126 HIV/HCV coinfected patients who received repeated liver biopsies; 68 had received hepatitis C treatment and 58 had not. About 80% were men and the average age at the time of first biopsy was 33 years. The median interval between first and last biopsy was 4 years (range 6 months to 15 years). The researchers compared factors linked to fibrosis progression and the impact of response to treatment.
- Interferon-based treatment was associated with reduced likelihood of fibrosis progression, with the best outcomes seen in people who achieved a cure:
o Untreated patients: 35 of 58 (44%) with worse fibrosis over time;
o Treated non-responders and relapsers: 22 of 50 (44%) with worse fibrosis;
o Treated with sustained virological response (SVR): 5 of 18 (28%) with progression.
- The likelihood of liver fibrosis progression was significantly lower among patients achieving SVR compared with untreated and non-responder/relapser patients (odds ratio 3.16 for improvement vs stability vs worsening; P < 0.02).
- This pattern persisted after adjusting for other known predictors of liver fibrosis, hepatitis B triple infection, CD4 T-cell count, and alcohol consumption (adjusted odds ratio 2.89; P = 0.03).
"HCVtreatment can stop fibrosis progression and induce its regression," the study authors concluded.
Non-responders to treatment may still experience rapid fibrosis progression, they continued. "It remains to be clarified if the same factors that induce non-response to treatment may also induce faster fibrosis progression."
P Ingliz, MA Valantin, P Preziosi, et al. Influenceof interferon-based therapy on liver fibrosis progression in HIV/HCV coinfected patients: a retrospective repeated liver biopsy analysis. Journal of Hepatology 56(1):49-54. January 2012.