Patients with hepatitis C virus (HCV)-associated B-cell non-Hodgkin’s lymphoma (B-NHL) show a sustained and positive response to antiviral therapy, justifying its recommended use as a first-line treatment for those not needing immediate conventional treatment, researchers reported. The analysis, “The anti-lymphoma activity of antiviral therapy in HCV-associated B-cell non-Hodgkin lymphomas: a meta-analysis,” was published in the Journal of Viral Hepatitis.
An association between chronic HCV infection and B-NHL has been documented in many epidemiological studies. According to the National Institutes of Health (NIH), HCV infection increases the risk of developing non-Hodgkin’s lymphoma by as much as 30 percent. But the strongest evidence of causality between HCV infection and lymphoma development rests in observations of NHL regression after HCV is eradicated through antiviral therapy.
Researchers conducted an extensive literature review to find studies that included patients with B-NHL associated with hepatitis C, and who had received AVT to treat both the lymphoma and HCV. The primary endpoint for this study was correlation of sustained virological response (SVR) with lymphoma response to antiviral therapy. Secondary endpoints included overall lymphoma response rates and HCV-NHL response in correlation with lymphoma subtypes. Twenty reports that evaluated AVT efficacy in HCV-NHL were assessed, with a total of 254 patients evaluated.
Overall lymphoma response rate to AVT was found to be 73 percent. Moreover, a strong association was reported between SVR and lymphoma response (83%) compared to the failure to achieve SVR (53%). Additionally, researchers reported a trend toward favorable response for AVT in HCV-associated marginal zone lymphomas (response rate 81%) compared to nonmarginal zone origin (71%).
“In the current meta-analysis, the overall response rate of HCV-NHL under AVT justifies the recommendation for AVT as first-line treatment in patients who do not need immediate conventional treatment. The strong correlation of SVR and lymphoma regression supports the hypothesis of a causal relationship of HCV and lymphomagenesis,” the authors concluded.