HIV-infected individuals on antiretroviral therapy who also have chronic coinfection with hepatitis B or C virus have an increased risk of developing non-Hodgkin lymphoma, according to new research published in Annals of Internal Medicine.
Lead author Qing Wang, PhD, of the Basel Institute for Clinical Epidemiology & Biostatistics at University Hospital Basel, Switzerland, and her coauthors said there is growing evidence of an association between both chronic hepatitis B virus infection (HBV) and chronic hepatitis C virus infection (HCV), and non-Hodgkin lymphoma, with chronic immune activation and B cell proliferation suggested as potential mechanisms. However, the impact of chronic coinfection in individuals with HIV is unclear.
Researchers undertook a cohort study of 52,479 treatment-naive individuals with HIV infection, using 18 of 33 cohorts from the Collaboration of Observational HIV Epidemiological Research Europe. Of these participants, 1,336 had chronic HBV and 7,506 had chronic HCV infection, and more than three-quarters (77%) later started treatment with antiretroviral therapy.
After 13 months of follow-up in the treatment-naive group and 50 months in the antiretroviral group, there were 252 cases of non-Hodgkin lymphoma in the treatment-naive group and 310 cases in the treated group ().
Antiretroviral-treated patients with chronic hepatitis B showed a significant 74% greater risk (95% confidence interval, 1.08-2.82) and those with hepatitis C showed a 73% greater risk (95% CI, 1.21-2.46) of non-Hodgkin lymphoma compared to treated individuals with neither coinfection. However, the differences in non-Hodgkin lymphoma rates in treatment-naive HBV and HCV coinfected individuals were not significant, which the authors suggested could be due to lower numbers of events and limited follow-up.
“The median CD4 count at the time of NHL diagnosis was less than 0.250 x 109 cells/L in both ART-naive and treated patients coinfected with HBV and HCV, indicating that coinfected patients with NHL initiate ART late or have insufficient HIV viral control and immune recovery that may be due to multiple reasons,” the authors wrote. “This unfavorable constellation is aggravated by the fact that chronic HBV infection attenuates immune recovery in ART-treated patients; whether this is also the case for chronic HCV infection is less clear.”
The authors said routine screening for chronic HBV and HCV infection, in conjunction with early diagnosis and treatment of HIV infection, was essential to reduce morbidity and mortality from non-Hodgkin lymphoma.
“Our findings provide strong evidence that HCV coinfected patients with poor immune status or restoration (CD4 count lower than 0.250 x 109 cells/L) are at high risk for NHL and death and deserve high priority for access to well-tolerated, interferon-free, direct-acting antiviral treatment programs similar to those for patients with advanced liver fibrosis or cirrhosis.”
The study was supported by the European Union Seventh Framework Programme, Schweizerische Krebsliga, Agence Nationale de Recherches sur le SIDA et les Hepatites Virales (ANRS), Paris; the HIV Monitoring Foundation, Amsterdam; and the Augustinus Foundation, Copenhagen. Eleven authors declared grants, personal fees, and other support from pharmaceutical companies including those involved in the manufacture of HIV and hepatitis drugs. No other conflicts of interest were reported.