The association between hepatitis B virus infection and nonliver malignancies in persons living with HIV: results from the EuroSIDA study. HIV Medicine
Mocroft and Miró et al. aimed to determine whether people living with HIV (PLWH) and hepatitis B virus (HBV) in the EuroSIDA study are at increased risk for nonliver cancer compared to PLWH without HBV.
All participants from the EuroSIDA study with known HBV status were included. HBV coinfection was defined as positive HBsAg, and the main outcome was the occurrence of any nonliver malignancy, including anal cancer, lung cancer, non-Hodgkin’s lymphoma and other cancers. Multivariable Poisson regression was used to compare incidence rates between individuals with and without HBV coinfection. The roles of HBV treatment and detectable HBV DNA were explored in additional models.
The study included 17’485 individuals, contributing 151’766 person-years of follow-up (PYFU). The median age was 41 years (IQR 35-49), median CD4 count 440 cells/μL (IQR 284-634), and 4’601 (26.3%) were women. HBV coinfection was present in 1’269 (7.2%) cohort participants. A total of 1’360 nonliver cancers occurred in 1’298 individuals (incidence rate [IR] 8.55 per 1’000 PYFU, 95% CI 8.09-9.92). The most common cancers were anal cancer (188 events), lung cancer (147 events) and non-Hodgkin’s lymphoma (131 events). In a multivariable analysis adjusted for age, CD4 cell count, HIV viral load, liver fibrosis and smoking status, individuals with HBV coinfection were at increased risk for the development of any nonliver malignancy compared to those without HBV (incidence rate ratio [IRR] 1.23, 1.00-1.51). The increased risk for HBV infected vs. HBV uninfected PLWH was most pronounced in individuals who did not receive tenofovir, emtricitabine or lamivudine during follow-up (IRR 1.45, 1.04-2.01), and in persons with detectable HBV DNA (IRR 1.37, 1.00-1.89 compared to HBV negative individuals).
In summary, the present study indicates that people living with HIV and HBV may be at increased risk for nonliver cancer. The association was strongest for individuals without HBV-active treatment and detectable HBV DNA, suggesting a role of HBV replication as a possible risk factor for the development of nonliver malignancies.