Studies have provided conflicting data for calendar trends in anal cancer among HIV+ individuals, one of the most frequent cancers in this population. Our objective here was to compare the risk of anal cancer between HIV+ and HIV- individuals in North America, and how this relationship has changed over time.
We conducted a cohort study involving 12 cohorts from North America followed between 1996 and 2007. Anal cancer incidence rates were compared between HIV+ men who have sex with men (MSM), HIV+ non-MSM (including women), and HIV- individuals. We calculated rate ratios (RRs) using multivariable Poisson regression with adjustment for age, sex, race/ethnicity (26% imputed), and calendar era. We next determined whether the adjusted RR for HIV+ compared with HIV- controls has changed over time. Since only a subset of cohorts contributed HIV- controls, we also computed age- and sex- and race-standardized incidence ratios (SIR) using national U.S. SEER rates.
Cohort-specific HIV+ anal cancer incidence rates ranged across cohorts from 0 to 154 cases per 100,000 person-years. The cohort-specific prevalence of MSM explained 58% of the total variability in rates. Overall, there were 111 anal cancer diagnoses among 15,907 HIV+ MSM, 38 diagnoses among 18,239 HIV+ non-MSM, and 79 diagnoses among 115,469 HIV- individuals. The corresponding adjusted RRs were 66.6 (95% CI: 36.9-120.2) for HIV+ MSM and 23.4 (95% CI: 11.9-46.1) for HIV+ non-MSM compared with the HIV- control group. For both HIV+ MSM and non-MSM, the RR was highest in 1999-2002, but the RR decreased for both groups in the most recent calendar era, 2003-2007 (Table 1), although the differences were not statistically significant (p>0.2) comparing RRs across eras. Inferences were similar for SIRs.
Table 1. Anal cancer RR (95% CI) for HIV+ MSM and HIV+ non-MSM compared with HIV- controls (reference) and national US SEER rates.
Despite an aging HIV+ population with presumed longer exposure to the oncogenic effects of human papillomavirus, the relative incidence of anal cancer among HIV+ individuals in the most recent calendar era has not increased. It is possible that improvements in immune function resulting from effective antiretroviral therapy contributed to this result.
The abstract is submitted on behalf of the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD).
This article has been published as part of Infectious Agents and Cancer Volume 5 Supplement 1, 2010: Proceedings of the 12th International Conference on Malignancies in AIDS and Other Acquired Immunodeficiencies (ICMAOI).The full contents of the supplement are available online at http://www.biomedcentral.com/1750-9378/5?issue=S1.