875
Cancer Risk in 57,350 HIV-Infected Individuals in the US (1991-2002): Relationship with Immunosuppression and Changes Over Time
Eric Engels*1, J Goedert1, I Hall2, H Cross3, A Crutchfield4, J Finch4, B Grigg5, T Hylton5, K Pawlish3, and R Biggar1
1NCI, Rockville, MD, US; 2CDC, Atlanta, GA, US; 3New Jersey Dept of Hlth and Senior Svcs, Trenton, US; 4Colorado Dept of Publ Hlth and Environment, Denver, US; and 5Florida Dept of Hlth, Tallahassee, US
Background: HAART,
available since 1996, improves immunity in people with HIV (PWH). Although much
data exist on cancer risk in persons with AIDS, population-based data for less
advanced HIV disease, and the relation of immunity and HAART to cancer risk, are
limited.
Methods: We linked HIV
and cancer registry data from 3 U.S.
states (CO, FL, NJ). Standardized incidence ratios
(SIRs) compared cancer risk in PWH (initially AIDS-free) during the 5-year
period after registration vs. general population. Poisson regression provided
relative risks (RRs) of selected cancers by AIDS onset, calendar year, and CD4
count at HIV registration, adjusted for sex and age.
Results: 57,350 PWH
were registered in 1991-2002. Baseline CD4 count was available on 27% (median CD4
491 cell/ul, IQR 356-685). 871 incident cancers arose during follow-up. SIRs were
elevated (p<0.05) for Kaposi sarcoma (KS, SIR 1251 [173 cases]); non-Hodgkin
lymphoma (NHL, 7.3 [203]), especially central nervous system NHL (246 [28]);
Hodgkin lymphoma (HL, 5.6 [36]); and cancers of lung (2.6 [109]), cervix (2.9
[28]), oral cavity (1.7 [26]), anus (9.2 [18]), liver (2.7 [14]), and penis
(5.4 [3]). Risk increased after AIDS onset during follow-up for KS (RR 7.2,
95%CI 5.3-9.7), NHL (4.1, 3.0-5.5), HL (3.0, 1.4-6.5), and cancers of cervix
(2.2, 0.9-5.5) and lung (2.1, 1.3-3.3). In 1996, risk declined for KS (RR 0.4,
95%CI 0.3-0.5) and NHL (0.7, 0.5-0.9); declines were strongest for PWH who had
developed AIDS. Cervix and lung cancer risk did not change in 1996, and HL risk
increased (RR 2.2, 0.9-5.7). Risk was inversely related to baseline CD4 for KS
(p<0.001) and NHL (p=0.02), but these associations attenuated after 1996 (p=0.007
and p=0.22). No CD4 association was seen for other cancers, although data were
sparse.
Conclusions: Our
population-based study of U.S. PWH is the largest to date. High cancer risk at some
sites reflects immunosuppression, viral coinfections, and smoking. Associations
with immunosuppression (AIDS onset, lower baseline CD4) were stronger for KS
than NHL. Notably, risk for these 2 cancers fell in 1996 coincident with HAART,
and declines were larger in PWH who had developed AIDS. In contrast, risks of
HL and cancers of cervix and lung increased with AIDS onset but were unrelated
to CD4 count, pointing to a more complex relationship with immunity. Indeed,
the rise in HL since 1996, previously reported for people with AIDS, suggests
that incomplete immune restoration increases HL risk.
|
