Health & Medical AIDS & HIV

Cancers Attributable to Infections Among Adults With HIV

Cancers Attributable to Infections Among Adults With HIV

Results


Table 2 shows the estimated numbers of incident cancer cases in the HIV-infected people in the year 2008 in the United States for each infection-associated cancer site or histological type. Of the estimated 6231 new cancer cases (95% CI 6041–6538), 2512 (95% CI 2375–2709) were attributable to infection (attributable fraction 40%, 95% CI 39–42). The most important infection-associated cancer sites were Kaposi sarcoma, lymphomas (especially NHL), and ano-genital cancers, comprising 85% of all cancer cases attributable to infection. Among ano-genital cancers, anal cancer was preponderant (Table 2), and 93% of anal cancer cases occurred in men. The three main infectious agents responsible for cancers in HIV-infected people were KSHV, which caused 789 cases [95% CI 703–882 (13% of all cancer)]; EBV, which caused 768 cases [95% CI 687–878 (12% of all cancer)]; and HPV, which caused 632 cases [95% CI 571–723 (10% of all cancer)]. Together, these three agents caused 2189 cases (95% CI 2059–2389), that is, 87% of all cancers attributable to infection and 35% of all cancers. HBV and HCV together caused 285 cases of liver cancer (95% CI 234–341), which corresponds to an attributable fraction of 94% (95% CI 90–97) of liver cancers for the two hepatitis viruses together. The contribution of HCV was nearly four-fold larger than the one of HBV (Table 2).

Figure 1 shows the burden of cancer attributable to infection in relation to the total cancer incidence (Fig. 1a), and the breakdown of infection-attributable cancer by agent (Fig. 1b) for both the general US population and the HIV-infected people (for further details, see Appendix Table 3). In the general US population, the proportion of cancers attributable to infection was 4% compared to 40% in the HIV-infected people (Fig. 1a). In a sensitivity analysis adjusting the age and sex distribution of the general population to match that of the HIV-infected population, the proportion of infection-attributable cancers in the general population increased from 4 to 5%, showing that the much higher proportion of infection-attributable cancer in HIV-infected people is not due to demographic differences. Figure 1b shows infectious agents among cancers attributable to infection. This represents the same cases as the upper panel, but shows the distribution after removing cancers nonattributable to infection (shown in gray in Fig. 1a). The spectrum of infectious agents causing cancer in the general population is quite different from the HIV-infected population. H. pylori causes a much smaller proportion of infection-attributable cancers in the HIV-infected population than in the general population. Conversely, EBV and KSHV cause a higher proportion of infection-attributable cancers. Liver cancers due to HBV and/or HCV account for a similar proportion of infection-attributable cancers in the HIV-infected people (11%) and the general population (13%) (data not shown).



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Figure 1.



Cancer attributable to infection in the general population and HIV-infected people in the USA in 2008. AF, attributable fraction; EBV, Epstein–Barr virus; H. pylori, Helicobacter pylori; HBV, hepatitis B virus; HCV, hepatitis C virus; HPV, human papillomavirus; KSHV, Kaposi sarcoma herpes virus.





Table 3 shows the breakdown of infection-associated cancers and corresponding attributable fractions by age, race/ethnicity, and combination of sex and risk groups. The attributable fraction in HIV-infected people was highest in young people (attributable fraction 69% in age group 20–29 years, 95% CI 65–72), and this decreased with age. Sixty-nine percent of the cases of infection-attributable cancers occurred in MSM and MSM-IDU, among whom the highest infection-attributable fractions are also found (attributable fraction 48%, 95% CI 46–50; and attributable fraction 46%, 95% CI 43–50, respectively), due to the high number of both Kaposi sarcomas (n = 631 in MSM, n = 60 in MSM-IDU) and anal cancers (n = 313 in MSM, n = 44 in MSM-IDU) in these groups compared to others.

Figure 2 shows age-specific incidence rates of cancer attributable to individual infections or nonattributable to infection (for further details see Appendix Table 4). The incidence rate of cancer nonattributable to infection steeply increased with age, but the incidence of infection-attributable cancers increased very little after the age 30 years. The composition of cancers due to different infectious agents, however, varied substantially by age group. Below the age of 30 years, nearly all infection-attributable cancers in the HIV-infected people were due to KSHV or EBV. Incidence rates of cancers attributable to HPV increased after age 30, and those of cancers attributable to HBV/HCV and H. pylori increased after age 40.



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Figure 2.



Estimated cancer incidence among HIV-infected people in the USA in 2008 by age. EBV, Epstein–Barr virus; H. pylori, Helicobacter pylori; HBV, hepatitis B virus; HCV, hepatitis C virus; HPV, human papillomavirus; KSHV, Kaposi sarcoma herpes virus.







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