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AIDS Res Hum Retroviruses. 2012 Sep;28(9):994-99. doi: 10.1089/AID.2011.0185. Epub 2012 Feb 2.

Opportunistic intestinal infections and risk of colorectal cancer among people with AIDS.

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Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA.


Because mucosal inflammation contributes to colorectal carcinogenesis, we studied the impact of intestinal infections on risk of this malignancy among people with AIDS (PWA). Using the population-based HIV/AIDS Cancer Match, which includes approximately half of all PWA in the United States, the cancer registries ascertained colorectal cancers (ICD-O3 codes C180-C189, C199, C209, and C260). During 4-120 months after AIDS onset, risk of cancer occurring after AIDS-defining intestinal infections (considered as time-dependent exposures) was estimated with hazard ratios (HR) and 95% confidence intervals (CI) calculated by Cox regression. Analyses included cancers overall and by histology and anatomic site. After excluding 118 squamous cell rectal cancers (possible anal cancers), we analyzed 320 incident colorectal cancer cases that occurred among 471,909 PWA. Colorectal cancer risk was marginally elevated following cryptosporidiosis (HR=2.08, 95% CI=0.93-4.70, p=0.08) and mucocutaneous herpes (HR=1.69, 95% CI=0.97-2.95, p=0.07) but not with Pneumocystis pneumonia (HR=0.79, 95% CI=0.57-1.10). Cryptosporidiosis was associated with rare colon squamous cell carcinoma [N=8, HR=13, 95% CI=1.5-110] and uncommon histologies [HR=4.4, 95% CI=1.1-18, p=0.04], but it was not associated with colorectal adenocarcinoma (N=269, HR=1.3, 95% CI=0.4-3.9, p=0.70). Mucocutaneous herpes was associated with colon squamous cell carcinoma (HR=13, 95% CI=2.4-67, p=0.003) but not with colorectal adenocarcinoma (HR=1.3, 95% CI=0.6-2.6, p=0.52) or uncommon histologies (HR=2.5, 95% CI=0.8-8.2, p=0.13). Colon squamous cell carcinoma risk was significantly elevated among PWA who had cryptosporidiosis or mucocutaneous herpes. These findings might suggest that HPV or inflammation from other infection may contribute to carcinogenesis.

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