[Preneoplastic anal lesions and anal canal carcinoma]

Anal canal cancer rate is relatively high among HIV-positive patients, particularly in homosexual men, where it is twice that of HIV-negative homosexual men. As for uterine cervix cancer, it is possible that anal canal cancer is linked to human papillomaviruses (HPV): in fact, its oncogenic serotypes are found in 60% of tumours. Most of anal mucosa in HIV-positive patients is infected by HPV. It causes Anal Squamous Intraepithelial Lesions (ASTI): low grade and high grade squamous intraepithelial lesions, which can probably progress to invasive anal cancer. In the anal mucosa, HPV induces clinically flat condylomata. They generally are invisible and revealed only by acetic acid application. Sixty percent of seropositive gay men and 26% of seropositive women have anal ASTI. This rate is higher than in the general population. A decreasing of systemic and local immunity and so probable interactions between HPV and HIV could explain the frequency of anal ASTI among seropositive patients. Introduction of highly active antiretroviral therapy does not really influence the evolution of anal dysplasia. Screening of preneoplastic lesion is possible with anal Pap smear, and when it is positive, patients must undergo high resolution anuscopy. Cost effectiveness analyses indicate that only the highest risk group (HIV-positive gay men) should have anal screening. Only high grade squamous intraepithelial lesions have to he systematically treated, low grade squamous intraepithelial lesions could he simply followed up. The best treatment of anal dysplasia is surgical excision, with careful follow-up, because of high recurrence rate among seropositive patients.