Objective: The incidence of anal cancer among homosexual men exceeds that of cervical cancer in women, and HIV-positive homosexual men may be at even higher risk than HIV-negative men. Cervical cancer is preceded by high-grade squamous intra-epithelial lesions (HSIL) and anal HSIL may similarly be the precursor to anal cancer. In this study, we describe the incidence of and risk factors for HSIL in HIV-positive and HIV-negative homosexual and bisexual men.
Design: Prospective cohort study of HIV-positive and HIV-negative homosexual men.
Setting: The University of California, San Francisco.
Patients: 346 HIV-positive and 262 HIV-negative men enrolled at baseline, 277 HIV-positive and 221 HIV-negative homosexual men followed after baseline.
Study design: A questionnaire was administered detailing lifestyle habits, medical history and sexual practices. Anal swabs for cytology and human papillomavirus studies were obtained, followed by biopsies of visible lesions. Human papillomavirus testing was performed using polymerase chain reaction (PCR) and ‘hybrid capture’. Blood was obtained for HIV testing and measurement of CD4 levels.
Main outcome measures: Incident HSIL.
Results: HIV-positive men were more likely to develop HSIL than HIV-negative men relative risk (RR), 3.7; 95% confidence interval (CI), 2.6–5.7. Life-table estimates of the 4-year incidence of HSIL was 49% (95% CI, 41–56) among HIV-positive men and 17% (95% CI, 12–23) among HIV-negative men. Among HIV-positive men, those with lower baseline CD4 counts (P = 0.007) and persistent infection with one or more human papillomavirus types, determined using PCR (P = 0.0001), were more likely to develop HSIL.
Conclusions: HIV infection, lower CD4 levels and human papillomavirus infection were associated with high rates of incident HSIL among homosexual men. However, high rates were found at all CD4 levels among HIV-positive men and among HIV-negative men.
1Departments of Laboratory Medicine, University of California San Francisco, San Francisco, California, USA
2Departments of Stomatology, University of California San Francisco, San Francisco, California, USA
3Departments of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, USA
4Departments of Pathology, University of California San Francisco, San Francisco, California, USA.
5Requests for reprints to: Dr Joel Palefsky, Box 0100, Department of Laboratory Medicine, University of California San Francisco, San Francisco CA 94143, USA.
Sponsorship: Supported by grant NCI R01CA54053. These studies were carried out in the General Clinical Research Center, University of California San Francisco with funds provided by the Division of Research Resources 5 M01-RR-00079, U.S. Public Health Service.
Date of receipt: 5 June 1997; revised 28 November 1997; accepted 5 December 1997.