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RESEARCH ARTICLE

14. Natural history of high-grade squamous intraepithelial lesions (HSIL) in homosexual men: early evidence from the Study of the Prevention of Anal Cancer (SPANC)

Andrew E. Grulich A , Fengyi Jin A , I. Mary Poynten A , Jennifer Roberts B , Annabelle Farnsworth B , David J. Templeton C , Sepehr N. Tabrizi D , Suzanne M. Garland D , Christopher Fairley E and Richard J. Hillman F G
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- Author Affiliations

A Kirby Institute, University of New South Wales, Sydney, NSW, Australia.

B Douglass Hanly Moir Pathology, Sydney, NSW, Australia.

C RPA Sexual Health, Royal Prince Alfred Hospital, Sydney, NSW, Australia.

D Royal Women’s Hospital, University of Melbourne, Melbourne, Vic., Australia.

E Melbourne Sexual Health Centre, Melbourne, Vic., Australia.

F Western Sydney Sexual Health Centre, University of Sydney, Sydney, NSW, Australia.

G St Vincent’s Hospital, Sydney, NSW, Australia.

Sexual Health 10(6) 576-576 https://doi.org/10.1071/SHv10n6ab14
Published: 22 November 2013

Abstract

Background: Screening for the anal cancer precursor HSIL is not recommended in national guidelines. A recent Cochrane review of HSIL treatment concluded there is no evidence of efficacy. In this context, we aimed to describe the natural history of anal HSIL, and association with human papillomavirus (HPV), in a community-recruited cohort of Australian homosexual men. Methods: The SPANC study is a three-year prospective study in men aged ≥35 years. At each visit, men undergo an anal swab for cytology and HPV genotyping (Roche Linear Array), followed by high-resolution anoscopy-aided biopsy. Anal HSIL is defined as having either anal intraepithelial neoplasia grade 2/3 on histology and/or HSIL/ASC-H on cytology. Results: Among 342 men recruited by March 2013, median age was 49 with 29% HIV positive. At baseline, prevalence of anal HSIL was 50% and 44% in the HIV-positive and HIV-negative groups, respectively (P = 0.303). Among those without HSIL at baseline, HSIL incidence was 28/100 person-years in both the HIV-positive and HIV-negative groups (P = 0.920). Among those with HSIL at baseline, the incidence of change to non-HSIL was 41 and 43/100 person-years (P = 0.851). Men with anal HPV16 at baseline were more likely to develop incident HSIL (57 vs 23/100 person-years, P = 0.010), and less likely to change to non-HSIL (18 vs 61/100 person-years, P = 0.001). Conclusions: Anal HSIL was highly prevalent in these homosexual men. Both incidence of HSIL and change to non-HSIL were common, and were closely associated with HPV16 status. HPV16 positivity may identify men with HSIL at higher risk of anal cancer.