1298. Risk of progression of high grade anal dysplasia to invasive squamous cell carcinoma of the anus
Session: Poster Abstract Session: Clinical Infectious Diseases: Sexually Transmitted Infections
Friday, October 28, 2016
Room: Poster Hall
  • stage 0 poster idweek REVISED.pdf (248.5 kB)
  • Background: Anal dysplasia is mediated by persistent HPV infection. While anal intraepithelial neoplasia, grade 3 (AIN 3) is thought to be the precursor of invasive squamous cell carcinoma of the anus (SCCA), the rate and predictors of progression of AIN 3 to SCCA are unclear.

    Methods: We identified 756 cases (78% HIV infected) of incident, pathologically-confirmed AIN 3 from the Surveillance, Epidemiology, and End Results (SEER) database linked to Medicare claims from 2000-2011. We compared baseline characteristics by HIV infection status using univariate tests. We compared outcomes such as progression to SCCA and overall survival by HIV infection status using Kaplan-Meier methods and methods accounting for competing risks. We fitted Cox regression models to adjust for potential confounders.

    Results: Compared to HIV uninfected patients, HIV infected patients were more likely to be male (95% vs 48%), younger (IQR 41-52 vs 51-70 years), and non-White (37% vs 22%), all p < .01. HIV infected patients were less likely to undergo treatment for AIN 3 (62% vs 77%), but more likely to undergo anal cytology (72% vs 24%) and anoscopy (54% vs 6%) thirty or more days after AIN 3 diagnosis (all p<.01). There were 41 cases of incident SCCA over the study period. AIN 3 progressed to SCCA at a rate of 0.9 per 100 person-years (95% CI 0.7-1.2). Median time to progression was 24 months (IQR 12-44 months). Cumulative risk of SCCA at 5 years was 5.7% (95% CI 4.2%-7.8%). Progression rates did not differ by HIV status (all p > .05). In our multivariable analysis, HIV infection was associated with a trend towards increasing hazard of progression to SCCA (HR 4.4, 95% CI 1.0-20.6, p = 0.06); surveillance cytology and anoscopy did not predict progression (all p > .05). Competing risk analysis yielded similar results. Overall survival did not differ by HIV status (p=0.98) despite the younger age of the HIV infected patients.

    Conclusion: In our population-based cohort of patients with AIN 3, we found rates of progression to invasive carcinoma similar to previous estimates. We did not detect a robust effect of HIV infection on rate of progression to SCCA; however our study lacked detailed data on AIN 3 treatment, CD4 count, and ART use, which may be more predictive of risk of progression than HIV status alone.

    Yotam Arens, MS41, Keith Sigel, MD, MPH2, Michael Gaisa, MD, PhD2, Annika Burnett, MS41 and Stephen Goldstone, MD3, (1)Icahn School of Medicine at Mount Sinai, New York, NY, (2)Dept. of Medicine, Division of Infectious Disease, Icahn School of Medicine at Mount Sinai, New York, NY, (3)Dept. of General Surgery, Icahn School of Medicine at Mount Sinai, New York, NY


    Y. Arens, None

    K. Sigel, None

    M. Gaisa, None

    A. Burnett, None

    S. Goldstone, None

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