Anal dysplasia: Diagnosis and Management, OR Everything you ever wanted to know about tushes and HPV...and then some
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Screening, treatment and prevention of Anal Intraepithelial Neoplasia (AIN) Presented by Joel Palefsky, UCSF School of Medicine, San Francisco at the 5th Annual Gay Men's Health Summit held in Vancouver, BC on November 9th and 10th, 2009.
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Anal dysplasia: Diagnosis and Management, OR Everything you ever wanted to know about tushes and HPV...and then some
- 1. Joel Palefsky Department of Medicine University of California, San Francisco Anal dysplasia: Diagnosis and Management Or Everything you ever wanted to know about tushes and HPV And then some…
- 2. 100 CD4>500 200-500 <200 HIV- HIV+ 80 60 40 20 Percent with anal HPV infection HIV+ HIV+
- 3. 80 CD4>500 200-500 <200 HIV- HIV+ Percent with abnormal anal cytology 60 40 20 HIV+ HIV+
- 7. Population-based data Chin-Hong et al Ann Int Med 2008; 149; 300-6
- 8. Anal and cervical HPV infection in HIV-positive women
- 9. Anal Cytology Screening for AIN in Men Screen Normal ASCUS LSIL HSIL Repeat in 12 months (HIV+) Repeat in 2-3 years (HIV-) Anoscopy with biopsy Treat or follow Treat No lesion seen Chin-Hong PV et al. J Infect Dis. 2004;90:2070-2076. LSIL HSIL
- 11. Diagnostic tests for AIN High resolution anoscopy Digital rectal exam
- 15. Condyloma … too large for TCA, could potentially be treated with IRC
- 16. Precancerous lesion AIN 3 … too large for TCA, IRC OK
- 17. Before treatment with IRC AIN 3
- 18. After treatment with IRC
- 19. After treatment with IRC
- 20. 6 months after treatment with IRC
- 23. Annual number of new cases of HPV-related cancers in American men American Cancer Society: Cancer Facts and Figures 2005 Kreimer AR, et al. Cancer Epidemiol Biomarkers Prev 2005; 14(2):467-75 Ryan DP, et al. N Engl J Med 2000; 342:792-800 Daling JR, et al. Int J Cancer 2005; 116:606-616 11,310 6,820 7,700 1,910 1,530 29,270 New Cases Oral Cavity Oropharynx Larynx Anal Canal Penis Total Anatomic Area 23% 36% 24% 88% 80% -- % With Detectable HPV 2600 2455 1850 1680 1225 9,810 New HPV-Related Cases
- 29. Baseline demographics N = Number of subjects randomized. Percent calculated as 100*(n/N) 4 (0.1) 1 (0.0) 3 (0.1) Missing or Unknown 2,518 (61.9) 1,286 (63.2) 1,232 (60.7) No 1,543 (38.0) 749 (36.8) 794 (39.1) Yes Circumcision 585 (14.4) 293 (14.4) 292 (14.4) Other 1,431 (35.2) 697 (34.2) 734 (36.2) White 3 (0.1) 1 (0.0) 2 (0.1) Native American 835 (20.5) 447 (22.0) 388 (19.1) Hispanic American 805 (19.8) 393 (19.3) 412 (20.3) Black 406 (10.0) 205 (10.1) 201 (9.9) Asian Race/Ethnicity 20 (15-27) 20 (16-27) 20 (15-26) Median (range) 20.5 +/- 2.0 20.5 +/- 2.0 20.5 +/- 2.0 Mean +/- SD Age (years) 4,065 (100) 2,036 (100) 2,029 (100) Male Gender (N = 4,065) n (%) (N = 2,036) n (%) (N = 2,029) n (%) Total Placebo GARDASIL™
- 30. Number of subjects enrolled by country HM = heterosexual men; MSM = men having sex with men.
- 32. Efficacy against HPV 6/11/16/18-related persistent infection and DNA detection * PERSISTENT INFECTION HPV DNA detection in anogenital specimens from > 2 consecutive visits > 6 months apart (± 1 month visit windows) or HPV 6/11/16/18-related disease with positivity to the same type at adjacent visit ** DNA DETECTION HPV DNA detection in anogenital specimens from > 1 visit Per-protocol population <0.001 <0.001 p-value 10.0 5.5 4.1 Inc. per 100 PY 0.6 Inc. per 100 PY Cases Cases 31.5, 55.6 44.7 241 136 DNA detection * Endpoint GARDASIL ™ (n = 1,390) Placebo (n = 1,400) % Efficacy 95% CI Persistent infection * 15 101 85.6 75.1, 92.2
- 33. Efficacy against HPV 6/11/16/18-related persistent infection in males Per-protocol population n = number of subjects randomized who received at least one injection and have follow-up after month 7; PY = person years; CI = confidence interval. 25 41 15 33 Cases 1 9 1 4 Cases 75.6, 99.9 96.0 1.0 1,347 0.0 1,327 HPV 18 55.5, 90.9 78.7 1.8 1,264 0.4 1,290 HPV 16 56.8, 99.8 93.4 0.6 1,238 0.0 1,239 HPV 11 1.4 Inc. per 100 PY 0.2 Inc. per 100 PY n n HPV Type GARDASIL ™ Placebo % Efficacy 95% CI HPV 6 1,239 1,238 88.0 66.3, 96.9
- 34. Efficacy against external genital lesions (EGL) Per-protocol population <0.001 p-value 1.1 Inc. per 100 PY 0.1 Inc. per 100 PY Cases Cases Endpoint GARDASIL ™ (n = 1,397) Placebo (n = 1,408) % Efficacy 95% CI All subjects 3 31 90.4 69.2, 98.1
- 35. Efficacy against external genital lesions (EGL) Per-protocol population *Two cases related to HPV 6 alone, and one case related to HPV 6/11/35 -- -- 0.0 0 0.0 0 Penile/perineal/ perianal cancer -- -- 0.0 1 0.0 0 PIN 2/3 -- -- 0.1 2 0.0 0 PIN 1 1.0 Inc. per 100 PY 0.1 Inc. per 100 PY Cases Cases Severity GARDASIL ™ (n = 1,397) Placebo (n = 1,408) % Efficacy 95% CI Condyloma 3* 28 89.4 65.5, 97.9
- 36. Adverse experience summary; days 1-15 following any vaccination visit 0.0 0 0.0 0 serious vaccine-related adverse experiences 0.1 1 0.3 5 With serious adverse experiences* 14.6 284 14.1 274 systemic adverse experiences 53.6 1,046 60.1 1,169 injection-site adverse experiences 58.2 1,134 63.9 1,242 With vaccine-related adverse experiences 31.4 613 31.6 615 systemic adverse experience 53.7 1,047 60.1 1,169 injection-site adverse experience 63.8 1,244 69.2 1,345 With one or more adverse experiences Number of subjects: 1,950 1,945 Subjects with follow-up % % n n GARDASIL ™ Placebo Subjects in analysis population 2,020 2,029
Editor's Notes
- HPV infection also causes cancer in ~10,000 American men every year. HPV-related head and neck cancers account for the majority of these cancers, followed by cancer of the anal canal and the penis. It is important to note that all of these cancers, with the exception of penile cancer, also affect women.
- This diagram summarizes how VLP-based vaccines are made. The first step is to isolate the DNA of a naturally occurring HPV and then clone the gene or open reading frame (ORF) encoding the L1 capsid protein into a plasmid. The plasmid containing the L1 gene is then introduced into a eukaryotic cell, the L1 gene is transcribed into mRNA and the cell then translate the mRNA into L1 capsid proteins. These capsid proteins then combine together to form a viral like particle. Since no viral DNA (except for the L1 gene) has been introduced into the eukaryotic cell, there are no viral genomes available to incorporate with the viral like particles so there is no danger of producing infectious virions. The VLPs are then purified and used to elicit an immune response in the host.