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Anal Dysplasia and Cancer in At-Risk Groups: What Providers Need to Know

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Anal Dysplasia and Cancer in At-Risk Groups: What Providers Need to Know Anal Dysplasia and Cancer in At-Risk Groups: What Providers Need to Know Lori Panther, MD, MPH Assistant Professor, Harvard Medical School BIDMC Division of Infectious Diseases Associate Director of Clinical Research The Fenway Institute Boston, MA Continuing Medical Education Disclosure Program Faculty: Lori Panther, MD, MPH Current Position: Clinical Director of the Infectious Diseases Dysplasia Clinic, Beth Israel Deaconess Medical Center; Medical Provider at Fenway Health, and Associate Medical Director for Clinical Research, The Fenway Institute, Fenway Health Disclosure: No relevant financial relationships. Content of presentation contains no use of unlabeled and/or investigational uses of products. It is the policy of The National LGBT Health Education Center, Fenway Health that all CME planning committee/faculty/authors/editors/staff disclose relationships with commercial entities upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflicts of interest and, if identified, they are resolved prior to confirmation of participation. Only participants who have no conflict of interest or who agree to an identified resolution process prior to their participation were involved in this CME activity. Learning Objectives Summarize the current epidemiology of anal HPV infection and anal cancer among MSM and women Describe the clinical manifestations of anal HPV infection Identify currently available screening methods for anal cancer Review methods of preventing HPV infection Learning Objectives Summarize the current epidemiology of anal HPV infection and anal cancer among MSM and women Human Papillomavirus (HPV) Noncoding regulatory region Transformation (inhibits p53) Genome copy Modulation Major capsid (inhibits pRb) protein Minor capsid DNA protein replication Membrane signaling protein incytepathology.wordpress.com Gene expression/ incytepathology.wordpress.com Assembly and release Life Cycle of HPV HPV infects basal cells Parabasal cells and HPV replicate together . E1, E2, E6, E7 expressed . E6 inhibits p53: cell immortalization . E7 inhibits RBP: accelerates cell cycle progression Suprabasal cells terminally differentiate; HPV replicates . L1, L2 expressed Surface cells die and lyse . millions of infectious HPV/cell released HPV Evades the Immune System Little tissue destruction associated with HPV . Target of infection not an antigen-presenting cell . Infected keratinocytes less susceptible to cytotoxic lymphocyte-mediated lysis No blood-borne phase of infection Limited and delayed expression of late viral capsid proteins (L1, L2) Tindle RW. Nat Rev Cancer. 2002;2:1–7; Scott M, Nakagawa M, Moscicki A-B. Clin Diagn Lab Immunol. 2001;8:209–220; Frazer IH. Nature Rev. 2004;4:46–54 Tindle RW. Nat Rev Cancer. 2002;2:1–7; Scott M, Nakagawa M, Moscicki A-B. Clin Diagn Lab Immunol. 2001;8:209–220; Frazer IH. Nature Rev. 2004;4:46–54 HPV Transmission HPV is released from infected desquamating cells Transmission mainly via direct contact with infected cells Transmission of genital HPV typically occurs through sexual contact ► Practically everyone gets infected at some point during their lives. HPV Clearance and Persistence ~80% of HPV infections are transient . 70% of new HPV infections clear within 1 year and 91% within 2 years . Median duration of infection = 8 months Persistence of high-risk HPV is crucial for development of disease Other associated factors: . Age at acquisition (≥30 years) . Immunosuppression . Infection with oncogenic HPV types (more likely to persist) 1. Meijer CJLM, Helmerhorst TJM, Rozendaal L, van der Linden JC, Voorhorst FJ, Walboomers JMM. Histopathology. 1998;33:83–86. 2. Schiffman M, Kjaer SK. J Natl Cancer Inst Monogr. 2003;31:14–19. 3. Ho GYF, Bierman R, Beardsley L, Chang CJ, Burk RD. N Engl J Med. 1998;338:423–428. Anal HPV Infection Cross sectional studies of any HPV detected in anal canal: . HIV neg MSM 40-60% . HIV pos MSM 60-90+% . HIV neg women 40% . HIV pos women 75% Factors: . Age . CD4 count Goldstone et al J Infect Dis. 2011 Jan 1;203(1):66-74. Palefsky et al J Infect Dis. 2001 Feb 1;183(3):383-91 Chin-Hong J Infect Dis. 2004 Dec 15;190(12):2070-6 Anal vs. Cervical HPV Infection in Women 90 80 70 60 50 % 40 Anal 30 Cervical 20 10 0 HIV- HIV+ CD4 HIV+ CD4 HIV+ CD4 >500 200-500 <200 Palefsky et al. HPV Causes Two Diseases 1. CANCER 2. WARTS . due to high risk . due to low risk (oncogenic) HPV (non-oncogenic) types: 16, 18, 31, HPV types: 6, 11, 33, 35, 39, 45, 51, 40, 42, 43, 44, 54 52, 58 1. Howley PM. In: Fields BN, Knipe DM, Howley PM, eds. Fields Virology. 4th ed. Philadelphia, Pa: Lippincott-Raven; 2001:2197– 2229. Reprinted with the permission of Lippincott-Raven. 2. Schiffman M, Castle PE. Arch Pathol Lab Med. 2003;127:930–934. 3. Wiley DJ, Douglas J, Beutner K, et al. Clin Infect Dis. 2002;35(suppl 2):S210–S224. 4. Muñoz N, Bosch FX, de Sanjosé S, et al. N Engl J Med. 2003;348:518–527. 5. Clifford GM, Smith JS, Aguado T, Franceschi S. Br J Cancer. 2003:89;101–105. Natural History of HPV Infection Transient Cleared HPV Infection Infection Initial HPV Warts Infection Low-Grade High-Grade Persistent Dysplasia Dysplasia Infection (X)IN 1 (X)IN 2/3 Invasive Cancer T I M E (YEARS) 0-2 2–5 4–12 9–20 HIV INFECTION COMPRESSES THE NATURAL HISTORY OF HPV INFECTION Adapted from: 1. Pagliusi SR, Aguado MT. Vaccine. 2004;23:569–578. 2. Pinto AP, Crum CP. Clin Obstet Gynecol. 2000;43:352–362. HPV: Terminology “low risk” “high risk” HPV type HPV type “low grade” “high grade” term term General General pathologic pathologic Normal ASCUS/LSIL HSIL CIS ICC Cytology Cytology (X)IN 1 (X)IN 2 (X)IN 3 Normal (moderate Invasive (condyloma/mild (severe dysplasia/CIS) Cancer dysplasia) dysplasia) Histology (X ) can be cervical (C), anal (A), penile (P), vulvar (V), vaginal (VA) HPV Infection Statistics: United States At least 80% of us will have an HPV infection by the time we reach 50 . 3/4 of first-time HPV infections occur at <25 y. o. About 20 million new infections annually . Half of these are 15-24 years of age . 5-30% of these infected with multiple HPV types 1. Centers for Disease Control and Prevention. Genital HPV infection fact sheet. CDC National Prevention Information Network; 2004. 2. Weinstock H et al. Perspect Sex Reprod Health. 2004;36:6–10. 3. Burk RD et al. J Infect Dis. 1996;174:679–689. 4. Bauer HM et al. JAMA. 1991;265:472–477. Who Gets Anal Cancer? In 2013: Estimated Cancer Cases, 2013 About 7,000 cases . 65% in women . 35% in men About 900 deaths of Number Cases CA CANCER J CLIN 2013;63:11–30 Incidence Rates of AIDS-defining and Non-AIDS-defining Cancer, 1996-2000 CANCER TYPE SIR (95%CI) AIDS-Defining KS 5600 (4400-7200) AIDS-defining cancer NHL 23.1 (17.8-30.0) Cervical 16.6 (9.3-27.4) Non-AIDS-defining cancer Non-AIDS-defining Head and neck 5.1 (2.8-8.6) Anus 39 (18.7-71.7) Liver 16.5 (8.8-28.2) Lung 29 (5.5-3.7-8.0) Hodgkin’s 9.8 (4.2-19.2) AIDS 2008, 22:489-496 Risk of HPV-Associated Cancers in HIV+ Patients Relative Risk Cancer Type [95% CI] Cervix 5.4 [3.9-7.2] Vulva/Vagina 5.8 [3.0-10.2] Penis 3.7 [2.0-6.2] Anus (female) 6.8 [2.7-14.0] Anus (male) 37.9 [33.0-43.4] Tonsillar cancer (men) 2.6 [1.8-3.8] Oropharynx 6.0 [3.5-9.7] Frisch et. al. Learning Objectives Describe the clinical manifestations of anal HPV infection Warts HPV 6 and 11 responsible for >90% of anogenital warts Peak prevalence . Women 20–24 years . Men 25–29 years vulvar internal anal meatal penile cervical lingual oral external anal Genital Warts: Statistics New cases per year in the United States: . 1 million Sexually active adults with visible genital warts: . 1 in 100 (1 in 20 HIV+ patients) People who will develop genital warts in their lifetime: . 1 in 10 Fleischer AB et al. Sex Transm Dis. 2001;28:643–647. 2. Koutsky L. Am J Med. 1997;102:3–8. 3. Franco EL et al. In: Franco EL, Monsonego J, eds. New Developments in Cervical Screening and Prevention. Blackwell Science; 1997:14–22. 1. Fleischer AB et al. Sex Transm Dis. 2001;28:643–647. 2. Koutsky L. Am J Med. 1997;102:3–8. 3. Franco EL et al. In: Franco EL, Monsonego J, eds. New Developments in Cervical Screening and Prevention. Blackwell Science; 1997:14–22. Invasive Anal Squamous Cell Carcinoma Incidence rate: 60-80 cases/100,000 HIV+ MSM . Twice that of HIV- MSM rates Typical HIV+ patient: MSM 42 years old CD4 count 200/mm3 or less Low nadir CD4 count Mortality rate at 5 years: 50-80% Perianal Squamous Carcinoma-in- situ (Bowen’s Disease) Symptoms: pruritis, mass, bleeding, pain Increased incidence in HIV+ patients, and not predictably associated with internal lesions Perianal Bowen’s has higher incidence of invasion (10- 14%) compared to SCCIS of other sites (3-4%) High rate of recurrence: 1/3 of cases recurred in 5 years Sarmiento et al., Dis Colon Rectum 40(8); 1997 Chin-Hong et al., Clin Inf Dis 35(9); 2002 HPV and Head and Neck Cancer Fakhry, JNCI 2008 Fakhry, JNCI 2008 # Lifetime Oral Odds OR, HPV16+ Sex Partners Ratio (OR) tumors 0 1 1 1-5 1.9 3.8 NEJM, May 2007 >6 3.4 8.6 NEJM, May 2007 Learning Objectives Identify currently available screening methods for anal cancer A Brief History of the Pap Smear 1915: initially noted cyclic changes in vaginal cytology of the guinea pig 1923: abnormal vaginal cytology in women with uterine cancer 1943: published “Diagnosis of Uterine Cancer by the Vaginal Smear” 1960s: noted decrease in cervical cancer from 1st George Nicholaus Papanicolaou, 1883-1962 to 3rd most common cancer in women Transformation Zones of ♀ and ♂ Have Identical Embryologic Origins How to Collect Anal Cytology 1.
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