Il vaccino contro l’Hpv (Human papilloma virus, il Papilloma virus umano) e’ in grado di difendere l’organismo dal cancro al collo dell’utero, alla vagina e alla vulva ma anche di ridurre l’insorgenza della neoplasia intraepiteliale cervicale (CIN, un precursore del cancro alla cervice), di diminuire il pericolo di sviluppare lesioni genitali esterne e di prevenire lo sviluppo di anomalie citologiche responsabili di diverse patologie. E’ quanto emerge da uno studio condotto dai ricercatori del National Institute of Cancer di Bogota’ (Colombia) diretto da Nubia Munoz, direttore della struttura, e pubblicato sul Journal of the National Cancer Institute.
Dallo studio e’ emerso che il vaccino, rivolto principalmente alle adolescenti e alle giovani donne, puo’ portare alla riduzione dello sviluppo dei condilomi genitali e di altre anomalie cellulari, spesso precursori dei tumori del collo dell’utero, della vulva e della vagina.
”I nostri risultati forniscono prove evidenti che suggerire l’attuale programma di vaccinazione contro l’HPV alle ragazze adolescenti e alle giovani donne portera’ entro alcuni anni a una notevole riduzione dei condilomi genitali e delle anomalie citologiche cervicali - spiegano gli autori -. Si prevede che tali riduzioni alla fine si tradurranno in tassi piu’ bassi di cancro alla cervice uterina, alla vulva e alla vagina”.
Impact of Human Papillomavirus (HPV)-6/11/16/18 Vaccine on All HPV-Associated Genital Diseases in Young Women
Nubia Muñoz, Susanne K. Kjaer, Kristján Sigurdsson, Ole-Erik Iversen, Mauricio Hernandez-Avila, Cosette M. Wheeler, Gonzalo Perez, Darron R. Brown, Laura A. Koutsky, Eng Hseon Tay, Patricía J. Garcia, Kevin A. Ault, Suzanne M. Garland, Sepp Leodolter, Sven-Eric Olsson, Grace W. K. Tang, Daron G. Ferris, Jorma Paavonen, Marc Steben, F. Xavier Bosch, Joakim Dillner, Warner K. Huh, Elmar A. Joura, Robert J. Kurman, Slawomir Majewski, Evan R. Myers, Luisa L. Villa, Frank J. Taddeo, Christine Roberts, Amha Tadesse, Janine T. Bryan, Lisa C. Lupinacci, Katherine E. D. Giacoletti, Heather L. Sings, Margaret K. James, Teresa M. Hesley, Eliav Barr, Richard M. Haupt
Affiliations of authors: Division of Research and Public Health, National Institute of Cancer, Bogotá, Colombia (NM); Department of Virus, Hormones and Cancer, Institute of Cancer Epidemiology, Danish Cancer Society/Rigshospitalet, University of Copenhagen, Denmark (SKK); National Cancer Detection Clinic, Icelandic Cancer Society, Reykjavik, Iceland (KS); Department of Clinical Medicine, University of Bergen, Bergen, Norway (O-EI); and Department of Obstetrics and Gynecology, Haukeland University Hospital, Bergen, Norway (O-EI); Institute of Public Health, Cuernavaca, Morelos, Mexico (MH-A); Department of Pathology and Department of Obstetrics and Gynecology, University of New Mexico Health Sciences Center, Albuquerque, NM (CMW); Obstetrics, Gynecology and Reproductive Health department at the Universidad del Rosario, Bogotá, Colombia Now at Merck Research Laboratories, West Point, PA. (GP); Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (DRB); Department of Epidemiology, University of Washington, Seattle, WA (LAK); KK Women’s & Children’s Hospital, Singapore (EHT); Epidemiology HIV and STD Unit, Universidad Peruana Cayetano Heredia, Lima, Peru (PJG); Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, GA (KAA); Microbiology and Infectious Diseases Department, Royal Women’s Hospital, Parkville, Victoria, Australia (SMG); Department of Obstetrics and Gynecology, University of Melbourne, Melbourne, Victoria, Australia (SMG); Department of Gynecology and Obstetrics, Medical University of Vienna, Vienna, Austria (SL, EAJ); Karolinska Institute at Danderyd Hospital, Stockholm, Sweden (S-EO); Department of Obstetrics and Gynecology, University of Hong Kong, Hong Kong Special Administrative Region (GWKT); Department of Family Medicine and Department of Obstetrics and Gynecology, Medical College of Georgia, Augusta, GA (DGF); Department of Obstetrics and Gynecology, University Central Hospital, Helsinki, Finland (JP); Direction Risques Biologiques, Environnementaux et Occupationnels, Institut National de Santé Publique du Québec, Montréal, QC, Canada (MS); Epidemiology Research Program, Institut Catala d’Oncologia, Institut d’Investigacio Bellvitge, Barcelona, Spain (FXB); Department of Medical Microbiology, Lund University, Lund, Sweden (JD); Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL (WKH); Department of Gynecology and Obstetrics, Department of Pathology, and Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD (RJK); Department of Dermatology and Venereology, Center of Diagnostics and Treatment of Sexually Transmitted Diseases, Warsaw Medical University, Warsaw, Poland (SM); Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC (ERM); Department of Virology, Ludwig Institute for Cancer Research, Sao Paulo, Brazil (LLV); Merck Research Laboratories, West Point, PA (FJT, CR, AT, JB, LCL, KEDG, HLS, MKJ, TMH, EB, RMH)
Correspondence to: Nubia Muñoz, MD, 24 Quai Fulchiron, 69005 Lyon, France (e-mail: nubia.munoz@free.fr ).
Background: The impact of the prophylactic vaccine against human papillomavirus (HPV) types 6, 11, 16, and 18 (HPV6/11/16/18) on all HPV-associated genital disease was investigated in a population that approximates sexually naive women in that they were “negative to 14 HPV types” and in a mixed population of HPV-exposed and -unexposed women (intention-to-treat group).
Methods: This analysis studied 17 622 women aged 15–26 years who were enrolled in one of two randomized, placebo-controlled, efficacy trials for the HPV6/11/16/18 vaccine (first patient on December 28, 2001, and studies completed July 31, 2007). Vaccine or placebo was given at day 1, month 2, and month 6. All women underwent cervicovaginal sampling and Papanicolaou (Pap) testing at day 1 and every 6–12 months thereafter. Outcomes were any cervical intraepithelial neoplasia; any external anogenital and vaginal lesions; Pap test abnormalities; and procedures such as colposcopy and definitive therapy. Absolute rates are expressed as women with endpoint per 100 person-years at risk.
Results: The average follow-up was 3.6 years (maximum of 4.9 years). In the population that was negative to 14 HPV types, vaccination was up to 100% effective in reducing the risk of HPV16/18-related high-grade cervical, vulvar, and vaginal lesions and of HPV6/11-related genital warts. In the intention-to-treat group, vaccination also statistically significantly reduced the risk of any high-grade cervical lesions (19.0% reduction; rate vaccine = 1.43, rate placebo = 1.76, difference = 0.33, 95% confidence interval [CI] = 0.13 to 0.54), vulvar and vaginal lesions (50.7% reduction; rate vaccine = 0.10, rate placebo = 0.20, difference = 0.10, 95% CI = 0.04 to 0.16), genital warts (62.0% reduction; rate vaccine = 0.44, rate placebo = 1.17, difference = 0.72, 95% CI = 0.58 to 0.87), Pap abnormalities (11.3% reduction; rate vaccine = 10.36, rate placebo = 11.68, difference = 1.32, 95% CI = 0.74 to 1.90), and cervical definitive therapy (23.0% reduction; rate vaccine = 1.97, rate placebo = 2.56, difference = 0.59, 95% CI = 0.35 to 0.83), irrespective of causal HPV type.
Conclusions: High-coverage HPV vaccination programs among adolescents and young women may result in a rapid reduction of genital warts, cervical cytological abnormalities, and diagnostic and therapeutic procedures. In the longer term, substantial reductions in the rates of cervical, vulvar, and vaginal cancers may follow.
Context and Caveats
Prior knowledge
Prevention of cervical cancer has focused on screening and prophylactic human papillomavirus (HPV) vaccination.
Study design
Two randomized, placebo-controlled, efficacy trials for an HPV vaccine provided data. The average follow-up was 3.6 years. All women underwent cervicovaginal sampling and Papanicolaou (Pap) testing. Outcomes were any cervical intraepithelial neoplasia, any external anogenital and vaginal lesions, any Pap test abnormality, and any procedure such as definitive therapy.
Contribution
In the group representing uninfected women, vaccination was up to 100% effective in reducing the risk of HPV16/18-related high-grade cervical, vulvar, and vaginal lesions and the risk of HPV6/11-related genital warts. In the intention-to-treat group representing the general population, vaccination statistically significantly reduced the risk of any high-grade cervical lesion, vulvar and vaginal lesion, genital wart, Pap abnormality, and definitive therapy, irrespective of causal HPV type.
Implications
HPV vaccination of adolescents and young women in the general population may reduce the incidence of genital warts and cervical cytological abnormalities, the associated number of diagnostic and therapeutic procedures performed, and eventually the rates of cervical, vulvar, and vaginal cancers.
Limitations
Only 14 of the 40 HPV types that infect the genital tract were assessed. The intention-to-treat population was not entirely representative of the general population because at most four sex partners and no past abnormal Pap test or external genital abnormality were required for entry.
From the Editors
