BACKGROUND: We describe the prevalence of 14 common types [human papillomavirus (HPV)-6/11/16/18/31/33/35/39/45/51/52/56/58/59] in vulvar intraepithelial neoplasia grades 1 to 3 (VIN 1-3) and HPV genotype-specific infection in relation to the development of VIN 1-3. METHODS: Data were analyzed from women enrolled in the placebo arms of three randomized double-blind trials. Anogenital examinations, including collection of labial/vulvar/perineal/perianal swabs, occurred at day 1 and every 6 to 12 months through 48 months. Lesions that were possibly, probably, or definitely HPV related or of unknown etiology were biopsied. Biopsies and swabs were HPV typed. Biopsies were read for endpoint determination (VIN 1-3) by up to four pathologists. RESULTS: Incident infection with HPV-16 was the most common (6.0/100 person-years). The mean time from incident infection to the development of VIN 1-3 was 18.5 months (95% confidence interval, 13.4-23.6). HPV-6 or -11 was observed in 64.5% of VIN 1 and 29.0% of VIN 2/3, whereas HPV-16 was observed in 6.5% of VIN 1 and 64.5% of VIN 2/3. CONCLUSION: A vaccine that includes both low- and high-risk types could prevent more than half of VIN 1-3 lesions, including the precursor lesions to HPV-related vulvar carcinoma. Understanding the incidence and duration of vulvar HPV infection and risk for progression to VIN 1-3 may inform therapeutic decisions for vulvar disease and mathematical models that assess the cost-effectiveness of vaccination.
RCT Entities:
BACKGROUND: We describe the prevalence of 14 common types [human papillomavirus (HPV)-6/11/16/18/31/33/35/39/45/51/52/56/58/59] in vulvar intraepithelial neoplasia grades 1 to 3 (VIN 1-3) and HPV genotype-specific infection in relation to the development of VIN 1-3. METHODS: Data were analyzed from women enrolled in the placebo arms of three randomized double-blind trials. Anogenital examinations, including collection of labial/vulvar/perineal/perianal swabs, occurred at day 1 and every 6 to 12 months through 48 months. Lesions that were possibly, probably, or definitely HPV related or of unknown etiology were biopsied. Biopsies and swabs were HPV typed. Biopsies were read for endpoint determination (VIN 1-3) by up to four pathologists. RESULTS: Incident infection with HPV-16 was the most common (6.0/100 person-years). The mean time from incident infection to the development of VIN 1-3 was 18.5 months (95% confidence interval, 13.4-23.6). HPV-6 or -11 was observed in 64.5% of VIN 1 and 29.0% of VIN 2/3, whereas HPV-16 was observed in 6.5% of VIN 1 and 64.5% of VIN 2/3. CONCLUSION: A vaccine that includes both low- and high-risk types could prevent more than half of VIN 1-3 lesions, including the precursor lesions to HPV-related vulvar carcinoma. Understanding the incidence and duration of vulvar HPV infection and risk for progression to VIN 1-3 may inform therapeutic decisions for vulvar disease and mathematical models that assess the cost-effectiveness of vaccination.
Authors: Krystle A Lang Kuhs; Paula Gonzalez; Ana Cecilia Rodriguez; Leen-Jan van Doorn; Mark Schiffman; Linda Struijk; Sabrina Chen; Wim Quint; Douglas R Lowy; Carolina Porras; Corey DelVecchio; Silvia Jimenez; Mahboobeh Safaeian; John T Schiller; Sholom Wacholder; Rolando Herrero; Allan Hildesheim; Aimée R Kreimer Journal: J Infect Dis Date: 2014-06-23 Impact factor: 5.226
Authors: Antonio Frega; Francesco Sopracordevole; Paolo Scirpa; Alberto Biamonti; Laura Lorenzon; Simona Scarani; Luana De Sanctis; Arianna Pacchiarotti; Massimo Moscarini; Deborah French Journal: Med Sci Monit Date: 2011-09
Authors: Ruth Tachezy; Jana Smahelova; Martina Salakova; Marc Arbyn; Lukas Rob; Petr Skapa; Tomas Jirasek; Eva Hamsikova Journal: PLoS One Date: 2011-07-13 Impact factor: 3.240
Authors: Elmar A Joura; Suzanne M Garland; Jorma Paavonen; Daron G Ferris; Gonzalo Perez; Kevin A Ault; Warner K Huh; Heather L Sings; Margaret K James; Richard M Haupt Journal: BMJ Date: 2012-03-27