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Rigshospitalet - en del af Københavns Universitetshospital
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Human Papillomavirus Genotypes From Vaginal and Vulvar Intraepithelial Neoplasia in Females 15-26 Years of Age

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  • Suzanne M Garland
  • Elmar A Joura
  • Kevin A Ault
  • F Xavier Bosch
  • Darron R Brown
  • Xavier Castellsagué
  • Alex Ferenczy
  • Daron G Ferris
  • Anna R Giuliano
  • Mauricio Hernandez-Avila
  • Warner K Huh
  • Ole-Erik Iversen
  • Susanne K Kjaer
  • Robert J Kurman
  • Joaquin Luna
  • Joseph Monsonego
  • Nubia Muñoz
  • Jorma Paavonen
  • Punnee Pitisuttihum
  • Brigitte M Ronnett
  • Marc Steben
  • Mark H Stoler
  • Cosette M Wheeler
  • Dorothy J Wiley
  • Gonzalo Perez
  • Alfred J Saah
  • Alain Luxembourg
  • Se Li
  • Mark J DiNubile
  • Monika Wagner
  • Christine Velicer
Vis graf over relationer

OBJECTIVE: To estimate the proportion of vulvar and vaginal low-grade and high-grade squamous intraepithelial lesions (LSILs and HSILs) in females 15-26 years of age attributable to 14 human papillomavirus (HPV) genotypes (6, 11, 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59).

METHODS: A post hoc analysis of prospectively diagnosed vulvar and vaginal LSILs and HSILs among females 15-26 years of age enrolled in the placebo arms of two phase 3, randomized HPV vaccine trials assessed 14 prespecified HPV genotypes associated with cervical cancers or anogenital warts using a type-specific multiplex polymerase chain reaction assay. The frequency of lesions associated with specific HPV genotypes was estimated by proportional and other attribution methods.

RESULTS: During approximately 4 years of follow-up in 8,798 females, 40 vulvar LSILs and 46 vulvar HSILs were diagnosed in 68 females, and 118 vaginal LSILs and 33 vaginal HSILs were diagnosed in 107 females. Females developing vulvar (41.2%) or vaginal (49.5%) lesions also had cervical lesions, whereas 6.5% of females with cervical lesions had vaginal or vulvar lesions. At least 1 of the 14 HPV genotypes was detected in females with vulvar LSIL (72.5%), vulvar HSIL (91.3%), vaginal LSIL (61.9%), and vaginal HSIL (72.7%). Considering only HPV-positive lesions, the nine most common genotypes causing cervical cancer and anogenital warts (6, 11, 16, 18, 31, 33, 45, 52, and 58) were found in 89.4% of vulvar LSILs, 100% of vulvar HSILs, 56.0% of vaginal LSILs, and 78.3% of vaginal HSILs.

CONCLUSION: Most vulvar and vaginal lesions were attributable to at least 1 of the 14 HPV genotypes analyzed. Effective immunization programs could potentially prevent substantial numbers of HPV-related vulvar and vaginal LSILs and HSILs.

CLINICAL TRIAL REGISTRATION: CLINICALTRIALS.GOV,: NCT00092521 and NCT00092534.

OriginalsprogEngelsk
TidsskriftObstetrics and Gynecology
Vol/bind132
Udgave nummer2
Sider (fra-til)261-270
Antal sider10
ISSN0029-7844
DOI
StatusUdgivet - aug. 2018

ID: 56089696