title: Comparison of measurements of human papillomavirus persistence for postcolposcopic surveillance for cervical precancerous lesions.
abstract: OBJECTIVE
  Following guidelines, women evaluated by colposcopy, but not found to have a precancerous lesion, could be tested again at 12 months for carcinogenic human papillomavirus (HPV). Compared with pooled-probe testing, measuring HPV genotype-specific persistence might better predict subsequent grade 3 cervical intraepithelial neoplasia (CIN3).
  
  
  METHODS
  For women enrolled in the immediate colposcopy arm of the Atypical squamous cells of undetermined significance (ASCUS) and Low-grade squamous intraepithelial lesion (LSIL) Triage Study (ALTS), who underwent enrollment colposcopy but were without prevalently detected CIN2 or worse (CIN2+; n = 671), we compared 1-year HPV persistence, as measured by a pooled HPV genotype test (hybrid capture 2; hc2) versus a research PCR HPV genotyping test (line blot assay; LBA) as predictors of "missed prevalent" or possibly incident CIN3 diagnosed between 12 and 24 months.
  
  
  RESULTS
  Thirty-two (4.8%) women were diagnosed with subsequent CIN3. Testing repeatedly hc2-positive (hc2+) was more common (49.0%) than genotype-specific persistence as detected by LBA (30.3%, P < 0.01). Although absolute risks of CIN3 following repeat hc2+ or genotype-specific persistence were similar (8.8% versus 8.4%, P = 0.86), repeat hc2+ was more sensitive for identifying CIN3 than genotype-specific persistence (90.6% versus 53.1%, P < 0.01). Among 329 women repeatedly hc2+, women with persistent HPV16 were at higher risk of CIN3 than non-HPV16-persistent women (23.1% versus 7.0%, P < 0.01).
  
  
  CONCLUSIONS
  For postcolposcopy management, 1-year HPV persistence as measured by hc2 would recall more women but was more sensitive and similarly predictive for CIN3 in the following year than detection of genotype-specific persistence by LBA.
  
  
  CONCLUSIONS
  Although find little utility for measuring type-specific persistence, testing for persistent HPV16 might be clinically useful.
authors.affiliation: Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, EPS/7013, Rockville, MD 20852, USA. gagej@mail.nih.gov
authors.forename: Julia C
authors.initials: JC
authors.lastname: Gage
authors.forename: Mark
authors.initials: M
authors.lastname: Schiffman
authors.forename: Diane
authors.initials: D
authors.lastname: Solomon
authors.forename: Cosette M
authors.initials: CM
authors.lastname: Wheeler
authors.forename: Philip E
authors.initials: PE
authors.lastname: Castle
mesh_terms: D000293:Adolescent; D000328:Adult; D002294:Carcinoma, Squamous Cell / Q000175:diagnosis / Q000473:pathology / Q000821:virology*; D015331:Cohort Studies; D003127:Colposcopy; D005260:Female; D005838:Genotype; D006801:Humans; D027383:Papillomaviridae / Q000235:genetics / Q000302:isolation & purification*; D030361:Papillomavirus Infections / Q000175:diagnosis / Q000473:pathology / Q000821:virology*; D012307:Risk Factors; D002583:Uterine Cervical Neoplasms / Q000175:diagnosis / Q000235:genetics / Q000821:virology*; D055815:Young Adult; D002578:Uterine Cervical Dysplasia / Q000175:diagnosis / Q000473:pathology / Q000821:virology*