Maria Teresa Bruno1,2, Nazario Cassaro3,4, Salvatore Giovanni Vitale5, Arianna Guaita6, Sara Boemi5. 1. Department of General Surgery and Medical Surgery Specialties, Gynecological Clinic, University of Catania, Catania, Italy. mt.bruno@unict.it. 2. Multidisciplinary Research Center in Papillomavirus Pathology, University of Catania, Catania, Italy. mt.bruno@unict.it. 3. Gynecological Oncology, Humanitas, Catania, Italy. 4. Multidisciplinary Research Center in Papillomavirus Pathology, University of Catania, Catania, Italy. 5. Department of General Surgery and Medical Surgery Specialties, Gynecological Clinic, University of Catania, Catania, Italy. 6. Department of Statistics, Sapienza University of Roma, Rome, Italy.
Abstract
BACKGROUND: The aim of this study was to evaluate the regression rate of CIN2 p16 positive lesions in women over 25 years of age and identify possible predictors of regression. METHODS: A total of 128 CIN2 p16 positive patients over 25 years old were considered. The women met the following inclusion criteria: HPV genotype 16, 18, 31, 33, 45 positive, HPV E6 / E7 mRNA test positive, without immune system pathologies, not pregnant and had completed at least two years of follow-up. At each follow-up examination patients were examined by colposcopy, HPV test, E6/E7mRNA, targeted biopsy and p16 protein detection. The final state after the two years of follow-up was classified as progression if the histology showed a CIN3, persistence if the lesion was a CIN2, regression if negative or LSIL. The predicted regression factors evaluated were: HPV E6/E7mRNA, protein p16. RESULTS: Overall, we had 35.1% (45 cases) of progression to CIN3, 41.4% (53 cases) of persistence and 23.4% (30 cases) of regression. The regression rate was higher in women with negative mRNA 92.8% (26/28), OR 312 (34.12-1798.76) p = 0.0001, while women with p16 negative had a regression of 22.6% (7/31), OR 0.94 (95% CI 0.36-2.46), p was not significant. We found no significant difference in regression between p16 positive (23.7%) and p16 negative (22.6%) CIN2 p16 lesions. p16 had a VPN of 22.6 (CI 95% 0.159-0.310), indicating that a p16 negative lesion does not exclude a CIN2 + . CONCLUSIONS: We had a regression rate of 23.4%, which was low if we consider that in the literature the regression rates vary from 55 to 63%. The discrepancy in the results may indeed be explained by the fact that all lesions in our study were hr-HPV positive and belonged to "older women" reflecting a more "high-risk" population. As regression factors we studied p16 and HPV E6/E7 mRNA. The results of our study show that HPV mRNA, if negative, appears to be able to identify CIN2 lesions with a higher probability of regression and underlines how a p16 negative is not an indicator of regression.
BACKGROUND: The aim of this study was to evaluate the regression rate of CIN2 p16 positive lesions in women over 25 years of age and identify possible predictors of regression. METHODS: A total of 128 CIN2 p16 positive patients over 25 years old were considered. The women met the following inclusion criteria: HPV genotype 16, 18, 31, 33, 45 positive, HPV E6 / E7 mRNA test positive, without immune system pathologies, not pregnant and had completed at least two years of follow-up. At each follow-up examination patients were examined by colposcopy, HPV test, E6/E7mRNA, targeted biopsy and p16 protein detection. The final state after the two years of follow-up was classified as progression if the histology showed a CIN3, persistence if the lesion was a CIN2, regression if negative or LSIL. The predicted regression factors evaluated were: HPV E6/E7mRNA, protein p16. RESULTS: Overall, we had 35.1% (45 cases) of progression to CIN3, 41.4% (53 cases) of persistence and 23.4% (30 cases) of regression. The regression rate was higher in women with negative mRNA 92.8% (26/28), OR 312 (34.12-1798.76) p = 0.0001, while women with p16 negative had a regression of 22.6% (7/31), OR 0.94 (95% CI 0.36-2.46), p was not significant. We found no significant difference in regression between p16 positive (23.7%) and p16 negative (22.6%) CIN2 p16 lesions. p16 had a VPN of 22.6 (CI 95% 0.159-0.310), indicating that a p16 negative lesion does not exclude a CIN2 + . CONCLUSIONS: We had a regression rate of 23.4%, which was low if we consider that in the literature the regression rates vary from 55 to 63%. The discrepancy in the results may indeed be explained by the fact that all lesions in our study were hr-HPV positive and belonged to "older women" reflecting a more "high-risk" population. As regression factors we studied p16 and HPV E6/E7 mRNA. The results of our study show that HPV mRNA, if negative, appears to be able to identify CIN2 lesions with a higher probability of regression and underlines how a p16 negative is not an indicator of regression.
Authors: J M Walboomers; M V Jacobs; M M Manos; F X Bosch; J A Kummer; K V Shah; P J Snijders; J Peto; C J Meijer; N Muñoz Journal: J Pathol Date: 1999-09 Impact factor: 7.996
Authors: Teresa M Darragh; Terence J Colgan; J Thomas Cox; Debra S Heller; Michael R Henry; Ronald D Luff; Timothy McCalmont; Ritu Nayar; Joel M Palefsky; Mark H Stoler; Edward J Wilkinson; Richard J Zaino; David C Wilbur Journal: J Low Genit Tract Dis Date: 2012-07 Impact factor: 1.925
Authors: Michelle G Discacciati; Carlos André S de Souza; Maria Gabriela d'Otavianno; Liliana A L Ângelo-Andrade; Maria Cristina A Westin; Silvia H Rabelo-Santos; Luiz C Zeferino Journal: Eur J Obstet Gynecol Reprod Biol Date: 2010-12-28 Impact factor: 2.435
Authors: Teresa M Darragh; Terence J Colgan; J Thomas Cox; Debra S Heller; Michael R Henry; Ronald D Luff; Timothy McCalmont; Ritu Nayar; Joel M Palefsky; Mark H Stoler; Edward J Wilkinson; Richard J Zaino; David C Wilbur Journal: Int J Gynecol Pathol Date: 2013-01 Impact factor: 2.762