2006
DOI: 10.1016/j.ygyno.2005.10.028
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Persistent HPV infection after conization in patients with negative margins

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Cited by 45 publications
(50 citation statements)
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“…We could not evaluate the performance of the generic assays for the screening of residual disease after treatment, as all 25 women treated for CIN 2/3 with adequate follow-up responded to therapy. Up to 20% of these women remain infected with HR HPV after treatment, as reported by others (1,19,20,22).…”
Section: Discussionsupporting
confidence: 55%
“…We could not evaluate the performance of the generic assays for the screening of residual disease after treatment, as all 25 women treated for CIN 2/3 with adequate follow-up responded to therapy. Up to 20% of these women remain infected with HR HPV after treatment, as reported by others (1,19,20,22).…”
Section: Discussionsupporting
confidence: 55%
“…Few studies have examined recurrence/persistence and direct HPV viral load. Song et al 15 reported that the pre-LEEP HR-HPV load was related to a higher risk of persistence of HPV in patients with negative margins after LEEP using multiple regression analysis. They used RLU/PC>500 as a cutoff value for a high viral load determined by HCII and reported that among the possible risk factors, including age, parity, conization grade, histology of colposcopic biopsy, and HPV load, HPV load was the only significant factor.…”
Section: Discussionmentioning
confidence: 99%
“…Several studies have suggested risk factors for the prediction of residual/recurrent disease CIN after LEEP, although the results have been somewhat inconsistent. [13][14][15] Age, cytology grade, menopause status, margin involvement, and HPV viral load have all been observed as risk factors for residual/recurrent disease in CIN treatment. Positive margins in the excised specimen was the greatest risk factors for the development of recurrent CIN in many studies, 13,14 while a few recent studies identified the HPV viral load before LEEP as a predictor of persistence/recurrent disease.…”
Section: Introductionmentioning
confidence: 99%
“…Some studies suggest a role for advanced age, infection with multiple HPV subtypes, infection with high-risk HPV subtypes, host immunodeficiency, and host genetics in the development of chronic HPV infection and eventual carcinoma [11,[13][14][15][16][17][18]. This process is thought to be exceedingly slow, with progression from high-grade dysplasia (CIN2/3) to cervical carcinoma requiring an estimated 20 years or more [19].…”
Section: Pathophysiology and Risk Factorsmentioning
confidence: 99%