Conservative management of cervical intraepithelial neoplasia 2 and prediction of its progression - a retrospective study

宫颈上皮内瘤变2型的保守治疗及其进展预测——一项回顾性研究

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Abstract

AIM: Cervical intraepithelial neoplasia 2 (CIN2) evolution is controversial, and some of them regress spontaneously in a two-year follow-up. The purpose of this work was to evaluate the percentage of CIN2 progression or persistence during a 24-month follow-up, using clinical predictors such as human papillomavirus (HPV) genotype and cytology results. PATIENTS, MATERIALS AND METHODS: This is a retrospective case-control study and included patients of reproductive age who had a new diagnosis of CIN2 who were monitored for lesion regression (Group 1, n=72 patients), and progression or persistence (Group 2, n=36 patients). A multinominal logistic regression was preferred to evaluate the impact that various categorical risk elements can lead to outcomes of persistence or progression of CIN2. We also performed a linear regression to assess the risk of CIN2 progression or persistence using the interaction between clinical predictors. RESULTS: A previous cervical cytology indicative of high-grade squamous intraepithelial lesion (HSIL) [relative risk ratio (RRR): 3.85, 95% confidence interval (CI): 1.66-8.90] or atypical squamous cells, cannot exclude HSIL (ASC-H) can highly raise the probability of a CIN2 progression or persistence. The presence of HPV16 increased the risk of CIN2+ with 3.77 (95% CI: 0.78-5.00), the presence of HPV18 increased the probability of CIN2+ with 4.39 (95% CI: 1.35-14.33), and other high-risk HPV (HR-HPV) strains increased the probability of CIN2+ with 3.62. The highest risk issue was produced by the interaction between HSIL* HPV16, ASC-H* HPV16, and ASC-H* HPV18. CONCLUSIONS: When discussing follow-up for CIN2 lesions, it is important to offer careful consideration and monitoring of patients with a previous HSIL or ASC-H cytology, with or without HPV 16, 18 or other HR-HPV strains, as their presence significantly increased the risk of CIN2 progression and persistence.

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