Zuna Rosemary E, Wang Sophia S, Schiffman Mark, Solomon Diane
Pathology Department, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Cancer. 2006 Oct 25;108(5):288-97. doi: 10.1002/cncr.22168.
Low-grade squamous intraepithelial lesion (LSIL) subsumes the formerly delineated cytologic categories of human papillomavirus (HPV)-associated cell changes (koilocytotic atypia) and low-grade dysplasia/cervical intraepithelial neoplasia (CIN) Grade 1 (CIN1). In this study, the objective was to determine whether these 2 morphologic subcategories are characterized by differences in risk for CIN3 and/or HPV type distribution.
Within the Atypical Squamous Cells of Undetermined Significance/Low-Grade Squamous Intraepithelial Lesion Triage Study, all cytologic interpretations of HPV cellular changes and CIN1 rendered by any of the pathology reviewers (community laboratory, clinical center, or Pathology Quality-Control Group) on referral Papanicolaou (Pap) tests or enrollment ThinPrep Pap tests were included for analysis. HPV testing was performed by Hybrid Capture 2 (HC2) and by polymerase chain reaction based reverse-line blot analysis for 27 HPV types. The absolute risks of cumulative detection of CIN3 or cancer (CIN3 +) and CIN2 or worse (CIN2 +) over 2 years of follow-up were calculated for the various cytologic interpretations.
For each review group and cytology preparation, most LSIL interpretations (from approximately 2 of 3 interpretations to 3 of 4 interpretations) were subcategorized as CIN1 rather than HPV cellular changes. HPV type 16 (HPV-16) was the most common HPV type and was identified in 21% to 24% of CIN1 and in 14% to 18% of HPV cellular changes. Nononcogenic types were identified alone in from 9% to 11% of CIN1 compared with 17% to 20% of HPV cellular change. The absolute risks of CIN1 and HPV cellular changes for cumulatively detected CIN3 + ranged from 12% to 16% for CIN1 and from 6% to 9% for HPV cellular changes.
Both cytologic subcategories of LSIL were associated predominantly with oncogenic HPV types; however, the proportion of nononcogenic HPV types was lower and the absolute risks for CIN3 + were higher for CIN1 compared with HPV cellular changes. The concordance in subcategorizing LSIL was low, and the authors concluded that the diagnostic distinction is of limited clinical utility for individual patient management.
低度鳞状上皮内病变(LSIL)涵盖了先前划定的人乳头瘤病毒(HPV)相关细胞改变(挖空细胞异型性)和低度发育异常/宫颈上皮内瘤变(CIN)1级(CIN1)的细胞学分类。在本研究中,目的是确定这两种形态学亚类是否具有CIN3风险和/或HPV类型分布差异的特征。
在意义不明确的非典型鳞状细胞/低度鳞状上皮内病变分流研究中,纳入了病理检查人员(社区实验室、临床中心或病理质量控制组)对转诊巴氏(Pap)试验或入组时的薄层液基Pap试验所做出的所有HPV细胞改变和CIN1的细胞学解释进行分析。HPV检测采用杂交捕获2代(HC2)法,并通过基于聚合酶链反应的反向线印迹分析检测27种HPV类型。计算了各种细胞学解释在2年随访期间累积检测到CIN3或癌症(CIN3 +)以及CIN2或更严重病变(CIN2 +)的绝对风险。
对于每个检查组和细胞学标本,大多数LSIL解释(约三分之二至四分之三的解释)被归类为CIN1而非HPV细胞改变。16型HPV(HPV-16)是最常见的HPV类型,在21%至24%的CIN1以及14%至18%的HPV细胞改变中被检测到。在9%至11%的CIN1中单独检测到非致癌型HPV,而在HPV细胞改变中这一比例为17%至20%。累积检测到CIN3 +时,CIN1和HPV细胞改变的绝对风险分别为12%至16%和6%至9%。
LSIL的两种细胞学亚类均主要与致癌型HPV类型相关;然而,与HPV细胞改变相比,CIN1中非致癌型HPV类型的比例更低,CIN3 +的绝对风险更高。LSIL亚分类的一致性较低,作者得出结论,这种诊断区分对个体患者管理的临床实用性有限。