PERSISTENT GENITAL HUMAN PAPILLOMAVIRUS INFECTION AS A RISK FACTOR FOR PERSISTENT CERVICAL DYSPLASIA
PERSISTENT GENITAL HUMAN PAPILLOMAVIRUS INFECTION AS A RISK FACTOR FOR PERSISTENT CERVICAL DYSPLASIA
复制标题
DOI：
10.1093/jnci/87.18.1365
复制
发表时间：
1995-09-20
影响因子：
10.3
通讯作者：
ROMNEY, S
中科院分区：
文献类型：
--
作者：
HO, GYF;BURK, RD;ROMNEY, S
背景：宫颈发育不良，也被称为细胞学上的鳞状上皮内病变（SIL）或组织病理学上的宫颈上皮内瘤变，被认为有可能进展为宫颈癌。然而，并非所有SIL的病例进展，大多数轻度病变自发消退。控制SIL的消退、持续和进展的因素尚不清楚。目的：我们的分析旨在确定决定SIL持续或消退的因素。方法：对70例经组织病理学证实的宫颈发育不良患者，每隔3个月随访15个月。每次就诊时，对宫颈进行巴氏涂片检查和阴道镜检查，并对脱落的宫颈阴道细胞进行人乳头瘤病毒（HPV） DNA分析。对于每个受试者，每两次连续访问的数据被分组为一对。如果在第1次就诊(t)和第2次就诊（t + 1）均检测到病变，则认为存在持续性SIL；如果第1次就诊（t + 1）未检测到病变，则认为不存在持续性SIL。时间相关数据的统计模型将持续性SIL与各种危险因素联系起来。结果：年龄、种族、教育程度、性行为、吸烟和口服避孕药的使用与持续性SIL无关。持续性SIL的风险与访诊t和t + 1时持续HPV感染相关（经Southern blot分析HPV阳性：优势比[OR] = 3.91, 95%可信区间[CI] = 1.58-9.65；经聚合酶链反应[PCR]检测HPV阳性：OR = 2.42, 95% CI = 1.03-5.67）和持续高病毒载量（OR = 4.07, 95% CI = 1.35-12.30）。当通过PCR分型时，与低水平的分型特异性持续感染或非分型特异性持续感染的个体相比，在第t次和第t + 1次就诊时发生型特异性持续感染的个体，特别是那些持续高病毒载量的个体（OR = 4.97; 95% CI = 1.45-17.02）发生持续性SIL的风险最高。在第t - 1次和第t次（之前的时间间隔）中持续HPV感染的存在也预测了第t次和第t + 1次的持续SIL，尽管关联强度较弱，表明持续HPV和SIL是同步发生的。结论：HPV感染及其相关宫颈病变往往同时发生，类型特异性持续HPV感染，特别是高病毒载量，可产生慢性宫颈发育不良。意义：生殖器HPV感染的自然史直接影响宫颈发育不良的预后，以病变的持久性来衡量。检测HPV感染可能是有价值的临床管理妇女宫颈发育不良。
Background: Cervical dysplasia, also referred to as squamous intraepithelial lesion (SIL) in cytology or cervical intraepithelial neoplasia in histopathology, is thought to have the potential to advance in progressive stages to cervical cancer. However, not all cases of SIL progress, and most of the mild lesions spontaneously regress. Factors that govern regression, persistence, and progression of SIL are poorly understood. Purpose: Our analysis sought to identify factors that determined persistence or regression of SIL. Methods: Seventy subjects with histopathologically confirmed cervical dysplasia were followed at 3-month intervals for 15 months. At each visit, the cervix was evaluated by Pap smear and colposcopy, and exfoliated cervicovaginal cells were analyzed for human papillomavirus (HPV) DNA. For each subject, data from every two consecutive visits were grouped as a pair. Persistent SIL was considered present if a lesion was detected at a visit (t) as well as at the next visit (t + 1) and absent if a lesion was detected at visit t but not at visit t + 1. A statistical model for time-dependent data correlated persistent SIL with various risk factors. Results: Age, ethnicity, education, sexual behavior, smoking, and the use of oral contraceptives did not correlate with persistent SIL. The risk of persistent SIL was associated with continual HPV infection in visits t and t + 1 (HPV positive by Southern blot analysis: odds ratio [OR] = 3.91, and 95% confidence interval [CI] = 1.58-9.65; HPV positive by polymerase chain reaction [PCR]: OR = 2.42, and 95% CI = 1.03-5.67) and a persistent high viral load (OR = 4.07, and 95% CI = 1.35-12.30). When typed by PCR, individuals with type-specific persistent infection in visits t and t + 1, and particularly those with a continual high viral load (OR = 4.97; 95% CI = 1.45-17.02), had the highest risk for persistent SIL compared with those with a low level of type-specific persistent infection or non-type-specific persistent infection. The presence of persistent HPV infection in visits t - 1 and t (the preceding time interval) was also predictive of persistent SIL in visits t and t + 1, although the strength of association was weaker, suggesting that persistent HPV and SIL occur synchronously. Conclusion: HPV infection and its associated cervical lesions tend to occur concurrently, and type-specific persistent HPV infection, particularly with a high viral load, produces chronic cervical dysplasia. Implications: The natural history of genital HPV infection directly influences the prognosis of cervical dysplasia as measured by persistence of the lesion. Testing for HPV infection may be valuable in the clinical management of women with cervical dysplasia.