Age-specific 3-year risk of cervical precancer among HPV-positive women attending screening: a post hoc analysis from a retrospective cohort.

IF 3.1 2区 医学 Q3 IMMUNOLOGY
Ruizhe Chen, Ying Li, Xiao Li, Xinyu Wang, Weiguo Lü, Yunfeng Fu
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引用次数: 0

Abstract

This post hoc analysis explored the age-specific risk of cervical precancer in women infected with human papillomavirus (HPV), using data from a cohort of 7263 participants aged 21-71years undergoing cervical screening. We found a slightly varied prevalence of high-risk HPV (hrHPV) in different age, with highest in women under 30 years old (9.28% for 13 hrHPVs tested by HC2-HPV, 10.82% for 14 hrHPVs tested by DH3-HPV). However, the prevalence of cytology abnormalities peaked in age 30-39 years (~ 3.6%). A total of 5840 women completed 3-year follow-up. Among them, 558 were positive for HC2 assay and 583 were positive for DH3-HPV at baseline. Of note, the 3-year cumulative risks for cervical intraepithelial neoplasia grade 2+ (CIN2+) or grade 3+ (CIN3+) in women infected with high-risk HPV did not increase with age but declined (e.g., 41.67%, 27.78%, 26.42%, 15.98%, and 18% for CIN2 + risk in HC2-positive women at year 25-29, year 30-39, year 40-49, year 50-59, and year 60-71, respectively). If stratified by the median age, younger women (25-48 years) positive with HC2-HPV at baseline had a higher 3-year CIN2+/CIN3 + risk than older women (49-71 years) [26.55% (95%CI = 21.8-31.92%) vs. 18.28% (95%CI = 14.11-23.34%), P = 0.019; 15.52% (95%CI = 11.81-20.14%) vs. 9.7% (95%CI = 6.71-13.83%), P = 0.039]. Similarly, for women positive with DH3-HPV at baseline, younger group had a higher 3-year CIN2+/CIN3 + risk than older group [26.44% (95%CI = 21.73-31.75%) vs. 17.01% (95%CI = 13.11-21.78%), P = 0.006; 15.25% (95%CI = 11.6-19.8%) vs. 9.03% (95%CI = 6.24-12.9%), P = 0.021]. These findings indicate the potential value of age-specific risk assessment in cervical cancer screening.

参加筛查的 HPV 阳性女性 3 年宫颈癌前病变的特定年龄风险:一项回顾性队列的事后分析。
这项事后分析探讨了感染人类乳头瘤病毒(HPV)的女性患宫颈癌前病变的特定年龄风险,数据来自接受宫颈筛查的 7263 名 21-71 岁参与者。我们发现不同年龄段的高危 HPV(hrHPV)感染率略有不同,其中 30 岁以下女性的感染率最高(HC2-HPV 检测的 13 种 hrHPV 感染率为 9.28%,DH3-HPV 检测的 14 种 hrHPV 感染率为 10.82%)。然而,细胞学异常的发生率在 30-39 岁达到高峰(约 3.6%)。共有 5840 名妇女完成了为期 3 年的随访。其中,558 人的 HC2 检测结果呈阳性,583 人的 DH3-HPV 检测结果呈阳性。值得注意的是,感染高危型 HPV 的妇女宫颈上皮内瘤变 2+ 级(CIN2+)或 3+ 级(CIN3+)的 3 年累积风险并没有随着年龄的增长而增加,反而有所下降(例如,HC2 阳性妇女在 25-29 岁、30-39 岁、40-49 岁、50-59 岁和 60-71 岁的 CIN2 + 风险分别为 41.67%、27.78%、26.42%、15.98% 和 18%)。如果按年龄中位数分层,基线时 HC2-HPV 阳性的年轻女性(25-48 岁)的 3 年 CIN2+/CIN3+ 风险高于年龄较大的女性(49-71 岁)[26.55% (95%CI = 21.8-31.92%) vs. 18.28% (95%CI = 14.11-23.34%), P = 0.019; 15.52% (95%CI = 11.81-20.14%) vs. 9.7% (95%CI = 6.71-13.83%), P = 0.039]。同样,对于基线 DH3-HPV 阳性的女性,年轻组的 3 年 CIN2+/CIN3 + 风险高于年长组 [26.44% (95%CI = 21.73-31.75%) vs. 17.01% (95%CI = 13.11-21.78%), P = 0.006; 15.25% (95%CI = 11.6-19.8%) vs. 9.03% (95%CI = 6.24-12.9%), P = 0.021]。这些研究结果表明,针对特定年龄的风险评估在宫颈癌筛查中具有潜在价值。
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来源期刊
Infectious Agents and Cancer
Infectious Agents and Cancer ONCOLOGY-IMMUNOLOGY
CiteScore
5.80
自引率
2.70%
发文量
54
期刊介绍: Infectious Agents and Cancer is an open access, peer-reviewed online journal that encompasses all aspects of basic, clinical, epidemiological and translational research providing an insight into the association between chronic infections and cancer. The journal welcomes submissions in the pathogen-related cancer areas and other related topics, in particular: • HPV and anogenital cancers, as well as head and neck cancers; • EBV and Burkitt lymphoma; • HCV/HBV and hepatocellular carcinoma as well as lymphoproliferative diseases; • HHV8 and Kaposi sarcoma; • HTLV and leukemia; • Cancers in Low- and Middle-income countries. The link between infection and cancer has become well established over the past 50 years, and infection-associated cancer contribute up to 16% of cancers in developed countries and 33% in less developed countries. Preventive vaccines have been developed for only two cancer-causing viruses, highlighting both the opportunity to prevent infection-associated cancers by vaccination and the gaps that remain before vaccines can be developed for other cancer-causing agents. These gaps are due to incomplete understanding of the basic biology, natural history, epidemiology of many of the pathogens that cause cancer, the mechanisms they exploit to cause cancer, and how to interrupt progression to cancer in human populations. Early diagnosis or identification of lesions at high risk of progression represent the current most critical research area of the field supported by recent advances in genomics and proteomics technologies.
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