A population-based prospective study of Chlamydia trachomatis infection and cervical carcinoma

被引:133
作者
Wallin, KL
Wiklund, F
Luostarinen, T
Ångström, T
Anttila, T
Bergman, F
Hallmans, G
Ikäheimo, I
Koskela, P
Lehtinen, M
Stendahl, U
Paavonen, J
Dillner, J
机构
[1] Karolinska Inst, Dept Mol Med, Stockholm, Sweden
[2] Univ Hosp No Sweden, Ctr Oncol, Umea, Sweden
[3] Finnish Canc Registry, Inst Stat & Epidemiol Canc Res, FIN-00170 Helsinki, Finland
[4] Univ Hosp No Sweden, Cytol Lab, Umea, Sweden
[5] Natl Publ Hlth Inst, Oulu, Finland
[6] Univ Hosp No Sweden, Dept Pathol, Umea, Sweden
[7] Univ Hosp No Sweden, Med Bank, Dept Publ Hlth & Clin Med, Umea, Sweden
[8] Oulu Univ Hosp, Clin Microbiol Lab, Oulu, Finland
[9] Natl Publ Hlth Inst, Dept Infect Dis & Epidemiol, Helsinki, Finland
[10] Univ Hosp No Sweden, Sect Gynecol, Dept Oncol, Umea, Sweden
[11] Univ Helsinki, Dept Obstet & Gynecol, Helsinki, Finland
[12] Lund Univ, Dept Med Microbiol, Malmo, Sweden
[13] Univ Tampere, Sch Publ Hlth, FIN-33101 Tampere, Finland
关键词
human papillomavirus (HPV); Chlamydia trachomatis; Pap smear; cervical cancer; cancer screening;
D O I
10.1002/ijc.10639
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Persistent human papillomavirus (HPV) infection is an established cause of cervical cancer, but the role of other sexually transmitted agents, most notably Chlamydia trachomatis, has not been well defined. The women participating in the population-based cervical cancer screening program in Vasterbotten county of Northern Sweden were followed up for up to 26 years to identify 118 women who developed cervical cancer after having had a normal Pap smear (on average 5.6 years later; range 0.5 months-26 years). As controls, we selected another 118 women who were matched by birth cohort, time-point of sampling of the baseline normal smear and who had a normal smear at the time when the corresponding case was diagnosed with cancer. The Pap smears and cervical cancer biopsies were analyzed by PCR for C. trachomatis DNA and for HPV DNA. At baseline, C. trachomatis DNA was present in 8% of cases but not among any one of the controls. The relative risk for cervical cancer associated with past C. trachomatis infection, adjusted for concomitant HPV DNA positivity, was 17.1 (95% CI 2.6-infinity). The presence of C. trachomatis and of HPV were not interrelated. Whereas C. trachomatis was primarily found in specimens taken many years before cancer diagnosis, HPV DNA was associated with a short lag time before cancer diagnosis. Whereas most women who were HPV DNA-positive in the prediagnostic smear were also positive for the same virus in the cervical cancer biopsy, none of the women were positive for C. trachomatis in both the prediagnostic smear and in the subsequent cervical cancer. In conclusion, a prior cervical C. trachomatis infection was associated with an increased risk for development of invasive cervical cancer. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:371 / 374
页数:4
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