Risk Factors for Cervical Precancer and Cancer in HIV-Infected, HPV-Positive Rwandan Women

被引:29
作者
Anastos, Kathryn [1 ,2 ]
Hoover, Donald R. [3 ,4 ]
Burk, Robert D. [5 ]
Cajigas, Antonio [6 ]
Shi, Qiuhu [7 ]
Singh, Diljeet K. [8 ]
Cohen, Mardge H. [9 ,10 ]
Mutimura, Eugene [11 ]
Sturgis, Charles [12 ]
Banzhaf, William C. [13 ]
Castle, Philip E. [14 ]
机构
[1] Montefiore Med Ctr, Dept Med, Bronx, NY 10467 USA
[2] Montefiore Med Ctr, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA
[3] Rutgers State Univ, Dept Stat, Piscataway, NJ USA
[4] Rutgers State Univ, Inst Hlth Hlth Care Policy & Aging Res, Piscataway, NJ USA
[5] Albert Einstein Coll Med, Dept Pediat, Div Genet, Bronx, NY 10467 USA
[6] Montefiore Med Ctr, Dept Pathol, Bronx, NY 10467 USA
[7] New York Med Coll, Dept Epidemiol & Community Hlth, Valhalla, NY 10595 USA
[8] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA
[9] John Stroger Hosp, Chicago, IL USA
[10] Rush Univ, Chicago, IL 60612 USA
[11] Womens Equ Access Care & Treatment, Kigali, Rwanda
[12] Providence Reg Med Ctr, Everett, WA USA
[13] Univ Chicago, Pritzker Sch Med, Evanston, IL USA
[14] NCI, NIH, US Dept HHS, Bethesda, MD 20892 USA
来源
PLOS ONE | 2010年 / 5卷 / 10期
基金
美国国家卫生研究院;
关键词
HUMAN-PAPILLOMAVIRUS INFECTION; NATURAL-HISTORY; NEOPLASIA; POPULATION; DIAGNOSIS; DNA; BIOPSY;
D O I
10.1371/journal.pone.0013525
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background: Although cervical cancer is an AIDS-defining condition, infection with human immunodeficiency virus (HIV) may only modestly increase the risk of cervical cancer. There is a paucity of information regarding factors that influence the natural history of human papillomavirus (HPV) in HIV-infected women. We examined factors associated with cervical intraepithelial neoplasia grade 3 or cancer (CIN3+) in Rwandan women infected with both HIV and HPV (HIV+/HPV+). Methods: In 2005, 710 HIV+ Rwandan women >= 25 years enrolled in an observational cohort study; 476 (67%) tested HPV+. Each woman provided sociodemographic data, CD4 count, a cervical cytology specimen and cervicovaginal lavage (CVL), which was tested for >40 HPV genotypes by MY09/MY11 PCR assay. Logistic regression models calculated odds ratios (OR) and 95% confidence intervals (CI) of associations of potential risk factors for CIN3+ among HIV+/HPV+ women. Results: Of the 476 HIV+/HPV+ women 42 (8.8%) were diagnosed with CIN3+. Factors associated with CIN3+ included >= 7 (vs. 0-2) pregnancies, malarial infection in the previous six months (vs. never), and >= 7 (vs. 0-2) lifetime sexual partners. Compared to women infected by non-HPV16 carcinogenic HPV genotypes, HPV16 infection was positively associated and non-carcinogenic HPV infection was inversely associated with CIN3+. CD4 count was significantly associated with CIN3+ only in analyses of women with non-HPV16 carcinogenic HPV (OR = 0.62 per 100 cells/mm(3), CI = 0.40-0.97). Conclusions: In this HIV+/HPV+ population, lower CD4 was significantly associated with CIN3+ only in women infected with carcinogenic non-HPV16. We found a trend for higher risk of CIN3+ in HIV+ women reporting recent malarial infection; this association should be investigated in a larger group of HIV+/HPV+ women.
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