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The incidence of cervical cancer has been changing at a global level, with increasing incidence in women below 40 years of age [9,10]. This may reflect age-cohort effects and the emergence of more aggressive histologies with a shorter natural history, possibly the result of HPV infection acquired at a younger age or of increased screening/awareness resulting in earlier detection of cervical cancer.
High-risk HPV types were detected in all (100%) of the HIV-positive women with cervical cancer and in 98/110 (89%) of HIV-negative women with cervical cancer (p = 0.1). In multivariate analysis, only HIV infection was associated with HPV infection among controls (OR = 3.0; 95% CI 0.7-13.5). A stronger association was observed among younger women, but the number of samples were small and the difference was not statistical significant (OR = 6.8; 95% CI 0.5-98.0).
Table 5 shows the characteristics of HIV-positive and HIV-negative women with cervical cancer. All HIV-positive case-participants had evidence of high-risk HPV infection. Among HIV-positive women, cervical cancer was detected at a younger age (median age 39 years (range 24-64)) than among HIV-negative women (median age 47 years (range 28-69)). Nevertheless, a similar percentage (50% each) of HIV-positive and HIV-negative women had advanced stage cervical cancer (Clinical Stage III or IV) at diagnosis. Only 18% of HIV-positive women with cervical cancer had CD4 counts below 200 cells/μl.
The results in this case-control study are consistent with established associations of cervical cancer with oncogenic types of HPV infection and with a potential association of cervical cancer with high parity both for older and younger women [5,18,33]. An association between HIV infection and cervical cancer was also noted especially in women aged
Young age and advanced stage of cervical cancer in HIV-infected women in this study were consistent with published findings of rapidly progressive or more advanced forms of cervical cancer at a young age . A possible explanation is that HIV infection may facilitate the progression of cervical HPV lesions to cancer in young women, and an inverse relationship of high-risk HPV prevalence and age has been described . However, among both the HIV-positive and HIV-negative patients in this study, those with cervical cancer had advanced clinical stages at the time of detection. This may reflect low prevalence of screening, and in a setting where preventive services are not developed, women may seek treatment only when they have advanced disease. There was no evidence that the relationship observed between HIV infection and cervical cancer reflected higher risk behavior among younger women, as numbers of sexual partners was adjusted for in the multivariate analysis.
Although HIV infection itself has been reported as a risk factor for cervical cancer [5,18,37], it may be that infection with high-risk types of HPV facilitates becoming infected with HIV if exposed . A higher prevalence of HPV infection in HIV-positive than in HIV-negative women has been described . Although the association of cervical cancer with HIV infection was observed only among the younger group of participants in our data, it may be that the lower prevalence of HIV infection among older participants resulted in an insufficient number of HIV-infected participants to detect a statistically significant difference in HIV-infection between cases and controls.
In interpreting the results of this study, a few limitations should be noted. First, controls who were recruited in the oncology and surgical outpatient clinics may not have been representative of the general population with respect to the probability of having HIV infection; however, if the pathology that resulted in their seeking care at the clinic had been related to HIV infection, the measure of effect would be biased towards the null hypothesis of no association between HIV infection and cervical cancer. Second, women who were recruited in university hospitals may not have been representative of women with cervical cancer in the general population in terms of probability of having HIV infection; to adjust for this potential bias (Berkson bias), control participants were selected from oncology and surgical outpatient clinics of the same institutions from which the case patients were selected. Third, control-participants were on average younger and had a higher socioeconomic status than did case-participants; however, these differences were addressed in multivariate analysis, and therefore were unlikely to affect validity of results. Fourth, the few cervical cancer specimens in which high-risk HPV DNA was not identified were probably false negatives, but their number was sufficiently small that their inclusion in the case group would not have appreciably altered the conclusions of this study.
The data presented here using confirmatory HIV testing, HPV DNA testing, and histologically confirmed biopsies support associations of cervical cancer with high-risk HPV infection and with parity observed in previous studies. In addition, strong association of HIV infection and cervical cancer was observed among young women, with a high prevalence of high-risk HPV DNA in women with HIV infection. In this study population, few participants had ever had a Pap smear, and cervical cancer was observed at a young age among women with HIV infection in the absence of extreme immunosuppression. The findings overall add support to the association of invasive cervical cancer among HIV-infected persons, an association on which the recommendation for annual cervical cytology screening in persons with HIV infection is based.
Another risk factor for positive HIV status was the number of sexual partners reported, P
A strong public health initiative to prevent HIV infection and STIs is critical at this time to prevent the prevalence rate of HIV from increasing in the young women in particular and in the Ghanaian population in general. Included in this initiative should be educational information concerning STIs and an inclusion of the significance of STIs as a facilitator of HIV infection. 041b061a72