Genital Dysplasia in Women Infected with Human Immunodeficiency
Genital Dysplasia in Women Infected with Human Immunodeficiency
Background: Women infected with human immunodeficiency virus (HIV) are at increased risk for the development of dysplastic genital lesions. Traditionally, markers of immunosuppression were predictive of the development of dysplasia. Recent advances in antiretroviral medications allow restoration of a once-depressed CD4 cell count and suppression of HIV replication. In this new era, additional predictive markers of genital dysplasia are needed for management of women infected with with HIV.
Objective: To find predictive markers of genital dysplasia in women infected with HIV.
Design: Observational study of a consecutive sample of 200 women infected with HIV from an urban university clinic. Measurements of histopathology, CD4 count, CD4 nadir, HIV viral load, human papillomavirus (HPV), and usage of highly active antiretroviral therapy (HAART) were evaluated for an association with genital dysplasia.
Results: There was a trend toward a protective effect against any genital dysplasia when HAART had been prescribed [relative risk = 0.77, 95% confidence interval (CI) 0.56, 1.06] and HAART therapy resulted in an immune response (relative risk, 0.61; 95% CI, 36, 1.02). High-risk HPV DNA was a strong predictor of dysplasia (P = .0003). A lower CD4 count nadir was strongly associated with genital dysplasia (P = .0003).
Conclusion: A history of greater immunosuppression, as measured by the nadir of a patient's CD4 count, is the strongest predictor of genital dysplasia in women infected with HIV.
There is an increase in the rates of both detection and persistence of human papillomavirus (HPV) infection in women coinfected with human immunodeficiency virus (HIV). Up to 20% of these coinfected patients develop HPV-induced premalignant lesions of the uterine cervix within 3 years of HIV diagnosis. The progression of an untreated HPV-induced dysplastic lesion may lead to invasive cervical cancer, an AIDS-defining illness.
Before highly active antiretroviral therapy (HAART) became the standard of care in the treatment of persons infected with HIV, the risk of cervical dysplasia increased progressively as a patient's immune function declined, as measured by the decrement of CD4 cells. It has also been observed that women with low CD4 counts experience greater rates of cervical lesion recurrence and progression when treated by the traditional ablative methods of loop electrosurgical excision procedure or cone biopsy. With the advent of newer antiretroviral medications and HAART therapy, it became possible to reverse the depletion of CD4 cells in a person infected with HIV. Opposing studies with small numbers of HIV-positive patients have revealed minimal to no effect of antiretroviral agents on the incidence of cervical dysplasia. Two of the studies that failed to reveal a positive effect were performed before HAART became the standard of care. Current guidelines suggest yearly Papanicolaou smears for HIV-positive women with a history of a normal Papanicolaou smear in the past, and every 6 months if the patient's CD4 count is below 200. These guidelines do not acknowledge the influence of HAART on immune perimeters and cervical dysplasia. It is unclear whether immune restoration brought about by HAART will be protective against genital dysplasia or influence the natural course and treatment of HPV-related genital dysplasia. Markers that may be predictive of genital dysplasia in HIV-positive patients need to be extrapolated from those who have been treated with antiretroviral agents. To investigate whether HAART has an affect on cervical dysplasia, we collected data on a consecutive sample of women infected with HIV undergoing colposcopic examination, starting in 1997, after the widespread institution of HAART.
Background: Women infected with human immunodeficiency virus (HIV) are at increased risk for the development of dysplastic genital lesions. Traditionally, markers of immunosuppression were predictive of the development of dysplasia. Recent advances in antiretroviral medications allow restoration of a once-depressed CD4 cell count and suppression of HIV replication. In this new era, additional predictive markers of genital dysplasia are needed for management of women infected with with HIV.
Objective: To find predictive markers of genital dysplasia in women infected with HIV.
Design: Observational study of a consecutive sample of 200 women infected with HIV from an urban university clinic. Measurements of histopathology, CD4 count, CD4 nadir, HIV viral load, human papillomavirus (HPV), and usage of highly active antiretroviral therapy (HAART) were evaluated for an association with genital dysplasia.
Results: There was a trend toward a protective effect against any genital dysplasia when HAART had been prescribed [relative risk = 0.77, 95% confidence interval (CI) 0.56, 1.06] and HAART therapy resulted in an immune response (relative risk, 0.61; 95% CI, 36, 1.02). High-risk HPV DNA was a strong predictor of dysplasia (P = .0003). A lower CD4 count nadir was strongly associated with genital dysplasia (P = .0003).
Conclusion: A history of greater immunosuppression, as measured by the nadir of a patient's CD4 count, is the strongest predictor of genital dysplasia in women infected with HIV.
There is an increase in the rates of both detection and persistence of human papillomavirus (HPV) infection in women coinfected with human immunodeficiency virus (HIV). Up to 20% of these coinfected patients develop HPV-induced premalignant lesions of the uterine cervix within 3 years of HIV diagnosis. The progression of an untreated HPV-induced dysplastic lesion may lead to invasive cervical cancer, an AIDS-defining illness.
Before highly active antiretroviral therapy (HAART) became the standard of care in the treatment of persons infected with HIV, the risk of cervical dysplasia increased progressively as a patient's immune function declined, as measured by the decrement of CD4 cells. It has also been observed that women with low CD4 counts experience greater rates of cervical lesion recurrence and progression when treated by the traditional ablative methods of loop electrosurgical excision procedure or cone biopsy. With the advent of newer antiretroviral medications and HAART therapy, it became possible to reverse the depletion of CD4 cells in a person infected with HIV. Opposing studies with small numbers of HIV-positive patients have revealed minimal to no effect of antiretroviral agents on the incidence of cervical dysplasia. Two of the studies that failed to reveal a positive effect were performed before HAART became the standard of care. Current guidelines suggest yearly Papanicolaou smears for HIV-positive women with a history of a normal Papanicolaou smear in the past, and every 6 months if the patient's CD4 count is below 200. These guidelines do not acknowledge the influence of HAART on immune perimeters and cervical dysplasia. It is unclear whether immune restoration brought about by HAART will be protective against genital dysplasia or influence the natural course and treatment of HPV-related genital dysplasia. Markers that may be predictive of genital dysplasia in HIV-positive patients need to be extrapolated from those who have been treated with antiretroviral agents. To investigate whether HAART has an affect on cervical dysplasia, we collected data on a consecutive sample of women infected with HIV undergoing colposcopic examination, starting in 1997, after the widespread institution of HAART.
Source...