Is HPV screening for cervical cancer predictive of risk of anal cancer?

June 25, 2019
Ben Schwartz
Ben Schwartz

Ben Schwartz is Associate Editor, Contemporary OB/GYN.

A new systematic review sheds light on whether routine cervical cancer screening results might predict anal HPV16 infection, anal high-grade squamous intraepithelial lesions (HSIL), and anal cancer

Testing for human papillomavirus (HPV) is proven to be predictive of cervical cancer risk, but whether the results can identify women at risk of anal cancer remains largely unknown. A new systematic review, published in Lancet Infection, sheds light on whether routine cervical cancer screening results might predict anal HPV16 infection, anal high-grade squamous intraepithelial lesions (HSIL), and anal cancer.

Included in the analysis were 36 studies of cervical determinants for anal HPV and HSIL published up to August 31, 2018 representing data from 13,427 women with paired cervical and anal samples. The authors compared anal high-risk HPV prevalence by HIV status, cervical high-risk HPV, cervical cytohistopathology, age, and their combinations.

The researchers found that cervical and anal HPV infections were highly correlated. In HIV-negative women, prevalence of anal HPV16 was 41% (447/1097) in those who screened positive for cervical HPV16, compared with 2% (214/8663) in HIV-negative women who screened negative for cervical HPV16 (prevalence ratios [PR]16.5, 95% CI 14.2 – 19.2, P< 0.0001). HIV-positive women had similar results; anal HPV16 prevalence was 46% (125/273) in cervical HP16-positive women versus 11 % (272/2588) (PR 4.4, 95% CI 3.7-5.3, P< 0.0001).

An association between anal HPV16 and cervical cytohistopathology was also significant, with a prevalence of 44% (101/228) for cervical cancer in HIV-negative women (PR vs normal cervical cytology 14.1, 11.1-17.9, < 0.001). Anal HSIL was associated with high-risk cervical HPV in both HIV-negative and HIV-positive women. In HIV-negative women, anal HSIL was found in 2% (11/527) of those who were negative for cervical high-risk HPV and 24% (33/138) who were positive for cervical HPV16 (PR 12.9, 95% CI 6.7-24.8, P< 0.0001). In HIV-positive women, rates were 8% (84/1094) and 17% (31/186), respectively (PR 2.3, 1.6-3.4, P< 0.0001). 

Anal HSIL was also associated with cervical cytohistopathology. Prevalence in HIV-negative women was 1% (5/498) in normal cytology up to 22% (59/273) in women with cervical HSIL (PR 23.1, 9.4 - 57.0, P< 0.0001). Prevalence in HIV-positive women was 7% (105/1421) to 25% (25/101), respectively (PR 3.6, 2.5-5.3, < 0.0001). Prevalence of HPV16-positive anal HSIL among HIV-negative women was higher in cervical HPV16-positive women over 45 years (5/20) compared with women younger than 30 years (2/46) (PR 5.8, 95% CI 1.2-27.2, = 0.0273). In HIV-positive women, these values were 23% (12/52) and 2% (1/55), respectively (PR 12.7, 95% CI1.7-94.2, = 0.0130).

 

The authors believe their study illustrates how cervical screening programs can help classify anal cancer risk, regardless of HIV status. The strongest indicators for anal cancer risk are a diagnosis of cervical cancer and cervical HPV16 positivity. Ob/gyns should reiterate the importance of regular cervical screening to their patients, and especially to older women who may have missed out on HPV vaccination.