Updated guidelines for papanicolaou tests, colposcopy, and human papillomavirus testing in adolescents

Abstract

Worldwide, cervical cancer is a major health concern for women of all ages; however the epidemiology and biology of human papillomavirus (HPV) infection differs in female adolescents and adults. In the United States, 50% of adolescent and young women acquire HPV within 3 years after initiating sexual intercourse, resulting in relatively high prevalence rates. Most infections, however, are transient and clear within several months. Consequently HPV infections detected in adolescents are likely to reflect benign disease, whereas infections detected in older women are likely to reflect persistent infections and a higher risk of advanced cervical intraepithelial lesions that can lead to invasive cervical cancer. This article reviews the most recently published guidelines for the prevention of cervical cancer through screening and management of abnormal cervical cytologic and histologic findings, which have been updated to reflect the differences in HPV infections and cervical abnormalities in female adolescents and adults.

Figure 1

Life cycle of the human papillomavirus (HPV). HPV requires direct access to basal cells through a wound or inflammation. HPV then requires cell differentiation for its own transcription and replication process. As cells mature and move through the epithelium, the early protein, E6 and E7, are expressed while the infected cell is present in the basal cell layers. As the infected cell matures, other proteins are expressed, including E4, which is known to induce the cytopathic effect referred to as koilocytosis. The late proteins, L1 and L2, which are responsible for the outer capsid, are not expressed until the cells are fully mature. At the time, the infectious viral capsid is released as the anucleated cells are desquamated. (Reprinted from von Knebel Doeberitz M. New markers for cervical dysplasia to visualise the genomic chaos created by aberrant oncogenic papillomavirus infections. Eur J Cancer 2002;38:2292–42, with permission from Elsevier.)

Figure 2

Role of persistent HPV infection in cervical cancer. CIN 3 = cervial intraepithelial neoplasia grade 3. (Reprinted from Moscicki AB. Updating the natural history of HPV and anogenital cancer. Vaccine 2006;24(Suppl 3):42–51, with permission from Elsevier.)

Figure 3

Comparison of cervical cytology descriptive systems. CIN = cervical intraepithelial neoplasia; WHO = World Health Organization. (Based on Solomon D, et al. The 2001 Bethesda System: Terminology for reporting results of cervical cytology. JAMA 2002 287:2114–9.)

Figure 4

Algorithms for Management of Adolescent Women with Abnormal Cytology. Reprinted from The Journal of Lower Genital Tract Disease Vol. 11 Issue 4, with the permission of ASCCP © American Society for Colposcopy and Cervical Pathology 2007. No copies of the algorithms may be made without the prior consent of ASCCP. (A) Management of adolescent women with either atypical squamous cells of undetermined origin (ASC-US) or low-grade squamous intraepithelial lesion (LSIL). (B) Management of women with atypical squamous cells cannot exclude high-grade SIL (ASC-H). (C) Management of adolescent women (20 years or younger) with high-grade squamous intraepithelial lesion (HSIL).

Figure 5

Algorithms for Management of Adolescent Woment with CIN. Reprinted from The Journal of Lower Genital Tract Disease Vol. 11 Issue 4, with the permission of ASCCP © American Society for Colposcopy and Cervical Pathology 2007. No copies of the algorithms may be made without the prior consent of ASCCP. (A) Management of adolescent women (20 years or younger) with a histologic diagnosis of cervical intraepithelial neoplasia grade 1 (CIN 1). (B) Management of adolescent and young women with a histological diagnosis of cervical intraepithelial neoplasia grade 2,3 (CIN 2,3).