Background: Previous studies demonstrated the etiological role of human papilloma virus (HPV) in cervical carcinogenesis. Assessing the distribution of HPV may elucidate these observations.
Materials and methods: In total, we examined 3839 specimens, of which 187 abnormally classified cervical smears were immunostained using the p16(INK4A) assay. DNA was extracted from 182 specimens, and polymerase chain reaction (PCR) was performed. Participants' socio-demographics, sexual and reproductive history, HIV status, contraceptive use, and Pap smear history were recorded.
Results: Subject ages, number of sexual partners, and age at first sexual encounter ranged from 15 to 49 years, from 1 to 37 partners, and from 13 to 34 years, respectively. P16 immunoreactivity was detected in 60.4% of cases. The distribution of epithelial lesions and P16 overexpression (bracketed) was: 28 (5) atypical squamous cells of undetermined significance (ASC-US), 96 (50) lower grade squamous intraepithelial lesion (LSIL), 9 (7) atypical squamous cells-cannot exclude HSIL (ASC-H), and 54 (51) higher grade squamous intraepithelial lesion (HSIL). Ninety-four percent of HSIL expressed P16. Fifty-two percent of LSIL expressed P16. P16 expression declined from 61% (25-34 year age group) to 5% (45-49 year age group) for different age groups. HPV-DNA by PCR was detected in 94.5% of P16-positive samples. Type-specific PCR (HPV 16 and 18) was found in 12.2% and 14.5% of abnormal lesions, respectively. Younger age at first sexual encounter and HIV infection predominated in HPV type(s) 16 and/or 18 positive subjects.
Conclusion: This study reinforced the value of the p16(INK4A) surrogate marker in identifying women with progressive cervical disease.
Keywords: Cervical cancer; Namibia; human papilloma virus; p16INK44A stain.