DISPARITIES IN MEAN AGE AND HISTOPATHOLOGIC GRADE BETWEEN HUMAN-PAPILLOMAVIRUS TYPE-SPECIFIC EARLY CERVICAL NEOPLASMS

Noninvasive squamous and glandular precursor lesions associated with h uman papillomavirus (HPV) types 16 and 18 have been reported to vary i n morphology. HPV 16 is associated predominantly with high-grade squam ous intraepithelial lesions (HSIL; cervical intraepithelial neoplasia (GIN 2 and 3), and HPV 18 is associated with low-grade squamous intrae pithelial lesions (condyloma/CIN 1) and CIN 3/adenocarcinoma in situ ( ACIS). This study explored the relationship of morphologic growth patt ern in these precursor groups with age of presentation. One hundred fo urteen CIN lesions (including those with ACIS), associated with HPV 16 or 18, were subdivided into well-differentiated low-and high-grade SI L, (CIN 1 and 2, respectively), poorly differentiated HSIL (GIN 3) wit h or without ACIS. I-IPV was detected by polymerase chain reaction (PC R) amplification with L1 consensus or type-specific E7 primers and typ ed by restriction fragment length polymorphism (RFLP) analysis. Age of the patient was obtained from the pathology report Mean age for each group was as follows: Low-risk HPVs, 25 years; HPV 18 CEN 1-2, 21.6 yr s; HPV 18 CIN 3/ACIS, 35.2 yrs; HPV 16 CIN 1,2, 25.9 ys; and HPV 16 CI N 3, 29.8 ys. There were significant differences in mean ages between HPV 18 CIN 1 and 2 and HPV 16 CIN 1 to 2 (P =.04), HPV 16 CIN 1-2 and CIN 3 (P =.01) and HPV 18 CIN 1 to 2 and HPV 18 CIN 3/ACIS (P =.00001) . None of the cases of HPV 18-associated CIN3/ACIS was associated with a CINI lesion. The disparity in mean ages between well and poorly dif ferentiated HPV 16/18 related that precursor lesions could reflect fac tors such as morphologic progression with increasing age, different ra tes of lesion persistence, depending on grade, or efficiency of detect ion between the two groups. The marked difference in mean age between HPV 18-associated CIN 1-2 and CIN 3/ACIS, combined with their lack of coexistence in the same cervix, raises alternate possibilities that sp ecific viral or host factors may determine the morphological phenotype associated with some HPV 18 infections. In the latter, the possibilit y that age independently confers an increased risk for higher-grade le sions should be considered. Copyright (C) 1997 by W.B. Saunders Compan y.