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High‐risk HPV presence in cervical specimens after a large loop excision of the cervical transformation zone: Significance of newly detected hr‐HPV genotypes
Author(s) -
van Ham Maaike A.P.C.,
van Hamont Dennis,
Bekkers Ruud L.M.,
Bulten Johan,
Melchers Willem J.G.,
Massuger Leon F.A.G.
Publication year - 2007
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20800
Subject(s) - medicine , cervical intraepithelial neoplasia , cervical canal , genotype , human papillomavirus , hpv infection , squamous intraepithelial lesion , virology , cervical cancer , gynecology , cervix , biology , gene , cancer , biochemistry
Large loop excision of the cervical transformation zone (LLETZ) is a well‐established treatment for high‐grade cervical intraepithelial neoplasia. It has even been postulated that LLETZ is responsible for the elimination of the infectious agent, human papillomavirus (HPV), causing the lesion. Most studies on HPV detection after LLETZ have focused on the persistence of high‐risk (hr‐) HPV to identify women at risk for residual or recurrent disease. Therefore, the appearance and significance of hr‐HPV types newly detected after surgical treatment has not been studied extensively so far. The presence of hr‐HPV in 85 high‐grade squamous cervical LLETZ biopsies and in the first follow‐up smear was determined. In 80 (94%) of the LLETZ biopsies hr‐HPV was detected in contrast to 30 (35%) hr‐HPV positive follow‐up scrapes. Twenty of the 80 hr‐HPV positive women (25%) had the same hr‐HPV genotypes in their follow‐up cervical smears as was found in the corresponding biopsies. In the follow‐up smear of 13 women a new hr‐HPV genotype was detected and HPV 18 was newly detected in 8 of them. The remarkably high presence of newly detected HPV 18 genotypes may argue for a release or re‐activation of this virus from proximal layers of the cervical canal incised during surgery. J. Med. Virol. 79:314–319, 2007. © 2007 Wiley‐Liss, Inc.