Incidence risk of cervical intraepithelial neoplasia 3 or more severe lesions is a function of human papillomavirus genotypes and severity of cytological and histological abnormalities in adult Japanese women
Incidence risk of cervical intraepithelial neoplasia 3 or more severe lesions is a function of human papillomavirus genotypes and severity of cytological and histological abnormalities in adult Japanese women
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DOI:
10.1002/ijc.27680
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发表时间:
2013-01-15
影响因子:
6.4
通讯作者:
Sakuragi,Noriaki
中科院分区:
文献类型:
--
作者:
Hosaka,Masayoshi;Fujita,Hiromasa;Sakuragi,Noriaki
We examined incidence probabilities of cervical intraepithelial neoplasia 3 (CIN3) or more severe lesions (CIN3+) in 1,467 adult Japanese women with abnormal cytology in relation to seven common human papillomavirus (HPV) infections (16/18/31/33/35/52/58) between April 2000 and March 2008. Sixty‐seven patients with multiple HPV infection were excluded from the risk factor analysis. Incidence of CIN3+ in 1,400 patients including 68 with ASCUS, 969 with low grade squamous intraepithelial lesion (LSIL), 132 with HSIL without histology‐proven CIN2 (HSIL/CIN2(−)) and 231 with HSIL with histology‐proven CIN2 (HSIL/CIN2(+)) was investigated. In both high grade squamous intraepithelial lesion (HSIL)/CIN2(−) and HSIL/CIN2(+), HPV16/18/33 was associated with a significantly earlier and higher incidence of CIN3+ than HPV31/35/52/58 (p= 0.049 andp= 0.0060, respectively). This association was also observed in LSIL (p= 0.0002). The 1‐year cumulative incidence rate (CIR) of CIN3+ in HSIL/CIN2(−) and HSIL/CIN2(+) according to HPV genotypes (16/18/33vs. 31/35/52/58) were 27.1%vs. 7.5% and 46.6%vs. 19.2%, respectively. In contrast, progression of HSIL/CIN2(+) to CIN3+ was infrequent when HPV DNA was undetected: 0% of 1‐year CIR and 8.1% of 5‐year CIR. All cervical cancer occurred in HSIL cases of seven high‐risk HPVs (11/198) but not in cases of other HPV or undetectable/negative‐HPV (0/165) (p= 0.0013). In conclusion, incidence of CIN3+ depends on HPV genotypes, severity of cytological abnormalities and histology of CIN2. HSIL/CIN2(+) associated with HPV16/18/33 may justify early therapeutic intervention, while HSIL/CIN2(−) harboring these HPV genotypes needs close observation to detect incidence of CIN3+. A therapeutic intervention is not indicated for CIN2 without HPV DNA.