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
Sakuragi,Noriaki
中科院分区:
医学1区
文献类型:
--
作者:
Hosaka,Masayoshi;Fujita,Hiromasa;Sakuragi,Noriaki

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我们研究了2000年4月至2008年3月期间1,467名与7种常见人乳头瘤病毒(HPV)感染(16/18/31/33/35/52/58)相关的细胞学异常的日本成年女性中宫颈上皮内瘤变3(CIN 3)或更严重病变(CIN 3+)的发生概率。67例多重HPV感染患者被排除在风险因素分析之外。研究了1,400例患者的CIN 3+发生率,包括68例ASCUS患者、969例低度鳞状上皮内病变(LSIL)患者、132例HSIL患者(无组织学证实的CIN 2)(HSIL/CIN 2(-))和231例HSIL患者(有组织学证实的CIN 2)(HSIL/CIN 2(+))。在高度鳞状上皮内病变(HSIL)/CIN 2(-)和HSIL/CIN 2(+)中,HPV 16/18/33与CIN 3+的发生率显著早于HPV 31/35/52/58(分别为p= 0.049和p = 0.0060)。在LSIL中也观察到这种关联(p= 0.0002)。根据HPV基因型,HSIL/CIN 2(-)和HSIL/CIN 2(+)中CIN 3+的1年累积发病率(CIR)(16/18/33 vs. 31/35/52/58)分别为27. 1%和46. 6%。相比之下,当HPV DNA未检出时,HSIL/CIN 2(+)进展为CIN 3+的情况很少:1年CIR为0%,5年CIR为8.1%。所有宫颈癌均发生在7种高危HPV的HSIL病例中(11/198),但未发生在其他HPV或未检测到/阴性HPV的病例中(0/165)(p= 0.0013)。总之,CIN 3+的发生率取决于HPV基因型、细胞学异常的严重程度和CIN 2的组织学。与HPV 16/18/33相关的HSIL/CIN 2(+)可能需要早期治疗干预,而携带这些HPV基因型的HSIL/CIN 2(-)需要密切观察以检测CIN 3+的发生率。治疗性干预不适用于无HPV DNA的CIN 2。
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.