阴道微生态与人乳头瘤病毒感染和宫颈病变的相关性

Correlations of vaginal microecology with human papilloma virus and cervical lesion

  • 摘要:
    目的 评估阴道微生态与人乳头瘤病毒(HPV)感染和宫颈病变发生的相关性。
    方法 选取薄层液基细胞学(TCT)初筛结果异常患者772例, 按照病变的程度实行分级,并分析感染高危型人乳头瘤病毒(HR-HPV)情况。选取同期TCT初筛未见上皮内病变细胞和恶性细胞(NILM)且HPV分型为阴性的患者156例。将所有患者分为TCT异常HPV阳性患者、TCT异常HPV阴性患者、TCT正常HPV阴性患者,均行阴道微生态检查。评估阴道微生态状况与HR-HPV感染和宫颈病变之间的相关性。
    结果 772例TCT结果异常患者中HPV感染率为48.06%; 其中多种型别感染占HPV感染者的22.37%; 感染率较高的亚型依次为HPV52、HPV16、HPV58。772例患者中,高级别鳞状上皮内病变(HSIL)患者HPV感染率高于低级别鳞状上皮内病变(LSIL)患者和无明确诊断意义的不典型鳞状细胞(ASCUS)、不典型腺上皮细胞(AGC)患者,差异有统计学意义(P < 0.05)。阴道微生态研究中, TCT异常HPV阳性患者唾液酸酐酶阳性率、白细胞酯酶阳性率、细菌性阴道病(BV)患病率与TCT异常HPV阴性患者比较,差异有统计学意义(P < 0.05)。TCT异常HPV阳性患者过氧化氢、唾液酸酐酶、白细胞酯酶、β-葡萄糖醛酸酶、凝固酶阳性率、BV、需氧菌性阴道炎(AV)、阴道混合感染患病率、阴道微生态失调比例、清洁度(Ⅲ~Ⅳ)占比、乳酸杆菌阳性率与TCT正常HPV阴性患者比较,差异有统计学意义(P < 0.05)。过氧化氢、唾液酸酐酶、白细胞酯酶阳性、BV、混合感染、阴道微生态失调、清洁度(Ⅲ~Ⅳ)是HR-HPV阳性和/或宫颈细胞学异常的危险因素(OR>1, P < 0.05), 乳酸杆菌阳性是HR-HPV阳性和/或宫颈细胞学异常的保护因素(OR < 1, P < 0.05)。
    结论 阴道微生态与HR-HPV感染和宫颈病变有相关性,阴道微生态失衡更易导致HR-HPV感染,促进宫颈病变的发生发展。

     

    Abstract:
    Objective To evaluate the associations of vaginal microecology with human papilloma virus (HPV) infection and cervical lesions.
    Methods A total of 772 patients with abnormal preliminary screening results of thin layer liquid based cytology (TCT) were selected, were graded according to the degree of lesions, and the infection of high-risk human papillomavirus (HR-HPV) was analyzed. A total of 156 patients without intraepithelial pathological cells and malignant cells (NILM) and negative HPV typing were selected in the initial TCT screening during the same period. All patients were divided into TCT abnormal HPV-positive patients, TCT abnormal HPV-negative patients and TCT normal HPV-negative patients. All patients underwent vaginal microecological examination. Associations of vaginal microecology with HR-HPV and cervical lesion were evaluated.
    Results Among 772 patients with abnormal TCT results, the HPV infection rate was 48.06%. Among them, multiple types of infection accounted for 22.37% of HPV infections. The higher infection rate of the subtypes were HPV52, HPV16 and HPV58. The HPV infection rate in the 772 patients with high-grade squamous intraepithelial lesions (HSIL) was higher than that in the patients with low-grade squamous intraepithelial lesions (LSIL), atypical squamous cells of undetermined significance (ASCUS) and atypical glandular epithelial cells (AGC), and the difference was statistically significant (P < 0.05). In the vaginal microecological study, the positive rates of sialic ananase, leukocyte esterase and bacterial vaginosis (BV) in TCT abnormal HPV-positive patients were compared with those in TCT abnormal HPV-negative patients, and the differences were statistically significant (P < 0.05). The level of hydrogen peroxide, sialic anhydrolase, leucocytoesterase, β-glucuronidase, coagulase positive rate, BV, aerobic vaginitis (AV), vaginal mixed infection, proportion of vaginal microecological disorders, cleanliness (Ⅲ to Ⅳ) and lactobacillus positive rate in HPV-positive patients with abnormal TCT were compared with those in normal HPV-negative patients, the difference was statistically significant (P < 0.05). Hydrogen peroxide, sialic anhydrase, leocytoesterase positive, BV, co-infection, vaginal dysbiosis, cleanliness (Ⅲ to Ⅳ) were risk factors for HR-HPV positive and/or cervical cytology abnormalities (OR>1, P < 0.05), and lactobacillus positive was a protective factor for HR-HPV positive and/or cervical cytological abnormalities (OR < 1, P < 0.05).
    Conclusion Vaginal microecology is related to HR-HPV infection and cervical lesions, and the imbalance of vaginal microecology is more likely to lead to HR-HPV infection and promote the occurrence and development of cervical lesions.

     

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