目的:人乳头瘤病毒(HPV)的持续存在被认为是肿瘤进展的主要危险因素,和证据表明,调节性T细胞在病毒消除失败中起重要作用。调节性T细胞可能参与维持有利于病毒持久性和新可塑性的微环境。通过局部免疫反应的失调。免疫功能改变与慢性感染发展之间的关联,癌症(实体和血液学),自身免疫性疾病在文献中有记载。这项回顾性分析的目的是评估由于15年的子宫颈抹片检查异常而参加阴道镜检查的妇女中HPV宫颈感染与淋巴瘤发生率之间的可能相关性。
方法:横断面研究参与者:我们回顾性调查了2004年至2019年期间转诊至我们中心的21-84岁女性的血液病发病率。
方法:大学医院方法:在我们的分析中,我们纳入了在检测到异常巴氏涂片和HPV感染后诊断为HL和NHL的女性.我们排除了在巴氏涂片和HPV检测异常之前诊断为淋巴瘤的患者。结果我们将患者分为两组,以分析标准发生率(SIR):HL患者(19/7064,0.26%),和NHL患者(22/7064,0.31%)。在我们的样本中,我们报告说,与普通人群相比,患淋巴瘤的风险很大,对于HL和NHL疾病,年龄<45岁。关于HL,<45岁女性的SIR为4.886(95%CI2.775-9.6029),45-59岁女性的SIR为2.612(95%CI0.96-7.108804).另一方面,对于<45岁女性的NHL,我们报告的SIR约为3.007(95%,CI1.273-7.101575),在45-59岁的女性中,SIR为4.291(95%CI2.444-7.534399),在60-74岁的女性中,SIR为3.283(95%CI1.054-10.22303)。这项回顾性分析是在意大利北部的一个中心进行的,没有考虑该国在HPV基因型方面存在的所有区域间差异。种族,和人口特征。关于HL和NHL的SIR分析,由于病例样本少,我们没有将疾病分为亚型。最后,我们在分析中只考虑子宫颈抹片检查异常的女性,而不考虑一般人群.结论结论,患有慢性和持续性HPV感染的女性患淋巴瘤的相对风险较高.这种可能的关联可能是由免疫系统对HPV的反应失调和病毒清除失败引起的。尤其是年轻女性。
OBJECTIVE: Human papillomavirus (HPV) persistence is considered the main risk factor for neoplastic progression, and evidence suggests that regulatory T cells play an important role in the failure of viral elimination. Regulatory T cells may be involved in maintaining a microenvironment favourable for viral persistence and neoplasticity, through a deregulation of the local immune response. The association between altered immune function and the development of chronic infections, cancer (solid and haematological), and autoimmune diseases is documented in the literature. The purpose of this retrospective analysis was to evaluate the possible correlation between HPV cervical infection and lymphoma incidence in women attending colposcopy due to an abnormal Pap smear during a period of 15 years.
METHODS: This is a cross-sectional study.
METHODS: We investigated retrospectively the incidence of haematological diseases in women aged 21-84 with an abnormal Pap smear who referred to our centre between 2004 and 2019.
METHODS: This study was conducted at the university hospital.
METHODS: In our analysis, we included women with diagnoses of HL and NHL after the detection of abnormal Pap smears and HPV infections. We excluded patients with a diagnosis of lymphoma preceding the date of the abnormal Pap smear and HPV test.
RESULTS: We divided the patients into two groups in order to analyse the standard incidence ratio (SIR): HL patients (19/7,064, 0.26%) and NHL patients (22/7,064, 0.31%). In our sample, we reported a significant risk of developing lymphoma compared to the general population, both for HL and NHL disease, at age <45 years. Regarding HL, the SIR of disease in women <45 years was 4.886 (95% CI 2.775-9.6029) and in women between 45 and 59 years was 2.612 (95% CI 0.96-7.108804). On the other hand, for NHL in women <45 years, we reported an SIR of about 3.007 (95%, CI 1.273-7.101575), in women aged 45-59 years, the SIR was 4.291 (95% CI 2.444-7.534399), and in women aged 60-74 years, the SIR was 3.283 (95% CI 1.054-10.22303).
CONCLUSIONS: This retrospective analysis was conducted in a single centre in Northern Italy and did not consider all interregional differences existing in the country in terms of HPV genotypes, ethnicity, and population characteristics. Regarding the analysis of SIR for HL and NHL, we did not divide the disease into subtypes because of the small sample of cases. Finally, we considered in our analysis only women with an abnormal Pap smear and not the general population.
CONCLUSIONS: Women with chronic and persistent HPV infections may have a higher relative risk of developing lymphoma. This possible association may be caused by the deregulation of the immune system response against HPV and the failure of viral clearance, especially in younger women.