Cervical glandular intraepithelial neoplasia, it is necessary to understand these

Cervical glandular intraepithelial neoplasia, it is necessary to understand these

Cervical glandular intraepithelial neoplasia is a disease that has attracted attention due to the increase in incidence in recent years. It is caused by human papillomavirus infection. The disease is very serious. If you suffer from this disease, your life may be in danger at any time. Therefore, patients need to learn more about treatment methods, seek medical treatment in time, cooperate with scientific care methods, and recover health as soon as possible.

1. Cervical glandular intraepithelial neoplasia

In the past, there was little research and the definition was not clear. However, due to the increasing incidence of cervical adenocarcinoma in recent years, it has attracted people's attention. Gloor and Hurlimann (1986) suggested the use of the name cervical glandular intraepithelial neoplasia, which is similar to squamous intraepithelial neoplasia and also includes glandular atypical hyperplasia and adenocarcinoma in situ. Some scholars describe glandular atypical hyperplasia as a glandular epithelial lesion between normal endocervical glandular epithelium and glandular carcinoma in situ, and believe that adenocarcinoma in situ is a precancerous lesion of invasive adenocarcinoma.

2. Epidemiology

A survey in areas with a high incidence of cervical cancer found that the peak ages for HPV, cervical atypical hyperplasia carcinoma in situ and invasive cancer were 25-29 years old, 30-34 years old, 40-44 years old and 45-54 years old, respectively, with a difference of 5-10 years between each age group. The age differences between invasive cancer and HPVI and atypical hyperplasia groups were 20-25 years and 10-15 years, respectively. Coppleson (1992) collected literature data and found that the peak age for atypical hyperplasia was 30-39 years old, and the average age for carcinoma in situ was 35-42 years old. Switzerland reported that the peak age of carcinoma in situ was 30 to 39 years old, with an average age of 37 years old. Kolstad et al. found that the age of onset of carcinoma in situ shifted to the left, 3 to 10 years earlier. In a group of 150 CIN reports, the median age was high at 43 years old, among which CIN grades I, II and III were 44.8 years, 43.8 years and 47.7 years old respectively. This may be related to the development of the census work, the different age composition of the examined population and the increase in HPV infection rate.

3. Causes

Human papillomavirus infection

With the deepening of research on the relationship between human papillomavirus (HPV) infection and the lower reproductive tract, it has been found that HPV infection is associated with the occurrence of cervical precancerous lesions. HPV infection, as a special type of sexually transmitted disease, is the cause of cervical intraepithelial neoplasia. Molecular biology and epidemiological studies have shown that human papillomavirus is carcinogenic. HPV can be divided into different types according to its carcinogenicity: HPV16, 18, 45, 56 are high-risk types, HPV31, 33, 35 and other 11 types are medium-risk types, and HPV6, 11, 26 and other 8 types are low-risk types. CINⅠ and subclinical HPV infection are usually HPV6 and 11, and 80% of CINⅢ are HPV16 infection

In patients with severe atypical hyperplasia of the cervix, the chromosomes in the cells are often accompanied by the integration of HPV genes, which activates the E1 and E2 genes and leads to the expression of viral genes in the cervical epithelium. Subsequently, the E6 and E7 genes encode the synthesis of multifunctional proteins, thereby interfering with cell growth. It plays an important role in cell carcinogenesis in patients infected with high-risk HPV types 16 and 18. The high-risk HPV E6 protein can bind to the tumor suppressor gene p53, leading to p53 degradation. The E7 gene product is a nuclear phosphoprotein that binds to the product of the tumor suppressor gene retinoblastoma gene (PRb), resulting in its functional inactivation, thereby affecting its effect of inhibiting cell growth.

Other factors

(1) Smoking: Smoking is related to the occurrence of cervical intraepithelial neoplasia. Nicotine, its degradation product, has a cervical irritation similar to that causing lung cancer and plays an important role in the occurrence of cervical intraepithelial neoplasia.

(2) Microbial infection: Neisseria gonorrhoeae, herpes simplex virus (HSV), and Trichomonas infection can increase susceptibility to HPV and thus be associated with the occurrence of cervical intraepithelial neoplasia.

(3) Endogenous and exogenous immunodeficiency: Infection with immunodeficiency viruses can increase the incidence of CIN, such as Hodgkin's disease, leukemia, collagen vascular disease and HPV infectious diseases.

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