Vulvar intraepidermal neoplasia

Introduction

Introduction of vulvar intraepithelial neoplasia Vulvarintraepithelialneoplasma (VIN) is a group of vulvar lesions, which are premature lesions of vulvar cancer. The lesions are characterized by epidermal hyperplasia, which may appear thickened plaque, nipple or small sputum; the surface may be grayish white, melanin Sink or dark red, the tumor surface is dry, desquamation, and the boundary is unclear. Tumor foci can often be multiple and can be fused together. The VIN of young patients often resolves naturally, but younger patients over 60 years old with immunosuppression may turn into invasive cancer. basic knowledge The proportion of illness: 0.004% Susceptible people: seen in women Mode of infection: non-infectious Complications: vaginal intraepithelial neoplasia

Cause

Vulvar intraepithelial neoplasia

Associated with HPV (human papillomavirus) infection (27%):

In VIN superficial cells, especially in VIN1 and VIN2, lesions caused by HPV infection are often seen, such as periplasmic vacuoles, cell membrane thickening, binuclear and multinuclear, etc. However, these viral changes are not the basis for the diagnosis of VIN-infected HPV. Vulvar genital warts are often associated with HPV6,11, and molecular biology techniques have shown that 80% VIN is associated with HPV16, and Basta et al found young patients with VIN and early vulvar cancer ( Among <45 years old, 61.5% of patients were infected.

Associated with immunodeficiency, vulvar malnutrition (25%):

The incidence of VIN is significantly higher in human immunodeficiency virus (HIV) infection, chronic lymphocytic leukemia, and long-term use of immunosuppressants (steroids and tissue transplant inhibitors). Vulvar intraepithelial neoplasia is more common in sclerosing atrophic moss than hypertrophic dystrophy.

Changes with sexual behavior and tobacco use (17%):

Smoking is often associated with an increased risk of VIN III. It is also found that the increase in the number of sexual partners is associated with the development of VIN III. Epidemiological studies have found that HPV infection is a sexually transmitted disease, and HPV infection is common in young VIN patients. And related to the history of sexual life (including the number of sexual partners, the first sexual life age).

Relationship with cervical lesions (10%):

Another study found that VIN is associated with cervical lesions due to the same risk factors, and approximately 15% of patients with VIN have cervical lesions.

Relationship with vulvar cancer (6%):

The relationship between grade I and vulvar cancer in vulvar intraepithelial neoplasia has not been confirmed, but some epidemiological data suggest that this connection exists. For example, the average age of patients with VIN is less than that of invasive cancer patients 10 to 20 years old, 95 to 18%. VIN treatment was carefully examined and found to have invasive carcinoma. Jones and other 5 patients with VIN were followed up for 2 to 8 years, and 5 patients gradually developed into invasive carcinoma. Other authors reported VIN from 1973 to 1977 to 1988 to 1992. The incidence increased by a factor of three, of which 3.4% progressed to invasive cancer. Conversely, some authors reported that VIN is naturally degraded. Others reported that molecular DNA analysis can make a diagnosis of the malignancy of VIN lesions. Some types of HPV The etiology of VIN plays an important role, especially in some young patients, HPV6, 11, 16 and other subtypes can be isolated in VIN biopsy specimens, and HPV16 is present in 80% of VIN lesions by PCR.

Pathogenesis

Vulvar intraepithelial neoplasia often shows pathological mitosis, active mitosis in the upper and middle lining of the epithelium, increased nucleoplasmic proportion, increased multinuclear and immature cells, and non-specific changes such as hyperkeratosis and parakeratosis. According to cell maturity, nuclear heteromorphism, cell arrangement and mitotic activity, VIN can be divided into grade 1 (mild atypical), grade 2 (moderate atypical), grade 3 (severe atypical) Or carcinoma in situ).

1. Mild dysplasia epithelial hyperplasia and abnormal cell changes, limited to the lower third of the epithelium.

2. Moderate dysplasia epithelial layer The above changes are 2/3 of the epithelium.

3. The change of severe dysplasia epithelial layer exceeds 2/3. The atypical hyperplasia of carcinoma in situ affects the entire epithelial layer but does not penetrate the basement membrane.

The thickness of the normal vulvar epithelium varies from site to site: vestibule often <0.3mm, labia minora 0.3mm, labia majora 0.4mm, and average thickness in VIN is 0.57mm, and due to age (postmenopausal or premenopausal) , the location (located in the center or side of the hair follicle), the thickness of the hyperkeratosis (small or more lesions) can fluctuate 0.1 to 0.2 mm, and the mechanism of HPV-induced tumorigenesis is caused by abnormal gene expression. Intracellular protein production, such as L2 and E7 mRNA, is increased in VIN lesions. In addition, HPV proto-oncogenes E6 and E7 inactivate tumor suppressor genes RB and P53.

Prevention

Vulvar intraepithelial neoplasia prevention

Patients with genital itching and discomfort, rash-like changes, should seek medical advice in a timely manner, and should pay attention to keep the genital area clean, because 80% of vulvar intraepithelial neoplasia with HPV (type 16) infection, it should promptly diagnose and treat HPV infection, due to There are risk factors such as anal-genital tumor-like lesions, immunosuppression, and smoking, so it is especially important to prevent and treat these risk factors.

Complication

Vulvar intraepithelial neoplasia Complications of vaginal intraepithelial neoplasia

About 50% of patients with VIN have intraepithelial neoplasia at other sites, more often with Cervical intraepithelial neoplasia (CIN), and 30% of patients with vulvar intraepithelial neoplasia have cervical neoplasia. 4% with vaginal neoplasia, 3% with cervical and vaginal tumors, these are more obvious in patients with immunosuppression and anal genital syndrome.

Symptom

Vulvar intraepithelial neoplasia common symptoms itching burning pain pimples atypical hyperplasia nodules

1.20% to 48% of patients are asymptomatic.

2. About 60% of the most common symptoms of vulvar intraepithelial neoplasia are genital itching and burning sensation. The size of the labia is more common, followed by the clitoris, and less common in the urethra and its surroundings.

3. About 17% of patients complained of finding vulvar nodules.

Examination revealed that 90% of patients had papules or spots on the skin of the vulva. The color could be gray, red, brown, brown or white. It could be single or multiple, fusion or dispersion. These lesions can occur in any part of the vulva. The most common site is the right side, 8 points at the bottom of the labia minora. The white irregular lesions above the skin surface should be highly suspected of VIN. The doctor must carefully examine the perineum, including the vulva, during the annual routine examination. Rectum, anus, single VIN is mainly located in the scaphoid fossa and the labia near the labia minora, occasionally in the posterior part of the perineal body or around the clitoris, rarely occurs in the hair growth site and the clitoris gland, while multiple VIN can invade the clitoris Foreskin, labia minora, boat-like fossa and perineal body, about 1/3 of cases have infiltration of the labia majora and the posterior part of the perineal body. When the posterior part of the perineal body infiltrates, it often involves the anus and the medial gluteal groove. The anal canal mucosa is also often affected. That is, dysplasia lesions can develop upwards and extend to the junction of the anal canal scales, the clitoris glands are rarely involved, and the urethral infiltration is rare.

Examine

Examination of intraepithelial neoplasia

Patients with intraepithelial neoplasia should be tested for anal genital tract, including:

1. Cervical cytology, anal cytology, cytological examination of keratinized epithelium

After soaking the horns with saline gauze, the surface tissue is scraped off with a blade, and then the epithelium underneath is scraped for cytological examination. The depth of the material should be determined according to the condition of the lesion. Generally, the subcutaneous fat layer is not required, and the anus is not required. Cytological examination should choose cytoplasmic brush. Although cytological examination of keratinized epithelium can not replace biopsy, in repeated, persistent HPV infection patients, because of the persistent, weak vinegar white epithelium, this test can reduce duplication. The number of biopsy, if the cytology examination is atypical, biopsy should be performed, biopsy should be performed on the suspected lesions, and multiple sampling biopsies are needed. Multi-point biopsy can determine the depth of subepithelial diffusion to guide The depth of the operation can be partially sprayed with lidocaine before the biopsy to reduce the discomfort of the operation. It is especially important to use a laser-free treatment without specimens to eliminate infiltration.

2. Colposcopy and anoscope

Colposcopy can improve the sensitivity of detecting adjacent tissue lesions. Some studies have found that about 80% of VIN lesions around VIN primary lesions occur mainly in young patients, and in women over 40 years old, around the primary lesions. About 35% of VIN lesions are present, and it is very important that the entire vulva should be thoroughly examined for some high-risk, especially young women.

Colposcopy can improve the sensitivity of detecting adjacent tissue lesions. Some studies have found that about 80% of VIN lesions around VIN primary lesions occur mainly in young patients, and in women over 40 years old, around the primary lesions. About 35% of VIN lesions are present, and it is very important that the entire vulva should be thoroughly examined for some high-risk, especially young women.

Diagnosis

Diagnosis and diagnosis of intraepithelial neoplasia

The diagnosis of vulvar intraepithelial neoplasia should be based on histopathological examination, symptoms and signs.

Differential diagnosis

Because many genital diseases can cause atypical hyperplasia, such as vulvar genital warts, vulvar white lesions, sputum, seborrheic keratomas and black acanthoma, in addition to the identification of these diseases, but also need to pay attention to these vulvar diseases and epidermis Coexistence of tumors.

1. vulvar atrophic sclerosing moss (lichen sclerosiset atrophicus)

It occurs mostly in women aged 41-60 years. The skin lesions are ivory white papules, which are fused into plaques of various sizes and shapes. The skin lesions are purple, the boundary is clear and shiny, the palpation is hard, and the vulva skin is white and dry. , hard, rough, microscopically seen epidermal atrophy, hyperkeratosis, disappearance of nails, basal liquefaction degeneration, lymphatic infiltration in the dermis.

2. Vulvar hyperplasia malnutrition

Occurred in women over the age of 40, often in the female vaginal mucosa, the inside and outside of the labia minora, clitoris, and then extended to the inside of the labia majora showing gray-white plaques, keratinized surface, rough, accompanied by infiltration and hypertrophy, often itching, Microscopically, the proliferative lesions of the mucosal epithelium or epidermis were seen, and the vaginal mucosa showed granular keratinization, but generally no keratinized cells.

3. Vulvar sweat duct tumor

Is a kind of tumor, a considerable number of patients have a family history, more common in adolescent and middle-aged women, associated with endocrine, can be located alone in the vulva, can also be in the upper and lower eyelids and other parts of the face, for a waxy luster of flat papules The color is almost skin color. Under the microscope, the tumor cells are often located in a small area of the dermis. There are very large catheters in the fibrous interstitial, which are shaped like commas or scorpions. There may be cystic catheter cavities near the epidermis.

4. Condyloma acuminata

More common in young people, mostly 16 to 25 years old sexually active, occurs in the size of the labia, clitoris, vagina and cervix, microscopic hyperkeratosis with parakeratosis, epidermal hyperplasia or pseudoepithelial neoplasia The acanthosis is thick, the hollow cells are focal, scattered and flaky, HPV6, 11 positive.

5.paget disease

Occurs in postmenopausal women, the naked eye sees a red eczema-like plaque with a clear boundary, and the red lesion can form a white suede. After the suede is removed, the erosion surface of bright red particles is exposed. The microscopic surface is visible in the deep surface of the epidermis. Single or small group of Paget cells.

6. Superficial extensible melanoma

Common in the back and calf, the skin lesions are slightly uplifted, and there are various shades of yellowish brown, brownish black, pink, blue and gray. Under the microscope, the epidermis is thick, and the whole epidermis is scattered with large round melanocytes, single or Nesting is located in the lower part of the epidermis. Most of the melanocytes have atypical nuclei, deep staining, abundant cytoplasm and contain unequal amounts of melanin.

7. Vulvar early cancer

Often manifested as nodular mass or slight pain, genital itching is the most common symptoms, microscopic appearance of nuclear abnormalities, nuclear large deep staining, pathological mitosis, visible interstitial infiltration, poor prognosis.

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