Vulvar white lesions before and after perimenopause
Introduction
Introduction to white lesions of the vulva before and after menopause Around the menopause, due to the gradual decline of ovarian function to the cessation of ovarian function, the gradual loss of estrogen production caused a series of physiological changes in the external genitalia, mainly varying degrees of atrophic changes. Usually, the skin ages around 40 years old, and it changes obviously 5 to 10 years after menopause. White lesions of the vulva, refers to a group of female genital skin, mucosal dystrophy caused by tissue degeneration and pigment changes. The genital itching, ulceration, severe pain, skin changes are characteristic, treatment is difficult, and recurrence is very painful for patients. The disease is a chronic disease process, the duration of the disease varies, and the elderly can reach decades. Because the cause is not clear, the naming and treatment methods are not uniform. In the past, vulvar skin and mucous membranes were whitened, thickened or shrunken. The vulvar disease was collectively called vulvar leukoplakia. It was even considered to be a precancerous lesion. Therefore, it was advocated for early resection. Later, some people thought that it must be atypical in pathological sections. The proliferating cells are diagnosed as "white leukoplakia". Due to different diagnostic criteria, different nature and prognosis of the disease, it causes confusion and understanding of the disease. In order to unify understanding, many scholars at home and abroad have white lesions on female genital. The naming and classification were further analyzed and discussed. In 1877, Schwimmer first whitened the buccal mucosa, and the keratinization was called white spot. Later, in 1985, Breisky reported that the genital lesion was called leukoplakia. Disease, later Taussig (1923, 1930) specific classification of vulvar leukoplakia named early vulvar leukoplakia (hypertrophic period) and late (atrophic period), this view has been used by future generations, in 1961 Oberqield review related literature and according to their own materials Observation, suggesting that the Taussig leukoplakia atrophy period is actually a sclerosing atrophic moss, but Clark and Woodruqq apply the nuclides side. The 3H ()-labeled thymidine assay confirmed that the epidermis of sclerosing atrophic moss has a strong metabolic function and does not shrink. Therefore, some people think that the name of sclerosing atrophic moss is not enough, and the word "atrophy" should be removed. It should be renamed "sclerosing moss". Some people think that the initial lesions and intrinsic lesions of this disease are the damage of connective tissue fibers and matrix under the epidermis. The thinning of the epidermis is secondary, which is consistent with the opinions of Oberqield and Stelguler, so from the formation mechanism It is believed that the name of sclerosing moss is more precise. For a long time, the clinical practice of vulvar leucorrhea is called vulvar leukoplakia. In the past 20 years, the concept of leukoplakia has been limited to the atypical hyperplasia under the epidermis of the mucosa. The same term has different meanings. In order to avoid confusion, most scholars advocate discarding. The name of the disease of leukoplakia. The 9th International Conference on Vulvar Diseases in 1987 proposed new classifications as follows: 1 non-neoplastic skin, mucosal epithelial lesions including sclerosing moss, squamous epithelial hyperplasia, other skin diseases; 2 vulvar intraepithelial neoplasia (VIN) Including mild, moderate, severe atypical hyperplasia and carcinoma in situ. There is no unified naming in China at present, and each scholar named and classified according to his own viewpoint. Some authors believe that the initial diagnosis of the clinic failed to judge whether there is dysplasia or not. Therefore, before the disease examination, it can be collectively referred to as vulvar white lesion or vulvar white skin disease including hyperplasia. Sexual vulvar skin lesions and sclerosing moss, genital atypical hyperplasia, vulvar vitiligo and so on. basic knowledge The proportion of illness: 0.001% Susceptible people: women Mode of infection: non-infectious Complications: vaginitis
Cause
The etiology of vulvar white lesions around menopause
(1) Causes of the disease
Some cases of senile skin diseases belong to aging physiological changes, while others belong to pathological changes, and some are unique or prone to old age lesions, which generally occur due to the interaction of multiple factors, except for the same points as general skin diseases. There are also a few special aspects:
Skin aging sign
Mainly physiological, due to aging and shrinkage of the skin and its accessory organs, resulting in dry skin, increased wrinkles, hair thinning, shedding, whitening, nails becoming brittle, itchy skin and dark spots, white spots, senile sputum, hemangioma, capillary Vasodilatation, etc., these lesions increase with age.
2. The role of physical and chemical factors
Various stimuli can cause skin damage. If dermal collagen fibers, elastic fibers are denatured and destroyed, skin atrophy, keratinization, and even canceration.
3. The impact of systemic diseases
Some elderly people with high blood pressure, arteriosclerosis, diabetes, etc. can cause skin diseases. For example, skin itching in diabetics is a good example. Diabetic people can also cause pyogenic bacteria and fungal infections in the skin, caused by arteriosclerosis. Skin malnutrition, lower extremity ulcers, necrosis, etc.
The exact cause of the white lesion of the vulva is unknown. Some people have exchanged the skin of the vulva with the normal skin of the patient's thigh. After a period of time, the transplanted lesion is found to be normal, but the normal skin transplanted to the vulva becomes sick. The skin, thus inferred, may be a neurovascular dysregulation in the connective tissue of the vulva, leading to lesions in the skin covering it. In recent years, it has been found that there is a stimulator in the dermis that causes local connective tissue to proliferate and promote it. Epidermal metabolism, while in the epidermis, there is a chalon that inhibits the division and growth of epidermal cells. This hormone is a tissue-specific protein hormone that acts on the epidermis. Under normal conditions, the two are in balance. In the state, once the balance is destroyed, the lesion is produced. When the stimulant in the dermis is active, and the statin in the epidermis is reduced, the cells divide and grow in a large amount, so that the epidermis is thickened, and when the epidermis is excessively produced, the epidermal growth is affected. Suppressed so that the epidermis becomes thinner.
Atrophic type often occurs in menopausal or postmenopausal women, sometimes in middle-aged women with artificial menopause after radiation therapy or bilateral ovariectomy, so ovarian function declines or disappears, estrogen deficiency may be the cause, but There are also some cases that have nothing to do with estrogen deficiency. It is therefore conceived that this disease may be caused by an unknown factor that causes the vulva tissue to lose its response to estrogen. It seems that it has nothing to do with marital status and the number of births. There is no obvious connection between local diseases.
In recent years, a large number of studies have confirmed that patients with sclerotic moss (hard moss) have immunological diseases, and their serum CD3, CD4, CD5 and HLA-DR have different degrees of change, and 10% of patients with hard moss have autoimmune. Diseases, such as hyperthyroidism, hypothyroidism, diabetes, etc., have found that malnutrition such as estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR) are reduced to varying degrees, including hard moss The lowest, the level of dihydrotestosterone in the serum of patients with vulvar dystrophy is significantly lower than that of normal people, suggesting that testosterone deficiency may be one of the causes. Some studies have shown that human epidermal growth factor (EGF) content in vulvar dystrophy skin tissue is significantly higher than that. The surrounding normal skin, and the latter is significantly higher than the normal human vulva skin, suggesting that the incidence of vulvar malnutrition is related to the increase of EGF content and dysfunction. In recent years, some authors believe that the occurrence, development and changes of vulvar malnutrition are related to The role of free radicals is closely related. When the content of superoxide dismutase (SOD) and whole blood glutathione (GSH) in local skin tissue is significantly decreased, free radicals are continuously produced and accumulated. The production of free radicals increases the oxidative damage to collagen fibers, reticular fibers, elastic fiber tissue cells and blood vessels, nerve biomolecules such as proteins, nucleic acids, fats, etc., and the physiological structure of skin tissues. Destroyed, metabolic disorders, nutritive metabolism blocked, leading to vulvar malnutrition, there are reports that patients with sclerotic moss have a higher positive rate of HLA ~ B40, clinical family cases are also common, in recent years, people have found HLA ~ DQT Positive.
For proliferative patients, the cause is still unknown, but according to some scholars' research, some nutrient deficiencies (hydrochloric acid, iron, vitamin B2, folic acid, vitamin A, D, B12, etc.) are found to be local vascular changes, estrogen deficiency, chronic stimulation, Bruises, neuropsychiatric factors and certain external stimuli may be the predisposing factors of this disease.
Xue Xiang et al. used the monoclonal antibody against apoptosis-inhibiting gene BCL-2 and immunohistochemical LSAB method, and found that BCL-2 protein was weakly positive in normal vulva, skin basal layer, proliferative malnutrition, atypical hyperplasia and vulva. The expression rate of cancer tissues increased in different degrees, and there was significant difference between hard moss and mixed type, but there was no significant difference between proliferative and atypical hyperplasia BCL-2 gene expression (P>0.05), and the expression rate of vulvar cancer was the highest. It is speculated that the incidence of hyperplastic vulvar lesions has a certain relationship with BCL-2.
Anti-epidermal growth factor receptor (EGFR), monoclonal antibody and immunohistochemical ABC method were used to detect the expression of EGFR in vulvar squamous cell carcinoma, vulvar white lesions and atypical hyperplasia. Results: vulvar squamous cell carcinoma and dysplasia The positive rate was significantly higher than other types of vulvar white lesions (P<0.05). This different expression indicates that the proliferation of EGFR and squamous cells is related to the occurrence of squamous cell carcinoma.
Vitiligo, its etiology is not clear, may be related to genetic, autoimmune and nervous system factors, patients often have a family history, generally considered autosomal dominant inheritance, vitiligo often with multiple immune diseases, patients with stomach wall antibodies and thyroid The globulin antibody is increased, and anti-melanin antibody can be confirmed in serum. Many clinical observations show that the disease is closely related to the nervous system. The damage is often distributed along the nerve or meridian. Post-operative and trauma can induce vitiligo. Recently, it has been proposed. The so-called melanin self-destruction theory believes that melanocytes are destroyed by the toxic effects of the precursors formed by them. In addition, certain chemicals and photosensitivity drugs can also induce the disease. The pathogenesis of vitiligo is to damage the local dermal junction. The lysin system, which loses its function, cannot oxidize tyrosine to dihydroxyphenylalanine (Dopa) and thus impairs melanin formation.
(two) pathogenesis
1. Under light microscopy, the proliferative type is squamous epithelial cell hyperplasia. The main lesions are epidermal hyperkeratosis and parakeratosis. The spinous cell layer is irregularly thickened, the epithelial foot extends downward, and the dermis has lymphocytes and a small amount. Infiltration of plasma cells, the main lesions of hard moss type are hyperkeratosis, visible angle plug formation, atrophy of the Marquis layer, liquefaction denaturation of basal cells, significant edema of collagen fibers in the upper part of the dermis (homogeneous, hyaline degeneration), inflammatory infiltration in the middle of the dermis, often It is distributed in a strip shape.
2. Under electron microscope, the epithelial cells atrophied, the intercellular space increased, the microvilli and cell gap desmosomes on the cell surface decreased, the melanin particles in the cells decreased or disappeared, vacuoles formed around the nucleus, mitochondria swollen or vacuolar degeneration occurred. The collagen fibers in the superficial dermis have different degrees of dissolution or rupture, and the fibroblasts decrease or disappear.
Prevention
Prevention of vulvar white lesions around menopause
Some patients with severe vulvar white lesions are regularly followed up to prevent malignant transformation.
Protection of the skin before and after menopause:
1. Avoid all kinds of bad physical and chemical stimuli: Because the old skin is relatively dry and less water, try to use less salt water, soap to wash, especially alkaline soap is more irritating to the skin, winter bathing should not be too diligent, after bathing can be coated A solution or cream that lubricates, protects, and prevents moisture from evaporating.
2. Good and comfortable living environment: Due to the reduced vascular regulation function of the elderly skin, the adaptability to external temperature changes is poor, the living environment should be relatively stable, the indoor temperature should be kept proper, the clothes and shoes are loose, soft and warm, the size is appropriate, and the traumatic bacteria are avoided. infection.
3. Reasonable dietary arrangements: due to poor gastrointestinal adaptability and weak digestion ability, avoid overeating, food should be diversified, should enter low-fat, high-protein, green leafy vegetables, eat more vitamins A, C, E Food, carrots, greens, fruits, egg vegetable oil, animal liver, etc.
4. Pay attention to the prevention and treatment of skin diseases and systemic diseases: pigment spots on the skin of the elderly, skin damage such as senile sputum, etc., are generally benign and do not require special treatment, but if the generalized senile convulsions suddenly appear in the short term, it indicates that there is The possibility of combining visceral malignant tumors should be vigilant. For some elderly skin diseases with malignant transformation, such as white lesions of the vulva, it should be followed regularly. Many systemic diseases can cause skin diseases such as hypertension and diabetes. Active prevention and treatment of various systemic geriatric diseases is beneficial to the health of the skin.
Complication
Complications of white lesions around the peri-menopausal period Complications vaginitis
Due to the decreased immunity of the patients in this period, the lesion area is also complicated by vaginal infection under the infection conditions.
Symptom
Peri-menopausal symptoms of white lesions of the vulva Common symptoms Itching vulvar ulcer edema vulva burning stimulation genital vulvar atrophy dysfunctional difficulty fatigue hardening vulvar leukoplakia
1. dermatitis: mainly occurs in the labia majora and labia minora, sometimes affecting the anus around the anus, caused by external stimuli, including dermatitis, folliculitis, urticaria and non-specific due to mental factors and excessive fatigue. Dermatitis, the main symptoms are the itching of the heart, acute phase, congestion, edema, erosion, ulcer pain and increased secretions, etc., due to constant scratching or scalding, the vulva skin gradually thickens and rough, leather, chronic phase pigment disappears There is a tough white lichen-like change. The vulvar dermatitis has a long course of disease and can be recurrent. No matter the severity of the disease, the length of the disease, the vulva does not deform, and the labia minora does not stick. This is the difference between vulvar dermatitis and hard moss.
2. Vulvar Sclerosis (Lichen Sclerosis): more common in women around 40 years old, can also be seen in young girls under 10 years old, the main symptoms of this disease are dry itching, pain, erosion and whitish, early vulva no obvious Deformation, the lesion is limited to the inside of the labia minora, the mucous membrane is whitish. As the disease progresses, the lesion develops to the clitoris, the labia majora, the posterior joint and the anus. The labia minora gradually shrinks and disappears. The vulva is atrophied and deformed in the middle and late stages. Postoperative shape, the skin gradually thins and shines, even thin as cigarette paper, small labia adhesions, causing difficulty in urinating, narrowing of the vaginal opening, can cause joint laceration after difficulty in sexual intercourse, vulva due to poor blood supply, malnutrition, it is easy to smash , chapped or formed a small ulcer, when burned by urine, there is a burning sensation, the clitoris foreskin hypertrophy and the rough texture of the labia majora are white plaque changes.
3. leukoderma: generally no pruritus, can occur on the vulva skin or mucous membrane, localized as a clear-cut sheet, whitish, the affected hair is also white, and the vulva skin texture, shape and gloss no change It has good elasticity and can be pigmented around.
Examine
Examination of white lesions of the vulva before and after menopause
Vaginal secretion examination, bacterial culture, tumor marker examination.
Histopathological examination: In order to improve the diagnostic accuracy, biopsy should be performed in the presence of cleft palate ulcers, induration or rough, and should be selected from different lesions. For the biopsy of suspected positive areas, the following fixed biopsy methods are available. .
1. The lesion was coated with 1% toluiduie blue.
2. Observe the lesion with a colposcope.
3. Position the biopsy using the HPD laser fluorescence method.
4. Position the biopsy using intrinsic fluorescence.
Diagnosis
Diagnosis and diagnosis of white lesions of the vulva before and after menopause
diagnosis
As with the diagnosis of general skin diseases, it must be based on a comprehensive analysis of medical history, physical examination, laboratory examination and pathological examination, but also consider the characteristics of senile skin diseases, systemic examination, suspected malignant transformation or skin tumor Biopsies should be performed early and pathological sections are the means of diagnosis.
Differential diagnosis
It should be differentiated from skin diseases such as skin itching, neurodermatitis, and chronic eczema. Some people in China have the most common disease, such as senile skin itching, eczema, neurodermatitis, and rickets. The prevalence rate is above 10%.
It should also be identified whether cancer has occurred: in the past, vulvar leukoplakia was considered to be a malignant potential, and the cancer rate was as high as 10% to 15%. From the literature, the cancer rate of vulvar white lesions is very different, ranging from 2% to 50%. % has not been equal. In recent years, domestic and foreign scholars have seriously explored the cancerous potential of this disease. Neurodermatitis in other parts of the body, hard moss has little or no malignant potential, but dysplasia can occur in the vulva. It may be related to the situation of the female genitals, because there are many secretions, damp heat, poor ventilation and long-term inflammatory stimulation.
As early as 1840, Taussig emphasized that half of the vulvar leukoplakia evolved into cancer within 10 years, and 70% of vulvar cancer with leukoplakia. For a long time, vulvar vaginal vaginal habits have been routinely performed. The modern literature has clarified this, Gardner et al. Long-term observation of leukoplakia, cancer rate is 2% to 5%, Shanghai data atypical hyperplasia detection rate is 1.5%, cancer detection rate is 1.8%, domestic reports 1% to 4%, according to Jeffcoate 136 exception Patients with yin dystrophy were observed for 2 to 25 years and found that the cancer rate was less than 5%. The detection rate of dysplasia was generally 2% to 3%. The selective cases could be as high as 10%. Kaufman believes that vulvar malnutrition is in treatment. There is very little cancer, Meadams and other reports that atypical hyperplasia has a cancer metastasis rate of 10% in 3 to 25 years. Therefore, the viewpoint that Taussig overemphasizes cancer and advocates surgical treatment has been abandoned, but there is still a warning about dysplasia of vulvar malnutrition. Regular follow-up, the expression of proliferating cell nuclear antigen PCNA and EGF in atypical hyperplasia vulvar dystrophy tissue was significantly higher than other types, but no significant difference with grade I squamous cell carcinoma, increased PCNA and continuous activation of EGF-R. It is one of the causes of obvious malignant transformation, and dystrophic vulvar dystrophy has potentially malignant characteristics.
In the past, it has been thought that hard moss is a degenerative disease without cancer, but it has been suggested that hard moss also has malignant potential. Barker Gross et al reported that 3% hard moss is associated with cancer, Hebei Medical College reported 0.6%, some scholars believe that hard moss The atrophic epithelium is not atrophic. The irradiated or fluorescently treated hard moss epithelium has two types of cells: "active" or "inactive". The former has a metabolic activity 3 to 6 times higher than that of the normal epithelium, and has the same malignant potential as the proliferative epithelium.
