What to do with vaginal ulcers

Gynecological diseases in women can be said to be relatively common diseases for young women nowadays. There are many causes of these diseases. Some are caused by sexual life, and some are caused by personal hygiene. No matter how they are caused, friends should pay attention to the details in this regard and protect their bodies reasonably. Today, the editor will talk to you about the problem of vulvar ulcers in women’s private parts. So what is the cause of vulvar ulcers? What should we do?

Causes of vaginal ulcers:

1. Infection

1. Virus: In the early days, it was believed that virus was the cause of the disease, but it was not further confirmed by epidemiological, tissue culture, serological, animal inoculation, immunofluorescence and electron microscopy examinations. The infection report believes that the onset of the disease may be related to autoimmune abnormalities caused by lentivirus infection; some reports have found evidence of the relationship between HSV-1 and the disease, such as evidence of the relationship between anti-HSV-1 in the patient's blood and the disease, such as increased anti-HSV-1 antibody titers in the patient's blood, HSV-1 affects CD4 lymphocytes and causes immune abnormalities, and HSV-1 has DNA homologous to the peripheral blood lymphocytes of the disease.

2. Streptococcus: Since some patients often suffer from diseases such as tonsillitis, pharyngitis and periodontitis, it is believed that the disease is related to the bacteria in these lesions. The study found that the titer of anti-streptococcal antibodies in the patient's serum was elevated; among the strains isolated from the patient's mouth, streptococci were the most closely related, especially Streptococcus sanguinis (both intradermal tests and macrophage migration inhibition tests with its bacterial components gave positive results; the 65-KDa heat shock protein test of streptococci could cause skin hypersensitivity reactions and systemic symptoms. These studies were mainly conducted by Japanese scholars, and although they were believed to play an important role in the onset of the disease, no consistent conclusion was reached.

3. Tuberculosis: Since 1964, there have been case reports in China that believe the disease is related to tuberculosis infection, that is, the patient had tuberculosis before the initial damage of Behct disease, such as pulmonary tuberculosis, lymph node tuberculosis and other tuberculosis lesions. It can be an old lesion, but active lesions are the majority. Most OT tests are strongly positive; anti-tuberculosis drug treatment not only has a significant effect on the primary lesions, but also improves the related damage of Behcet's disease, and is therefore considered to be an allergic manifestation of tuberculosis bacteria. The 65-KDa heat shock protein of Mycobacterium tuberculosis is also related to the occurrence of this disease.

2. Trace Elements

A few reports have found increased levels of multiple trace elements in patients' diseased tissues such as vascular endothelial cells, macrophages, sural nerves, as well as aqueous humor, serum, and neutrophils. The most studied are organochlorine, organophosphorus, and copper ions, among which the latter have the highest content, which may be due to occupational or environmental factors.

3. Genetic factors

The disease has a regional tendency to occur, such as being more common in Mediterranean coastal countries; there are consanguineous familial cases that can be seen in 2nd, 3rd or 4th generations, and the disease is more common in males. HLA-B5(+) is a marker of immune inheritance, and its positive rate can reach 67% to 88%, indicating that the disease is related to HLA-B5, and also has a certain relationship with HLA-D, especially HLA-DR. The Behcet's disease susceptibility gene is located on arm 6 of chromosome, between the HLA-B and TNF-beta loci, which may provide a direction for future research on gene therapy. Behcet's disease has no definite inheritance pattern and may be inherited in a systemic chromosomal recessive manner.

4. Immune abnormalities

Anti-oral mucosal antibodies and anti-arterial wall antibodies are present in the patient's serum. In addition, complexes are present in the serum, with a positivity rate of up to 60% and are related to disease activity. In addition to a slight increase in IgG, IgT and IgM, IgE is sometimes increased. DIF examinations revealed the presence of IgG, IgA, CIC and C3 in the blood vessel walls, especially the venous walls. In in vitro tests, the lymphocyte transformation test values ​​of these patients are generally low, the DNCB skin test is mostly negative, and the T-cell and TH cell values ​​are reduced; the infiltrating cells in erythema nodosum-like lesions are mainly T cells, especially TH and NK cells, while the infiltrating cells in the ocular tissue are mainly CD4 lymphocytes and macrophages, with very few B cells and NK cells. These CD4 lymphocytes and macrophages are HLA-DR(+). The above facts show that this disease has common manifestations of humoral immunity and cellular immunity, but it is generally believed that abnormal cellular immunity is more closely related to the occurrence of this disease.

V. Others

Although the cause of this disease is not clear, the onset is related to immune abnormalities. During the process of immune regulation and inflammatory response, changes in cellular components and the production of a variety of active substances, such as plasmin inhibitors, can reduce the activity of plasmin in dissolving fibrin, thereby increasing the fibrinogen content; as well as enhanced chemotaxis of neutrophils; production of tumor necrosis factor (TNF-beta), IL-2 and IL-6, etc., which may also play a certain role in the development of the lesion.

Mitigation methods

1. Colchicine: This drug has anti-chemotactic effect and is used to prevent ulcers, iritis, synovitis and phlebitis. 0.5 mg each time, 2 to 3 times a day. Toxic reactions include bone marrow suppression, nausea and vomiting, loss of appetite, diarrhea and constipation.

2. Adrenal cortical hormones: Generally, 30 to 40 mg of prednisone is used, taken orally once a day. For severe cases, hydrocortisone or dexamethasone can be injected intravenously. After the symptoms are relieved, switch to oral administration. Although adrenal cortical hormones can relieve oral ulcers and arthritis symptoms, the symptoms often recur after reducing the dosage or stopping the medication. Damage to the central nervous system is difficult to cure.

3. Immunosuppressants: Immunosuppressants for severe uveitis 50 mg, 3 times a day or 200 mg, intravenous injection, once a day or every other day. When using, you should pay attention to side effects such as leukocytopenia, adverse gastrointestinal reactions and hair loss. In recent years, cyclosporine A (CycosyrinA) has been tried and shown to have certain efficacy in treating eye diseases. The efficacy on damage to other systems is not obvious enough. Take 125-300 mg each time, once a day, and one course of treatment is 3 months. Tripterygium wilfordii glycosides, 30 mg each time, 3 times a day. There are side effects such as leukocytopenia, thrombocytopenia, loss of appetite, amenorrhea, and decreased sperm count. Immunosuppressants such as chloramphenicol and methotrexate can also be used.

4. Other treatments: Anti-tuberculosis drugs are given to people with tuberculosis.