What is the best ointment for folliculitis?

What is the best ointment for folliculitis?

Due to the relatively poor air quality and the irregular living and eating habits of most people, more and more people are suffering from skin inflammation. Among them, folliculitis, as a skin inflammation with an unclear cause, is relatively common, and people are more concerned about its treatment method. Among the many treatments for dermatitis, ointments are the most commonly used. So what ointment is best for folliculitis?

Dermatomyositis (DM) is a type of dermatomyositis, also known as poikilodermatomyositis. It is an autoimmune connective tissue disease and a non-suppurative inflammatory lesion that mainly affects striated muscle and is characterized by lymphocyte infiltration. It may be accompanied by or without a variety of skin lesions and may also be accompanied by various visceral lesions. Polymyositis (PM) refers to diseases in this group without skin lesions.

symptom

It initially appears as a red, solid papule, which then rapidly develops into a papular pustule, which then dries and forms a scab, leaving no trace after the scab falls off. Many rashes

Eating a light diet, avoiding spicy food, washing your face with cold water, keeping bowel movements smooth, not staying up late, and developing good living habits can effectively improve the situation.

Causes

The exact cause of the disease is not yet clear. It may be viral infection, abnormal self-recognition caused by the body's immune system, and vascular disease. The three may also be interrelated. For example, slow virus infection of striated muscle fibers can lead to changes in the antigenicity of muscle fibers, which are mistakenly identified as "foreign" by the immune system, thereby causing vasculitis and the disease.

(I) Immunological studies: Given the elevated serum immunoglobulins in patients, muscle biopsy specimens showed deposition of IgG, IgM, C3, and complement membrane attack complex C56-C9 in microvessels, and the degree of deposition seemed to be related to disease activity. Arahata and Engel confirmed that there was a significant increase in B cells in the inflammatory lesions of DM, suggesting an enhancement of local humoral effects. However, some scholars believe that the deposition of these antibodies is the consequence of muscle damage rather than its cause. Some scholars have also found that the conversion rate of peripheral blood lymphocytes of patients after the addition of striated muscle antigen and the control group of macrophage migration inhibition test were high and positively correlated with their activity. Reduced by glucocorticoids. The patient's peripheral blood lymphocytes have a cytotoxic effect on myoblasts in in vitro tissue culture. Its damaging effect may be the release of lymphotoxins or direct adhesion and invasion of muscle fibers.

Some people believe that this disease has many common clinical and immunological abnormalities with SLE and scleroderma. For example, LE cells, antinuclear antibodies and rheumatoid factor tests can be found in some cases, and immunoglobulin deposition can be seen in the epidermal basement membrane and blood vessel walls using fluorescent antibody technology. Anti-polymyositis antigen-1 (anti-PM-1 for short) and anti-myosin antibodies are found in the serum. Therefore, the theory of autoimmune disease is proposed. For example, in patients with concomitant malignant tumors, tumor resection can relieve the symptoms of this disease, and intradermal tests using patient tumor extracts show positive reactions, and passive transfer tests are also positive. Antibodies against tumors were found in the patient's serum. These malignancies act as the body's own antigens and induce the production of antibodies. In addition, tumor tissue can have cross-antigenicity with normal muscle fibers, tendon sheaths, blood vessels, and connective tissues in the body, and thus can undergo cross-antigen-antibody reactions with the antibodies produced, leading to lesions in these tissues, thus serving as the basis for the autoimmune theory of this disease.

(B) Sensory theory: In recent years, some scholars have observed the muscles and skin lesions of patients using electron microscopy and found particles similar to myxovirus or paramyxovirus in the nuclei of muscle cells, vascular endothelial cells, perivascular tissue cells and fibroblasts cytoplasm and nuclear membrane. Recently, a report of isolating Coxsackie A9 virus from the diseased muscles of an 11-year-old girl was published, so the infection theory was proposed. However, in animal experiments, it has not been possible to induce muscle inflammation by injecting patients' muscles or plasma, and antiviral antibodies cannot be detected in the patients' blood.

Children with dermatomyositis often have a history of upper respiratory tract infection before the onset of the disease, and their anti-streptococcal "O" value is increased. Treatment with antibiotics combined with corticosteroids can be effective, and the infection allergy theory is proposed.

(III) Vascular disease theory Vascular disease has been described, particularly in childhood DM. Any diffuse vascular disease can produce ischemia of skeletal muscle, resulting in necrosis of individual fibers and infarcted areas of muscle. In DM/PM, especially in children, there is evidence of capillary endothelial cell damage and thrombosis, as well as immune complex deposition in intramuscular vessels, thickening of the capillary basement membrane, and capillary loss, especially in the perifascicular region.

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