Discoid lupus erythematosus (DLE) is a chronic relapsing disease, a form of lupus erythematosus that primarily affects the skin and is characterized by well-defined red plaques (erythema), follicular embolism, scaling, capillary dilatation, and skin atrophy. The etiology is unclear. It is common in women, with the highest incidence around 30 years old. The prevalence of this disease varies among different races, with different strains of mice (NEB/NEWF, MRL1/1pr) showing spontaneous symptoms of SLE a few months after birth, and family surveys show that about 10% to 20% of the first and second degree relatives of SLE patients can have similar diseases, some with hyperglobulinemia, multiple autoantibodies and abnormal T suppressor cell function. HLA typing shows that SLE patients are associated with HLA-B8-DR2 and -DR3, and some patients may have a combination of complement C2C4 deficiency, and even TNFa polymorphisms are clearly associated; recently, the lack of pure C2 gene and high frequency of -DQ were found to be closely associated with DSLE; T cell The low level of TNFa may be the genetic basis of lupus nephritis. All of the above suggest that SL has a genetic predisposition, but according to the survey of 100 cases of SLE families in Huashan Hospital, it is polygenic, and environmental factors also play a role. 2.Drugs There are reports that among 1193 cases of SLE, the incidence is related to drugs accounting for 3%-12%. The first category is drugs that induce SLE symptoms, such as penicillin sulfonamides, botanicals, gold preparations, etc. These drugs enter the body and cause metabolic reactions first, and then stimulate lupus quality or potential SLE patients to develop idiopathic SLE or aggravate the disease of SLE already suffered from, and usually stopping the drugs cannot stop the development of the disease. The second group is drugs that cause lupus-like syndrome such as hydrazinophthalazine hydrochloride (hydrazinopyridazine), procainamide, chlorpromazine phenytoin sodium, isoniazid, etc. These drugs can cause clinical symptoms and laboratory changes of SLE in patients after prolonged application and larger doses. Their pathogenic mechanisms are less clear: for example, chlorpromazine is thought to bind slowly to double-stranded NDA, while UVA irradiation binds rapidly to denatured DNA clinically, skin exposure to sunlight can denature double-stranded DNA, which can easily bind to chlorpromazine to produce antigenic substances; also, hydrazinepyridazine binds to soluble nucleoproteins, which can enhance the immunogenicity of its own tissue components in vivo This type of drug lupus-like syndrome in HLA typing shows a significantly higher rate of DR4 positivity, which is recognized as the difference between drug-induced lupus-like syndrome and idiopathic lupus erythematosus: ① clinical Qinghai, involving the kidney, skin and nervous system less; ② older age of onset; ③ shorter and lighter disease duration; ④ no reduction of complement in blood; ⑤ serum single-stranded DNA antibody Positive. 3, infection It is believed that the onset of SLE is related to certain viral (especially lentivirus) infections from the patient’s glomerular endothelial cell pulp, vascular endothelial cells, skin lesions can be found similar to the inclusion body material at the same time the patient’s serum to the virus titer increased, especially to measles virus, parainfluenza virus type Ⅰ Ⅱ EBV, rubella virus and mucovirus, etc., in addition to the patient’s serum dsRNA, ds-DNA and The former can usually only be found in tissues with viral infection electron microscopic observation of these inclusion body-like material is small tubular mesh structure, 20-25 μm in diameter, distributed in clusters but can also be seen in dermatomyositis, scleroderma, acute sclerosing encephalitis in attempts to isolate the virus from tissues with inclusion body-like material was unsuccessful, so these substances and virus joints to be confirmed. Recently, it has been proposed that the pathogenesis of SLE is closely related to the C-type RNA virus. The authors measured serum interferon in 47 cases of SLE, and the results were 72.3% increased, which is alpha type, containing acid-stable and acid-unstable interferon concentrations parallel to the disease activity. It is known that alpha interferon is produced by leukocytes after stimulation by viruses, polynucleotides or bacterial lipopolysaccharides, etc. Whether this indirectly suggests the possibility of viral infection. It is also believed that the onset of LE is related to tuberculosis or streptococcal infection. 4, physical factors ultraviolet light can induce lesions or aggravate the existing lesions in a few cases and can induce or aggravate systemic lesions, about 1/3SLE patients are allergic to sunlight, Epstein ultraviolet irradiation skin type LE patients about half of the cases of clinical and histological typical lesions. Two months later the skin fluorescence band test was positive, such as premedication of adiponectin can prevent skin lesions normal human skin double-stranded DNA is not immunogenic, after UV irradiation occurs dimerization, that is, DNA depolymerization of thymine dimer into a stronger immunogenic molecule LE patients confirmed that there is a defect in repair of dimerized DNA. It is also believed that UV light first damages the skin cells, allowing antinuclear factors to enter the cells and interact with the nucleus to produce skin damage. The disease can also be triggered or aggravated by cold and intense electric light exposure. Some limited discoid lupus erythematosus can evolve into systemic type after exposure to sunlight, and the chronic type can evolve into acute type. 5. Endocrine factors Given that the disease is significantly more common in women than in men and develops mostly during the reproductive years, it is believed that estrogen is related to the development of the disease. The disease is significantly reduced, and in addition oral contraceptives can induce lupus-like syndrome. One author measured sex hormone levels in 20 men with SLE and found that serum estradiol levels were increased in 50% of patients (5% increased in controls), testosterone was decreased in 65% of patients (10% decreased in controls), and the estradiol/testosterone ratio was higher than in healthy controls. The above-mentioned images support the argument that the changes in SLE during pregnancy are also associated with increased levels of sex hormones. Afterwards, due to the rapid increase of progesterone level, the progesterone/estradiol ratio increases accordingly, thus the disease is relatively stable. The function is disturbed. When the genetic factors are strong, weak external stimuli can cause the onset of disease. Conversely, when the genetic factor is weak, a strong external stimulus is required for the onset of the disease. The disruption of immune stability in the body leads to a defect in the regulation of the immune system and the loss of suppressor T cells not only in number but also in function, which prevents them from regulating B lymphocytes that have the potential to produce autoantibodies, thus causing the formation of a large number of autoantibodies and causing the disease. In lupus rats, it was found that B cells were overactive in the early stages, but no defective regulatory T cells were seen, suggesting that the autoantibody-producing B lymphocyte strain escaped from the control of T cells, i.e., it could produce autoantibodies even when the regulatory function of T lymphocytes was normal, which is also known as the B cell escape theory of SLE. It has been suggested that this is due to the impaired immune regulation caused by the excessive function of helper T cells that produce large amounts of autoantibodies. It has also been suggested that the autoimmunity may be caused by the excessive activity of monocytes or macrophages, which usually produce some kind of factor to stimulate the helper T cells or directly stimulate the B cells, and that the “forbidden strain theory” is proposed by those who believe that the disruption of the immune stability of the body leads to an imbalance in the ratio of T and B cells or an imbalance in the ratio of B helper/inducer cells to T suppressor/cytotoxic cells. As a result, the forbidden strain of gonadotrophic cells loses control and overproliferates, causing autoimmune lesions. II. Disease characteristics At the beginning, the active damage is erythematous round scaly papules, 5-10 mm in diameter, with follicular embolism. The lesions occur on the prominence of the cheeks, the bridge of the nose, the scalp, and the external auditory canal and may persist or recur for several years. The lesions may spread to the upper trunk and the extremities. Photosensitivity is common and manifests itself as a patchy lesion of light-exposed skin. Mucosal involvement may be prominent, especially in oral ulcers. Untreated DLE lesions gradually expand outward, with atrophy in the central area of the lesion. Residual scarring does not shrink. When the scales are peeled off, spiny protrusions are seen on the scales, which are pinned inside the dilated hair follicle opening, called “carpet pegs”. There is extensive hair loss on the head and permanent scar formation. Although the disease is usually confined to the skin, nearly 10% of patients eventually develop systemic manifestations of varying severity, which are usually not severe and may manifest only as antinuclear antibody positivity. Leukopenia is common, as well as mild temporary systemic manifestations (e.g., arthralgia). Chronic bursitis occurs in only a minority of DLE patients, with no other “systemic” manifestations. The rash is usually found on exposed areas such as cheekbones, tip of nose, bridge of nose, nose, lips, head, neck, upper chest and back, upper extremities, back of hands, back of fingers (toes), and heels. The lesions start as one or several small round red patches or papules, and gradually expand into round or irregular-shaped patches, with light red or dark red rash, which may be accompanied by capillary dilation, covered with scales, with nail-like keratin plugs underneath the peeled scales, with clear and slightly elevated borders and slightly depressed central atrophy in the form of disks. 20% to 25% of patients may have oral lesions, with the lower lip, gingiva and cheek mucosa being more easily involved. Lip damage is more common in the lower lip, often forming a gray-white vesicular surface or shallow ulcers. Scarring of the scalp can lead to permanent hair loss. The disease can be aggravated by sun exposure or exertion. There are usually no systemic symptoms, but a few may have mild fever, fatigue and joint pain or muscle pain. The course of the disease is chronic and rarely resolves spontaneously, with occasional secondary carcinoma. 5% of discoid lupus erythematosus can be transformed into systemic lupus erythematosus. The active lesions are erythematous, round, scaly papules, 5-10 mm in diameter, with follicular embolism, and are found on the prominence of the cheeks, nose, scalp and external auditory canal, and can persist or recur for several years. Untreated DLE lesions gradually expand outward, with atrophy in the central area of the lesion and residual scarring that does not shrink. When the scales are peeled off with force, spiny protrusions are seen on the scales, which are pinned inside the dilated hair follicle opening, called “Carpettack”. There is extensive hair loss on the head and permanent scarring. Although the disease is usually confined to the skin, nearly 10% of patients eventually develop systemic manifestations of varying severity, which may be as simple as positive antinuclear antibodies, leukopenia, and mild temporary systemic manifestations (e.g., arthralgia) are common. Chronic bursitis occurs in only a minority of DLE patients, with no other “systemic” manifestations. Because the cause of discoid lupus erythematosus is unknown, its clinical manifestations are variable, and it involves more tissues and organs, the disease is complicated, especially in early atypical patients or those with only one or two organs involved, or those with no rash or even no clinical manifestations. The American Rheumatism Association (ara) revised the diagnostic criteria for discoid lupus erythematosus in 1982, with 10 items: ① zygomatic-cheek erythema; ② discoid lupus; ③ photosensitivity; ④ oral ulcers; ⑤ non-erosive arthritis; ⑥ proteinuria (>0,5g/d) or urinary cell tubularity; ⑦ seizures or psychosis; ⑧ pleurisy or pericarditis; ⑨ hemolytic anemia or leukopenia.