The systematic erythalamus (SLE) is a complex self-immunological disease, whose occurrence is caused by the interplay of multiple factors. Genetic factors play a key role in the systematic occurrence of red weeds. Research has shown that SLE has a certain family concentration. If there is a systematic erythalamus in the family, there is a significant increase in the risk of the disease among other family members. The mutation or polymorphism of certain genes may make individuals more vulnerable to self-immunization. For example, the human white cell antigen (HLA) genes are closely related to SLE morbidity. The HLA-II gene is involved in the antigen presentation process, and its specific gene type may lead to an erroneous identification of its own antigen by the immune system and to an immune response.
Moreover, it is not just a question of a single gene, but the unusual combination of multiple genes may together increase disease susceptibility. This genetic tendency is like a “time bomb” inside the human body, which is more likely to trigger systemic red hemorrhoids, triggered by other factors. Environmental factors are also an important cause of systemic red weeds. Ultraviolet exposure is a common trigger. Ultraviolet rays in the sun, especially UVB (UVB), can penetrate the skin, alter DNA in skin cells and produce immunogenic substances. These substances activate the immune system and induce the production of their own antibodies. For those with genetic susceptibility, overexposure to sunlight may be the “last straw” that triggers systemic red weeds. For example, some patients experience a marked increase in skin erythromatoma after long periods of sun tan, and even acute disease. Drug factors cannot be ignored. Some drugs may induce systemic red hemorrhoids, such as thorium, plucainamine, etc. These drugs may alter their own antigen structure or interfere with the normal functioning of the immune system during the internal metabolic process. In the case of thorium, for example, it can be integrated into the body with cell components, creating new antigens, stimulating the immune system to produce antibodies, and thus causing symptoms similar to systemic erythalamus, such as heat, joint pain, rashes, etc.
However, the systemic red hemorrhoids induced by drugs may gradually diminish after the relevant drugs have been discontinued. The infection also plays a role in the systematic occurrence of erythalamus. Virus infections, such as EB viruses, megacell viruses, etc., can induce disease through molecular simulation mechanisms. Some of the antigens of the virus are similar to the human own antigens, and when the immune system attacks the virus, they may be misidentified and lead to their own immune response. For example, after the infection of the EB virus, the protein of the virus may simulate some antigens within human cells, activate the T-cells and B-cells in the immune system and give them their own antibodies, thus triggering systemic red weeds. Endocrinological factors also have an impact on the incidence of systemic red lupus. Estrogen plays a prominent role in it. Female patients tend to suffer from an increase in the incidence or onset of disease during periods of high estrogen levels, such as adolescence and pregnancy. Estrogen regulates the immune system and promotes the activation of B cells and the generation of its own antibody. Relatively low estrogen levels in males may also be one of the reasons why men suffer from systemic red erythalamus, which is much lower than women. Systematic erythroacemia is the result of a combination of factors. Genetic factors provide the basis for morbidity, on which factors such as the environment, drugs, infections and endocrines play a role. Understanding these morbidity factors is important for disease prevention, early diagnosis and effective treatment.
