What is psoriasis Psoriasis, commonly known as “psoriasis”, is an ancient disease. Psoriasis has been recorded in Chinese medicine since long ago, but it is not called psoriasis, but has more names, such as “dry ringworm”, “naughty ringworm”, “pine skin ringworm”, “white H ” “white H wind” “snake wind and other names. Psoriasis is a chronic disease, and the characteristic damage of this disease is the repeated appearance of multiple layers of silvery-white dry scales on erythema, papules and plaques. The scales do not bond well with the skin beneath them and are easily shed, so it is often seen that the skin falls off easily on psoriasis patients. Psoriasis mainly occurs on the scalp and extremities. However, psoriasis can occur all over the body, even on the glans, fingernails and toenails. Most psoriasis tends to recur or worsen in winter and spring, while it remits or subsides in summer and autumn. Why psoriasis occurs In recent years, most scholars believe that psoriasis is related to genetics, infection, metabolic disorders, immune dysfunction, endocrine disorders and other factors. However, the etiology of psoriasis is complex and the exact cause is not yet clear. Therefore, psoriasis is one of the key diseases in current dermatology research. Although many scholars at home and abroad have conducted a lot of research on the etiology and pathogenesis of psoriasis and have made some achievements, no definite conclusion has been reached so far. There are the following common statements about the main causes or causative factors for the occurrence and development of this disease. Genetic factors It is now confirmed that the disease often has a family history of development and a genetic predisposition. This so-called genetic predisposition does not mean that if someone in the family has psoriasis, then the next generation will definitely get psoriasis. The genetic predisposition means that if someone in the family has psoriasis, then the next generation will have a greater chance of getting psoriasis than the average person, but it does not necessarily mean that they will get psoriasis. It is currently believed that the disease is controlled by multiple genes. Recently, a research group from the Institute of Dermatology of Anhui Medical University, the University of Michigan, the University of Washington and other research institutions have identified six new psoriasis susceptibility genes, which provide insight into the pathogenesis of psoriasis and psoriatic arthritis and offer new treatment pathways for psoriasis. Nearly 20 susceptibility genes for psoriasis have been identified and widely recognized internationally, and the discovery of the six susceptibility genes is bound to set off a new round of lively discussions on psoriasis genetics. All the relevant genes discovered now can only explain 40% of the genetic susceptibility mechanism of psoriasis, and there are still a lot of unknown mysteries waiting to be revealed by geneticists. Infectious factors It has been suggested that viral infections are responsible, as it has been observed that psoriasis can remit as a result of antiviral treatment in patients with concurrent viral infections. Similarly, colds may induce and exacerbate psoriasis. However, no virus has been cultured from psoriatic lesions or from the body to date. Therefore, further research is needed to determine the extent to which viral infections play a role in the development of psoriasis. Bacterial infections may also be an important predisposing factor for the disease, especially streptococcal infections. Because some patients with psoriasis often have upper respiratory tract infections and tonsillitis, their anti-“O” antibody values are increased. Especially in pediatric psoriasis, 10% to 20% of children often have a history of acute tonsillitis or upper respiratory tract infection, and antibiotic treatment with penicillin and other antibiotics often has a good effect. At the same time, the psoriasis rash also subsided after tonsil removal. This suggests the importance of bacterial infections in these patients. Psoriasis caused by bacterial infections is generally thought to be a metabolic reaction to bacterial toxins. Metabolic disorders Increased serum lipids, cholesterol, globulins, sugar, uric acid and potassium, and decreased folate levels have been reported, but no firm conclusions have been made. Increased polyamines and arachidonic acid in the lesions have also been reported. However, psoriasis lesions can also produce changes in the above-mentioned substances, so it is difficult to be sure whether the resultant changes in the above-mentioned substances in human body are caused by psoriasis itself or the cause of psoriasis. Endocrine factors The relationship between psoriasis and the function of endocrine glands has long received attention. Clinically, it has been observed that some female patients’ rashes can subside on their own during pregnancy and worsen again after delivery. But there are also a small number of patients who develop or aggravate during pregnancy, so the role of endocrine factors in the occurrence and development of psoriasis is not certain. Mental factors Mental trauma and emotional stress and overexertion can trigger the disease or aggravate it. Therefore, it is conjectured that mental factors have some correlation with the occurrence and development of psoriasis. However, mental factors cannot fully explain the etiology of psoriasis. Immune factors Some patients have low cellular immune function, some have increased serum IgG, IgA and IgE, and some have anti-IgG antibodies in their serum. The presence of anti-keratin autoantibodies within the epidermal stratum corneum of patients has been measured by immunofluorescence techniques. All these suggest that immunogenic factors play an important role in the occurrence and development of psoriasis, but the exact mechanism is not clear. Other factors Trauma, stimulation by certain physical and chemical factors and drugs, as well as climatic factors, are also relevant to the onset of psoriasis in some patients. For example, most patients have relapses and exacerbations in winter that remit or subside spontaneously in summer, but seasonal regularity disappears in those with long-standing disease.