The etiology of this disease is not completely clear, but in recent years most scholars believe that it is related to genetics, infection, metabolic disorders, immune dysfunction, endocrine disorders, etc. 1, genetic According to the clinical observations, the disease often has a family history and a hereditary tendency. Foreign countries have reported a family history of 30%; – 50%;, and even some individuals emphasize up to 100%;. Domestic reports of family history are 10%; -20%; about the mode of inheritance, some people believe that it is autosomal dominant with incomplete epistasis, while others believe that it is autosomal recessive or sex-linked inheritance. If one of the parents has psoriasis, the incidence of the offspring is as much as three times higher than that of the children of healthy individuals, and if both parents have psoriasis, the incidence of the offspring is even higher. Histocompatibility antigens (HLA) have been found to be significantly associated with psoriasis in recent years. The frequency of HLA-B13 and HLA-B17 antigens is reported to be significantly higher in psoriasis patients abroad, but there are also reports of increased HLA-B3, HLA-CT7 and HLA-W6 in psoriasis patients. In addition to HLA-B13 and HLA-B17 antigens, which were significantly higher than normal group, gene frequencies of HLA-DR7, HLA-A19, were also increased in our psoriasis patients. gene frequencies of HLA-BW35, HLA-DR9, HLA-C7, HLA-DQ were decreased. It is now believed that psoriasis is controlled by multiple genes and is also influenced by environmental factors. 2, infection Clinical practice has proved that the onset of psoriasis is related to upper respiratory tract infection and tonsillitis. Six percent; of psoriasis patients have a history of pharyngeal infection. We found that psoriasis in many children is closely related to tonsillitis. For example, one mother and her three children had acute tonsillitis at the same time, and after the disease was controlled, three developed psoriasis. Such patients were effectively treated with antimicrobials. After removal of the tonsils, the rash may improve significantly or subside, indicating that infection is an important factor in the development of psoriasis. Some scholars believe that the onset of the disease is related to viral infection. The presence of eosinophilic inclusion bodies in spinal cells has been confirmed, but others deny their presence. Inoculation has been performed on rat-by-mouse and lesions similar to the disease have appeared and inclusion bodies were found in their tissue sections. However, its incidence was only 7.5%;, experimental inoculation on chicken embryos has been performed and its success rate was 86.7%;, the cells of the disease have a vigorous nuclear division. Deoxyribonucleic acid (DNA) increased, so the viral theory seems to have some basis, but so far it has not been possible to culture the virus. Recently, Liu Zhengyu et al. in China studied the relationship between human cytomegalovirus (HCMV) infection and the development of psoriasis and tested 86 psoriasis patients for serum HCMV-specific antibody IgM, IgA and urinary HCMV-DNA positivity. The results showed that the rate of active HCMV infection in psoriasis patients was significantly higher than that in the control group, and the rate of positive HCMV-DNA in patients’ urine was also significantly higher than that in the control group, indicating that active HCMV infection existed in psoriasis patients and its onset was related to HCMV activation. 3, metabolic disorders The research on blood chemistry, skin histochemistry and skin pathophysiology of psoriasis has failed to obtain intentional results. In the past, it was thought that the onset of psoriasis was related to disorders of lipid metabolism. At present, the etiology of the disease can no longer be considered to be caused by disorders of lipid-like metabolism. Instead, it is mostly studied from the alteration of enzyme metabolism. Four enzymes are present in the normal human epidermis, while two of them are missing in the lesions of psoriasis patients, and two of them reappear after the lesions are cured. It is known that psoriasis lesions lack cyclic adenosine monophosphate (cAMP), an epidermal chalone, which inhibits epidermal cell division and maintains a balance between cell growth and disappearance. On the other hand, cAMP has the effect of activating phosphorylases and thus also affects glycogen metabolism. If epidermal glycogen increases, it can cause increased mitosis and faster conversion rate of epidermal cells. However, the metabolic abnormalities in psoriasis are multifaceted and not only cAMP deficiency, but also the increase in cyclic phosphoglycosides (cGMP), free arachidonic acid and polyamines on the surface of the lesions play an important role in epidermal cell proliferation. However, it is worth mentioning that some authors believe that the ratio of cAMP to cGMP is very important in determining epidermal cell proliferation and differentiation, and that the proliferation, incomplete differentiation and glycogen accumulation of epidermal cells in patients with psoriasis are due to low cAMP and high cGMP, but this has not been fully confirmed. In addition, adenylyl cyclase activity is abnormal in psoriasis, and epinephrine has a low response to stimulation of this enzyme, but a high response to prostaglandin E2, so that epidermal cell membrane β-adrenergic receptor activity is reduced in psoriasis. And prostaglandins also play an important role in the regulation of cyclic nucleotides. The proliferative response of cyclic nucleotides to cells is a direct regulation of the synthesis of cellular macromolecules. That is, cAMP directly regulates the synthesis of DNA, so cAMP has a direct effect on cell division and enzyme production. 4, immune dysfunction The relationship between psoriasis and immunity has been widely appreciated. The clinical treatment of this disease with immunosuppressants, commonly used are methotrexate (MTX), ethyliminocyclosporine A and so on, has remarkable effects. The presence of various local or systemic immune abnormalities in patients with psoriasis and the high correlation between the disease and the expression of antigens such as HLAB13 and B17 suggest that the disease is also an immune disease. The immunopathogenesis of the disease is not yet fully understood. The more popular view is that psoriasis is a proliferative disease of epidermal cells caused by activated T cells. The dermis of psoriatic lesions is infiltrated by activated T cells, which release γ-interferon and induce epidermal cells to synthesize tumor necrosis factor and interleukin 8 and interleukin 6 cytokines, which attract neutrophils to infiltrate in the epidermis, leading to dermal vasodilation and causing skin inflammation. In addition, interleukin 6 and interleukin 8 released by monocytes and epidermal cells also promote the proliferation of epidermal cells. This results in the coexistence of abnormal epidermal proliferation and skin inflammation in psoriatic lesions. Further studies on the initiating factors of T-cell activation in psoriatic lesions are needed. It may be related to infection, trauma, neuropsychiatric factors, etc. 5, endocrine disorders The relationship between psoriasis and hormones has long been paid attention to. This disease is related to pregnancy, childbirth, lactation and menstruation. We have observed clinically that some patients with psoriasis have their rashes reduced or receded during pregnancy. 43 cases were observed by Chuzch, and 38% of the patients’ skin lesions receded during pregnancy. 6.2% of 169 patients with psoriasis were reported by Liu Chenghuang and others to be endocrine-related. 5 cases had their skin lesions healed or reduced during pregnancy, but intensified after delivery. Xu Yanchun et al. reported that plasma estradiol levels were measured in 19 cases of female psoriasis patients aged 12–45 years and were significantly higher than those of normal controls, while plasma progesterone levels were significantly lower than those of normal controls. They therefore concluded that increased plasma estradiol levels and decreased progesterone levels may promote or exacerbate lesions in female psoriasis patients aged 12–45 years. However, in some women the lesions worsen or are exacerbated during pregnancy, and therefore some efficacy has been reported with the use of long-acting contraceptives for the treatment of this disease. In summary, it can be seen that this disease and endocrine changes have a certain relationship. 6, other such as mental trauma, trauma or surgery, humidity, changes in blood rheology, as well as physical and chemical factors and drug stimulation, etc., also have a certain relationship to the onset of psoriasis patients.