Causes of psoriasis
Last reviewed: 23.04.2024
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Currently, the most recognized theories of the emergence of psoriasis are hereditary, immune, neurogenic, endocrine and the theory of metabolic (carbohydrate, protein, fatty, cyclic nucleotides, cheylons, etc.) disorders.
The role of hereditary factors in the development of psoriasis is beyond doubt. A high incidence of psoriasis among relatives of patients was found, prevalent in several times in the population, higher concordance of monozygotic twins (73%) compared with dizygotic (20%), association with the HLA system. Psoriasis is a multifactorial disease. Depending on the age, onset, the HLA system and the course of the disease, two types of psoriasis are distinguished. Psoriasis of the first type is associated with the HLA system (HLA Cw6, HLAB13, HLAB17), occurs at a young age (18-25 years) in individuals whose family members and relatives have psoriasis. This type of psoriasis affects 65% of patients and the disease is more severe. Psoriasis of the second type is not associated with the HLA system and occurs in the older age group (50-60 years). These patients have almost no family cases and the process is often limited or more mild than in the first type of psoriasis.
It is assumed that the development of psoriasis involves various genes, either individually or in combination. The adhesion of dominant forms of psoriasis with the distal section of the 17th chromosome was found, genetic determination of lipid and carbohydrate metabolism disturbances and increased expression of a number of proteoglycogenes, in particular mys, fos, abl in the skin of patients.
According to the immune theory of the emergence of psoriasis, T-lymphocytes (CD4 + T-lymphocytes) play a key role, and enhanced proliferation and disturbances in the differentiation of epidermal cells are a secondary process. It is believed that the primary changes in psoriasis occur both at the level of the cells of the dermal layer and the epidermis. Perhaps the trigger factor is the inflammatory reaction of the dermis, which leads to a violation of the regulation of cell division in the epidermis, which is manifested by excessive proliferation. Hyperproliferation of keratinocytes leads to the secretion of cytokines (including the tumor necrosis factor alpha-TNF-a) and eicosanoids, which exacerbate inflammation in the psoriatic focus. In lesions, cells presenting an antigen produce interleukin-1 (IL-1), which is identical to the activation factor of T-lymphocytes (mostly helpers). This factor is produced by keratinocytes and activates lymphocytes of the thymus. IL-1 leads to chemotaxis of T-lymphocytes in the epidermis and these cells infiltrate the epidermis. T-lymphocytes produce interleukins and interferons that enhance the process of hyperproliferation of epidermal keratinocytes, ie, a vicious circle is created. As a result, kinetics of proliferation of keratinocytes occur. The cell cycle decreases from 311 to 36 hours, i.e. Keratinocytes are formed 28 times more than in norm. Trigger factors can be infectious diseases, stress, physical trauma, drugs, hypocalcemia, alcohol, climate, etc.
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