For several decades, psoriasis is a disease characterized by hyperplasia of epidermal and dermal inflammation. Additional characteristics based on histopathological changes were found in psoriatic plaques and laboratory data describing the cell cycle and transit time of cells in the epidermis. Thickened epidermis in psoriasis plaques and hyperplastic, and there are incomplete maturation of epidermal cells over the cell area germinatif. Rapid replication of cells germinatif very easily recognized, and there is a reduction in transit time for cells through the epidermal cells thick.
Cutaneous vascular abnormalities characterized by increased amounts of inflammatory mediators, namely lymphocytes, polymorphonuclear, leukocytes, and macrophages, accumulate in the dermis and epidermis. These cells can induce changes in the structure of the dermis well insial and advanced-stage disease.
There are several factors that act as the etiology of psoriasis, include the following:
1. Genetic Factors
Approximately 1/3 of people affected by psoriasis report a family history of disease who also suffer from psoriasis. At the risk of monozygotic twins suffering from psoriasis was 70% when one of his suffering from psoriasis. If parents do not suffer from psoriasis then the risk of having psoriasis by 12%, whereas if one parent has psoriasis the risk of psoriasis increased to 34-39%. Based on the onset of the disease are two types, namely:
a. Psoriasis type I with early onset, and familial
b. Type II psoriasis with late onset and non-familial
Another thing that supports the existence of genetic factors that psoriasi adalag associated with HLA. Psoriasis type I associated with HLA-B13, B17, Bw57 and Cw6. Type II psoriasis associated with HLA-B27 and Cw2, whereas psoriasis pustulosa associated with HLA-B27.
2. Immunologic factors
Genetic defect in psoriasis may be expressed in one of the three types of cells are T lymphocytes, antigen presenter cells (dermal) or keratinocytes. Keratinocytes in psoriasis require stimuli for activation. Lesions of psoriasis is generally full of mature T lymphocytes in the dermis which mainly consisted of CD4 T lymphocytes with little lymphocytic sebukan the epidermis. While new lesions are generally more dominated by CD8 T cells limphocyte. In the psoriasis lesions contained about 17 cytokine production increases. Langerhans cells also play a role in psoriasis imunopathogenesis. Epidermal proliferation begins with the movement of both endogenous and exogenous antigen by Langerhans cells. In psoriasis epidermis formation (turnover time) is faster, only 3-4 days, whereas in normal skin of 27 days duration.
Nickoloff (1998) concluded that psoriasis is an autoimmune disease. Over 90% can be in remission after being treated with immunosuppressive. Berbaga trigger factor in psoriasis are mentioned in the literature include psychological stress, focal infection, trauma (Fenomenan Kobner), endocrine, metabolic disorders, drugs, alcohol and smoking. Psychological stress is a major trigger factor. Hunungan focal infection has close links with one type of psoriasis is guttate psoriasis, while psoriasis vulgaris with no apparent. Guttate psoriasis has been reported recovery after tonsillectomy. Generally, the infection caused by Streptococcus. Endocrine factors generally affect the course of the disease. The peak incidence of psoriasis, especially during puberty and menopause. At the time of pregnancy generally improves while in the postpartum period is generally worse. Metabolic disorders such as dialysis and hypocalcemia were reported to be one trigger factor. Generally, drugs that can cause residif are beta adrenergic blocking agents, lithium, anti-malaria and the sudden cessation of systemic steroids.
There are several predisposing factors that can cause this disease, namely:
1. Hereditary factors are dominant autosomal with incomplete penetration.
2. Psychological factors, such as stress and disruption emotion. The study mentions that 68% of patients with psoriasis express stress, and anxiety caused more severe and severe disease.
3. Focal infection. Chronic infection in the nose and ears, pulmonary tuberculosis, dermatomycosis, arthritis and chronic inflammation of the kidneys.
4. Metabolic diseases, such as latent diabetes mellitus.
5. Digestive disorders, such as obstipate.
Weather factors. Some cases showed a tendency to heal in the summer, while in the rainy season will relapse and more severe