الفهرس 
Psoriasis vulgarisOnly 14 pages are availabe for public view
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Abstract
Psoriasis affects nearly 2-3% of the world’s population. Its profound effect on the patients’ quality of life as well as its associated co-morbidities caused it to be one of the most studied dermatological diseases.
Psoriasis is a chronic inflammatory skin disease characterized by hyper proliferation of keratinocytes, dilation and growth of dermal capillary vasculture, and cellular infiltrate of activated T cells, dendritic cells, monocytes, and neutrophils. Increased production of numerous cytokines, chemokines and growth factor has been found to be present within the skin as well as in the circulation in psoriasis patients.
Nowadays, it is believed that psoriasis is most likely a Th1/Th17 induced inflammatory disease, with interplay between genetic susceptibility, defects in skin barrier and dysregulation of innate and adaptive immunity. Environmental factors also play a role in the pathogenesis of psoriasis including drugs, skin trauma, infection and stress.
High mobility group box-1 (HMGB1), initially described as a non histone nuclear protein with transcriptional regulatory properties, is now recognized as a late mediator in septic shock as well as a pro- inflammatory cytokines. HMGB1 is expressed by almost all cells, and usually located in the nucleus. However, it has been reported that HMGB1 can be translocated to the cytosol and then released into the extracellular space.
There are two pathways in which HMGB1 can be released extracellularly. One is an active process which occurs when cells exposed to inflammatory mediators, such as lipopolysaccharide (LPS), (TNF)- α, and (IFN)-γ ; the other a passive process during cellular necrosis.
With the discovery of HMGB1 as a potent mediator of inflammation and the presence of extranuclear HMGB1 in several inflammatory conditions, investigations of possible beneficial effects of HMGB1-targeted therapies were initiated.
Many recent studies have concluded that HMGB1 is a key player in the pathogenesis of several autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and psoriasis vulgaris.
It was suggested that HMGB1 may constitute a proinflammatory loop and may act as an important player in the inflammatory processes in psoriasis vulgaris. Activated HMGB1 mediates cellular responses including chemotactic cell movement and release of proinflammatory cytokines such as tumor necrosis factor-, IL-1 β, and IL-6, and effects on various immune cells, such as macrophages, monocytes, T cells, and B cells.
This study included 20 randomly selected psoriasis vulgaris cases of different clinical variants and 20 healthy control subjects. Each patient was subjected to a detailed history taking and examination. Skin biopsies were taken from all subjects. Tissue levels of HMGB1 were assessed using an enzyme-linked immunosorbent assay before and after treatment. NB-UVB treatment sessions were given for the patient group three times per week for 3 months. Tissue HMGB1 levels and PASI scores were measured at the beginning of the study and after 3 months of treatment.
Results assessed revealed a statistically significant increase in the mean tissue HMGB1 level in patients with psoriasis vulgaris compared to healthy control subjects which supports the possible role of HMGB1 in psoriasis vulgaris. Tissue HMGB1 levels in patients with high PASI score before treatment were statistically higher than those with low PASI score after treatment which indicates that HMGB1 may be used in psoriasis vulgaris as marker of activity and a prognostic factor. No significant association between tissue HMGB1 level and the age or the sex of patients.
With reference to duration of disease, there was significant positive correlation between tissue HMGB1 levels and the disease duration.