الفهرس 
Clinical picture of psoriasisOnly 14 pages are availabe for public view
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Abstract
Psoriasis is a common chronic condition characterized by thick scaling red plaques which can be either localized or widespread. The disorder is characterized by spontaneous remissions and exacerbations. It affects approximately 2-3% of the population worldwide. Its etiology and pathogenesis result from a combination of genetic and enviromental factors. It is frequently inherited and passed from one generation to the next. The disease is sometimes triggered by obvious causes as trauma, drugs or bacterial superantigens. It can be both physically and emotionally debilitating. Disability and impact on life quality due to psoriasis parallels that of heart disease and arthritis.
Psoriasis is a chronic papulosquamous skin disease characterized by marked keratinocyte hyperproliferation, dense inflammatory infiltrate of T cells and neutrophils, vascular dilatation and proliferation. The primary defect in psoriatic patients was believed to be abnormal epidermal cells proliferation.
Recent progress in the understanding of psoriasis has attributed its pathogenesis to the important role of T cells; specifically Th1 and Tc1. Activated T-cells in psoriatic lesional skin secrete type 1 cytokines such as: TNF-α, IL-2 and IFN-. Interleukin 2 (IL-2) plays an important role in the immunological reactions in psoriasis by its effect on T lymphocytes and NK cells through interacting with cell membrane bound IL-2 receptors. The level of specific soluble IL-2 receptor in blood serum corresponds with the amount of receptor on cell membranes. An increased level of sIL-2R in the serum of psoriatic patients may thus act as a sensitive marker of the activity of this disease.
In psoriasis, the initial activation of T-lymphocytes requires three steps: binding, signal 1 and signal 2. Binding occurs between surface adhesion molecules of both T-lymphocytes and APCs, then additional interactions occur at “signal 1” between TCR on T-cell and MHC I or II on APC, a process that is followed by additional interactions “signal 2” which, in their absence, T-cells undergo anergy or apoptosis. The trafficking of T-cells into the skin involves three steps: rolling, binding and diapedesis. Activated T-cells produce Th-1 cytokines (IL-2, TNF-α, IFN-γ) which, along with chemokines and growth factors, are responsible for the inflammatory infiltrate, vascular changes and the epidermal hyperproliferation present in psoriasis.
Phototherapies such as NB-UVB therapy or PUVA have proven to be highly effective for the treatment of psoriasis. Currently, PUVA is considered first-line therapy in the treatment of moderate to severe psoriasis resistant to topical agents or UVB phototherapy. There is evidence that NB-UVB phototherapy source (TL-01) is more effective than conventional BB-UVB sources, and is possibly as effective as PUVA.
There is evidence that one of the mechanisms through which PUVA produces its therapeutic effect is through immunomodulation. The immunomodulatory effects of NB-UVB, however, are controversial. This work was performed to compare the effect of NB-UVB phototherapy and PUVA photochemotherapy on sIL-2R serum level as a marker of systemic T-cell activation in patients with psoriasis before and after treatment.
The present study was performed on 24 patients, (19) patients with moderate to severe psoriasis and five (5) patients with mild to moderate psoriasis resistant to topical treatments, of both sexes (13 males and 11 females) and of different age groups (13-75 years) who had not received any systemic treatment for at least 6 weeks prior to the study. Their psoriasis was considered mild if PASI was less than 15, moderate if PASI was more than or equal to 15-25 and severe if PASI was more than 25. Serum sIL-2R levels were measured by ELISA technique that probably reflects activation of T cell- mediated immunopathogenic mechanisms. Correlation between the serum concentration of sIL-2R and the PASI measurement of disease activity was done. We also determined the effects of PUVA and NB-UVB on the following indices of disease activity, sIL-2R levels and PASI scores, in psoriatic patients.
In our study, patients with psoriasis were found to have elevated levels of sIL-2R in comparison to normal controls. Posttreatment sIL-2R levels were significantly reduced in comparison to pretreatment levels in both groups. However, posttreatment sIL-2R levels were lower in PUVA-treated patients in comparison to NB-UVB-treated patients. There was also a significant correlation between the level of sIL-2R and PASI scores throughout the study.
In conclusion, our study provides further evidence on the importance of sIL-2R in the pathogenesis of psoriasis and shows its elevation in the serum of psoriatic patients that probably reflects activation of T cell mediated immuno-pathogenic mechanisms which are affected by both PUVA and NB-UVB. Soluble IL-2R level also appears to be a useful index of disease activity and a means of discerning the mode of action of various therapies in this disease as it is easy and time-sparing method. Finally, we are looking forwards to the application of the anti- sIL-2R biological therapy that might give us glimpse of hope as this major cytokine plays a significant role in various autoimmune and inflammatory diseases.