الفهرس 
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Abstract
Psoriasis is a chronic disorder with polygenic predisposition combined with triggering environmental factors. It is a chronic papulosquamous skin disease characterized by complex alterations in epidermal growth and differentiation and multiple biochemical, immunologic, and vascular abnormalities.
Psoriatic lesions probably evolve as interplay between cells and mediators of the immune system specifically, its innate and adaptive function, and skin epithelium and connective tissue. Psoriasis is characterized by a T-helper (Th1-Th17) immune response. Recent interest has focused particularly on interleukin17, produced by type 17 helper T (Th17) cells. This cell type is specialized in immunosurveillance of epithelium, and it also secretes interleukin-22, a key cytokine linking adaptive immune effectors and epithelial dysregulation in psoriasis. Interleukin 22 induces proliferation of keratinocytes as well as production of antimicrobial peptides and chemokine.
Immunoglobulin (E) is a class of antibody or immunoglobulin isotype that has been found only in mammals. IgE is produced by B cells in the spleen, lymph nodes, and locally such as sinus mucosa.
Induction of IgE synthesis in human B cells requires three types of signals. The first signal is delivered through the B cell antigen receptor, and the second signal is mediated by Th2 cytokines; IL-4 and IL-13. Finally, the third signal is provided via the interaction between the constitutively expressed CD40 molecules on B-lymphocytes.
IgE estimation was important in the investigation of allergic diseases, parasitic infestations, and certain types of cancer. In addition, it was found to be elevated in some dermatologic conditions other than atopic dermatitis, such as contact allergic dermatitis and systemic lupus erythomatosus.
Unfortunately, the levels of serum IgE in psoriasis have not been fully explored although elevation of serum IgE in several cases of erythrodermic psoriasis and senile erythroderma has been reported.
Previous data on serum IgE in patients with psoriasis are very limited and results are controversial. Therefore, the aim of this work was to assess the total serum levels of IgE in psoriasis, and compare its levels between patients with different types of psoriasis, and with healthy subjects.
In the current study, serum IgE levels were measured by ELISA technique in the sera of ninety psoriatic patients, who were divided into three equal groups namely, those with chronic plaque, erythrodermic and pustular psoriasis with exclusion of those with possible atopic disease, in addition to thirty healthy controls were chosen for comparison of the results obtained from the patients group.
Our results showed a median of 87.5 IU/ml in psoriasis group, while in the control group a median of 24 IU/ml was found with a highly statistically significant difference, where p-value is < 0.001. On comparing total serum IgE in the four groups, the median serum IgE in erythrodermic psoriasis was the highest followed by pustular psoriasis then chronic plaque psoriasis and controls and that difference was statistically highly significant.
This study also provided a correlation between the onset of erythrodermic psoriasis and the level of total serum IgE since the longer the duration of the disease was, the higher the level of IgE was present. We also resulted in: the more the severity of erythrodermic psoriasis and the higher the PASI score, the more the rise in the serum IgE levels.
from the previous data, we can confirm that serum IgE level is relatively elevated in psoriatic patients especially erythrodermic type and it is more elevated in patients with chronic disease which may denote a shift to Th2- directed immune mechanisms.