الفهرس 
ALOPECIA AREATAOnly 14 pages are availabe for public view
Abstract
A
lopecia areata (AA) is a heterogenous disease characterized by nonscarring hair loss on the scalp or any hair-bearing surface. A wide range of clinical presentations can occur ranging from a single patch of hair loss to complete loss of hair on the scalp; alopecia totalis (AT) or the entire body; alopecia universalis (AU). The course of disease is not predictable and it is often associated with periods of hair loss and regrowth.
Many factors such as genetic predisposition, autoimmunity, cytokines, chemokines and stress have been suggested as predisposing factors for AA. Basic research has established AA as a T cell-mediated autoimmune disease.
Perifollicular and intrafollicular mononuclear cell infiltrates directed at anagen hair bulbs are characteristic histological features. The inflammatory infiltrate is composed of activated CD4+ and CD8+ T cells, together with macrophages and Langerhans cells.
An aberrant expression of Th1 cytokines plays a critical role in the pathogenesis of AA. TNF-α has been shown to be inhibitory to hair follicle growth in in-vitro studies. The changes in hair follicles incubated with TNF-α are similar to those reported in AA. Also, IL-1α and IL1-β inhibit hair follicle growth and show similar follicle morphological changes. This may suggest that TNF-α plays an important role in AA. However, there are many reports of failure of anti- TNF-α agents in treating AA with reports of worsening or denovo induction of AA which made the role of TNF-α doubted and needs further investigations. Thus, this thesis was conducted to assess the presence of TNF-α in serum of patients of AA and to review its possible role in AA to pave the way for the development of new and safe targeted therapy for AA.
We can conclude that skin of early localized cases of AA have a high level of TNF-α (a normal inhibitor of hair follicle growth in- vitro). This high level may point to the important role of TNF-α in AA. Further studies should be conducted to detect the level of TNF-α in long standing AA and the more severe cases of AA (i.e. AT and AU). Also, studies to detect the level of TNF-α and IFN-γ in skin biopsies of AA before and after using an anti TNF-α agent are recommended to detect if the response is associated with a change in the TNF-α and IFN-γ levels or not. The serum level of Auto antibodies before and after using an anti TNF-α agent should be detected to confirm the role of autoimmunity in the failure of these drugs.