الفهرس 
Alopecia AreataOnly 14 pages are availabe for public view
 |  | from | 97 |  |  |
| | | from | 97 | | |
Abstract
Alopecia areata (AA) is a common form of non-scarring alopecia involving the scalp and/or body, characterized by hair loss without any clinical inflammatory signs. AA1 can present with different clinical manifestations varying from reversible patchy hair loss to complete baldness or complete body hair loss. The affected skin appears normal with no epidermal alteration grossly visible such as scaling or follicular abnormalities.
The diagnosis of AA is made on clinical grounds and a good physical examination is imperative to distinguish between the differentials. The course of AA is unpredictable. Up to 50% of patients will recover within 1 year even without treatment. However, most patients will have more than one episode of hair loss. Although diagnosing alopecia areata is usually easy, treating it is not. At present, only two approaches reach the level of evidence-based medicine: intralesional injections of glucocorticoids and the induction of contact allergy.
AA is a polygenic disease. Most likely, there is an interaction between genetic and environmental factors that trigger the disease. There is a high prevalence of mood adjustment, and anxiety disorders in patients with AA.
Autoimmunity is believed to play a central role in the development of AA. Patients with AA have been found to have an increased frequency of hair follicle-specific auto-antibodies. The inferior portion of the normal hair follicle is an “immune privileged” site which is protected from surveillance by T cells. The immune response in AA is associated with aberrant lesional expression of tumor necrosis factor-, interferon-, IL-2, and IL-1β, and overexpression of ICAM-1 and MHC molecules on hair follicle keratinocytes and dermal papilla cells.
Together with these cytokines, HMGB1 may constitute a proinflammatory loop and may act as an important player in the inflammatory processes in AA. 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.
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.
This study included 50 randomly selected alopecia areata cases of different clinical variants and 30 healthy control subjects. Serum levels of HMGB1 were detected using an enzyme-linked immunosorbent assay kit.
Statistical analysis revealed a statistically significant increase in the mean serum HMGB1 level in patients with AA compared to healthy control subjects which supports the possible role of HMGB1 in AA. We did not observe any significant association between serum HMGB1 level and the type or the severity of AA. Serum HMGB1 levels in patients with positive hair-pull test results were statistically higher than those with negative results which indicates that HMGB1 may be used in AA as marker of activity and a prognostic factor.
With reference to duration of AA, we found that serum HMGB1 levels were increased in patients with acute disease occurrence but there was no statistically significant difference. Moreover, our results showed that serum HMGB1 levels in patients with history of prior episodes of AA were increased than patients with the first episodes but it was statistically insignificant.