الفهرس 
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Abstract
Any hair-bearing area can be affected by alopecia areata that is a frequent non-scarring type of hair loss. It appears as an abrupt loss of hair without any scarring or inflammation. The pattern of this type could be localized to one or more patches or diffuse as in alopecia totalis, which affects the entire scalp, or alopecia universalis, which affects the entire body. The condition has an unpredictable history and is frequently accompanied by phases of hair loss and regrowth.
There are many theories explaining the disease etiopathogenesis but none of them is conclusive, however, the gold standard approach for understanding AA is the collapse of hair follicle immune privilege.
The exact auto antigen that initiates AA is unclear until now, but many researchers pointed to hair follicle melanocytes as a target for T-cytotoxic lymphocytes, as pigmented hairs are attacked first and gray/white hairs are usually spared in AA lesions.
The study was conducted on 18 patients presenting with patchy alopecia areata of the scalp. Cases were selected from those attending the dermatology outpatient clinic at Minia University Hospital. Written informed consent was taken from all participating patients or their parents.
This work was done to study the immunohistochemical characteristics of hair follicle melanocytes in AA patients and their relation to the perifollicular mononuclear inflammatory infiltrate.
By analysis of the data collected from patients included in the current study, the age ranged from 5 to 40 years, duration of illness varied from 5 days to 36 months. As regards hair pull test 9 (56.3%) were active and 7 (43.7%) were negative. No family history of other autoimmune diseases was found. One case gave a history of other autoimmune disease namely vitiligo.
Skin biopsies were obtained at the border of the lesions on each patient. The biopsies were processed for routine longitudinal sectioning after they were fixed in ten percent formalin. Histopathological examination was done for each case and every case was evaluated either it had a significant perifollicular inflammatory infiltrate or not, in longitudinal section, 8 cases had significant infiltrate, and for more illustration, we evaluated every follicle in each case either it had a significant perifollicular inflammatory infiltrate or not. The total number of follicles was 85, 52 of them had significant perifollicular mononuclear inflammatory infiltrate.
The histopathological study revealed that the transverse section is better than the longitudinal one in evaluating the inflammatory infiltrate in a case of alopecia areata.
An immunohistochemical study of 4 different immune stains (CD117, Sox10, Melan-A, HMB45) was done for all cases in the transverse section only. The results showed that these melanocytic markers were clearly expressed in cases of AA, CD117 was the most marker expressed and HMB45 was the least.
The Correlation was statistically significant between the expression of the immune stain markers and the existence of the perifollicular inflammatory infiltrate in cross-section. On the other hand, there were no significant correlations between expression of immune stain and disease duration and existence of perifollicular infiltrate in the longitudinal section.
In conclusion, the obvious expression of these melanocytic-related markers and the expression of these markers in immune-attacked follicles increased the chances that melanocytes have in the etiopathogenesis of alopecia areata.