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ORIGINAL ARTICLE
Year : 2017  |  Volume : 9  |  Issue : 4  |  Page : 154-159

Detection of tumor necrosis factor-alpha in nonlesional tissues of alopecia areata patients: A prove for a systemic disease


1 Department of Dermatology, Faculty of Medicine, Beni-Suef University, Beni Suef, Egypt
2 Department of Biochemistry, Faculty of Medicine, Beni-Suef University, Beni Suef, Egypt

Correspondence Address:
Yasser Mostsfa Gohary
Department of Dermatology, Faculty of Medicine, Beni-Suef University, Mohammed Hassan Street, Beni Suef
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijt.ijt_47_17

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Introduction: The pathogenesis of alopecia areata (AA) remains incompletely understood. Different cytokines may play a role in AA. Tumor necrosis factor-alpha (TNF-α) has been shown to be inhibitory to hair follicle growth in in vitro studies suggesting that it may play an important role in AA. This study was conducted to assess the presence of TNF-α in lesional and nonlesional skin of AA, to review its possible role in AA, and to show whether AA is a systemic or localized disease by comparing the level of TNF-α between lesional and nonlesional skin biopsies of the patients. Materials and Methods: Thirty patients with AA and thirty age- and sex-matched healthy controls were included in the study. A 4 mm punch skin biopsy was taken from lesional and nonlesional skin of every patient, as well as from the normal skin of each individual in the control group for immunohistochemical analysis of TNF-α. Results: The level of TNF-α in lesional skin biopsies was significantly higher than in nonlesional skin biopsies of patients as well as controls' biopsies. Furthermore, TNF-α level in nonlesional biopsies of patients was significantly higher than the level in controls' biopsies. Conclusions: We concluded that skin of AA has 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.


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