Doss Reham William, El-Rifaie Abdel-Aziz, Gohary Yasser M, Rashed Laila A
Department of Dermatology, Faculty of Medicine, Beni-Suef University, Beni-Suef, Egypt.
Department of Biochemistry, Faculty of Medicine, Cairo University, Cairo, Egypt.
Indian J Dermatol. 2015 Nov-Dec;60(6):544-8. doi: 10.4103/0019-5154.169123.
Vitiligo is a progressive depigmenting disorder characterized by loss of functional melanocytes from the epidermis. The etiopathogenesis of vitiligo is still unclear. Vitamin D has stimulatory effects on melanocytes and acts through its nuclear Vitamin D receptor (VDR) on target cells.
The purpose of this study was to declare the role of Vitamin D in the pathogenesis of vitiligo.
This case-control study included 30 vitiligo patients and 30 age, gender-matched healthy controls. Blood samples were withdrawn from the study subjects, and the serum 25(OH) D level was determined by an enzyme-linked immunosorbent assay technique. Serum 25(OH) D levels were divided into: Normal or sufficient (≥30 ng/ml), insufficient (< 30-> 20ng/ml), and deficient (≤20 ng/ml) levels. Skin biopsies were obtained from the depigmented lesions and clinically normal skin of vitiligo patients and from the controls, and VDR gene expression was determined using real-time polymerase chain reaction.
Only 10 patients with vitiligo (33.3%) had sufficient serum 25(OH) D levels (≥30 ng/ml), 12 patients (40%) had insufficient levels, and 8 patients (26.7%) had deficient levels. On the other hand, most of the controls (96.7%) had sufficient levels. The mean serum 25(OH) D level in patients was significantly decreased compared to controls (P < 0.001). The VDR-mRNA expression was also significantly decreased in lesional and nonlesional skin of patients compared to controls (P < 0.001, P < 0.001, respectively).
Vitamin D deficiency influences the extent of vitiligo and could contribute to the pathogenesis of vitiligo through its immunomodulatory role and its role in melanogenesis.
白癜风是一种进行性色素脱失性疾病,其特征是表皮功能性黑素细胞丧失。白癜风的病因发病机制仍不清楚。维生素D对黑素细胞有刺激作用,并通过其核维生素D受体(VDR)作用于靶细胞。
本研究的目的是阐明维生素D在白癜风发病机制中的作用。
本病例对照研究纳入30例白癜风患者和30例年龄、性别匹配的健康对照。从研究对象中采集血样,采用酶联免疫吸附测定技术测定血清25(OH)D水平。血清25(OH)D水平分为:正常或充足(≥30 ng/ml)、不足(<30->20 ng/ml)和缺乏(≤20 ng/ml)水平。从白癜风患者的色素脱失皮损和临床正常皮肤以及对照者身上获取皮肤活检样本,使用实时聚合酶链反应测定VDR基因表达。
只有10例白癜风患者(33.3%)血清25(OH)D水平充足(≥30 ng/ml),12例患者(40%)水平不足,8例患者(26.7%)水平缺乏。另一方面,大多数对照者(96.7%)水平充足。患者的平均血清25(OH)D水平与对照者相比显著降低(P<0.001)。与对照者相比,患者皮损和非皮损皮肤中的VDR-mRNA表达也显著降低(分别为P<0.001,P<0.001)。
维生素D缺乏影响白癜风的病情严重程度,并可能通过其免疫调节作用和在黑素生成中的作用促成白癜风的发病机制。