Vitamin D Receptor Expression in Vitiligo

被引:18
作者
Doss, Reham William [1 ]
El-Rifaie, Abdel-Aziz [1 ]
Gohary, Yasser M. [1 ]
Rashed, Laila A. [2 ]
机构
[1] Beni Suef Univ, Dept Dermatol, Fac Med, Mohammed Hassan St, Bani Suwayf, Egypt
[2] Cairo Univ, Dept Biochem, Fac Med, Cairo, Egypt
关键词
25-hydroxy Vitamin D; enzyme-linked immunosorbent assay; real-time polymerase chain reaction; Vitamin D receptor; Vitiligo; 1,25-DIHYDROXYVITAMIN-D-3; STIMULATION; SERUM;
D O I
10.4103/0019-5154.169123
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Background: Vitiligo is a progressive depigmenting disorder characterized by toss of functional melanocytes from the epidermis. The etiopathogenesis of vitiligo is still unclear. Vitamin D has stimutatory effects on melanocytes and acts through its nuclear Vitamin D receptor (VDR) on target cells. Aims and Objectives: The purpose of this study was to declare the role of Vitamin D in the pathogenesis of vitiligo. Materials and Methods: 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 Blood samples were withdrawn from the study subjects, and the serum 25(OH) D level was determined by an enzyme-linked immunosorbent assay technique.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 (>= 30ng/ml), insufficient (< 30-> 20ng/ml), and deficient (< 20ng/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. Results: Only 10 patients with vitihigo (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). Conclusion: 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.
引用
收藏
页码:544 / 548
页数:5
相关论文
共 24 条
  • [1] HORMONAL EFFECTS OF VITAMIN-D3 ON EPIDERMAL MELANOCYTES
    ABDELMALEK, ZA
    ROSS, R
    TRINKLE, L
    SWOPE, V
    PIKE, JW
    NORDLUND, JJ
    [J]. JOURNAL OF CELLULAR PHYSIOLOGY, 1988, 136 (02) : 273 - 280
  • [2] Interleukin 17, Interleukin 22 and FoxP3 expression in tissue and serum of non-segmental vitiligo: A case- controlled study on eighty-four patients
    Abou Elela, Mostafa
    Hegazy, Rehab A.
    Fawzy, Marwa Mohamed
    Rashed, Lalia A.
    Rasheed, Hoda
    [J]. EUROPEAN JOURNAL OF DERMATOLOGY, 2013, 23 (03) : 350 - 355
  • [3] Depigmentation therapies for normal skin in vitiligo universalis
    AlGhamdi, K. M.
    Kumar, A.
    [J]. JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY AND VENEREOLOGY, 2011, 25 (07) : 749 - 757
  • [4] Analysis of Vitamin D Receptor Gene Polymorphisms in Vitiligo
    Aydingoz, Ikbal Esen
    Bingul, Ilknur
    Dogru-Abbasoglu, Semra
    Vural, Pervin
    Uysal, Mujdat
    [J]. DERMATOLOGY, 2012, 224 (04) : 361 - 368
  • [5] Cellular and molecular mechanisms involved in the action of vitamin D analogs targeting vitiligo depigmentation
    Birlea, S. A.
    Costin, G. -E.
    Norris, D. A.
    [J]. CURRENT DRUG TARGETS, 2008, 9 (04) : 345 - 359
  • [6] The 25-hydroxyvitamin D threshold for better health
    Bischoff-Ferrari, Heike A.
    [J]. JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 2007, 103 (3-5) : 614 - 619
  • [7] Imiquimod: A cytokine inducer
    Dahl, MV
    [J]. JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 2002, 47 (04) : S205 - S208
  • [8] Hann SK, 2000, VITILIGO, P35, DOI 10.1002/9780470760116.ch6
  • [9] An update on vitamin D and human immunity
    Hewison, Martin
    [J]. CLINICAL ENDOCRINOLOGY, 2012, 76 (03) : 315 - 325
  • [10] Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease
    Holick, MF
    [J]. AMERICAN JOURNAL OF CLINICAL NUTRITION, 2004, 80 (06) : 1678S - 1688S