الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Vitiligo is an acquired chronic depigmenting disorder of the skin characterized
by circumscribed de-pigmented macules or patches due to selective destruction of
melanocytes.
Approximately 0.5–2% of the world population is affected. Adults and children
of both sexes are equally affected, although larger numbers of females consult the
dermatologist probably due to the greater psycho–social perceived impact of the
disease.
The course of vitiligo is unpredictable, vitiliginous skin lesions may remain
stable or slowly progress for years and complete depigmentation may occur. Vitiligo
has been classified into two major forms, segmental vitiligo (SV) and non-segmental
vitiligo (NSV), the latter including several variants (generalized vitiligo, acrofacial
vitiligo, universal vitiligo, focal vitiligo.
Different hypotheses have been proposed to explain this disorder and the
pathological mechanisms might include biochemical, oxidant– antioxidant, neural, viral
and autoimmune processes.
S100B is one of the S100 proteins family. It includes a multigene 21 proteins of
low-molecular weight. Expression of S100B has been presented in a diversity of tissues,
including astrocytes, melanocytes, Schwann cells, neural progenitors, epithelial cells,
oligodendrocytes, adipocytes, kidney, Langerhans cells, epithelial, cardiac, skeletal
muscle cells, and chondrocytes.
It acts as a stimulator of cell proliferation and migration and an inhibitor of
apoptosis and differentiation.
S100B was hypothesized to be involved in the pathogenesis of many skin
diseases such as Atopic dermatitis, psoriasis, and Systemic lupus erythematosus.
The aim of the present work was to assess serum level of (S100B) in patients
with non-segmental vitiligo and its relationship to disease severity and disease activity.
This case-control study was performed on 40 patients with different types of
non-segmental vitiligo and 40age and sex matched healthy volunteers as controls. The
Cases were selected from the Dermatology outpatient clinic at Menoufia University
Hospital between July 2016 and February 2017. A written consent form approved by the
Ethical Committee of Menoufia Faculty of Medicine was obtained from each participant
before the study initiation .
All studied cases were subjected to complete history taking, general and
dermatological examination. The activity of disease was assessed by (VIDA) score and
the severity of disease was assessed by (VASI) score.
Inclusion criteria were as follows: Vitiligo cases with various types of nonsegmental
vitiligo and those have no history of administering systemic treatment of
vitiligo for the previous 6 weeks or topical treatment for the prior 2 weeks Exclusion criteria were as follows: patients suffering from autoimmune/
inflammatory systemic diseases e.g.; psoriasis, atopic dermatitis or connective tissue
disease and who have skin diseases other than vitiligo.
Blood samples were taken and sent to Biochemistry Department, Faculty of
Medicine, Menoufia University. Detection of S100B was done by ELISA kit.
In the current study the serum level of S100B in studied cases showed
statistically significant elevation (p value=0.001) (188.58 ± 186.24) than the control
group (93.30 ± 39.56). These results showed that increased S100 protein may be
involved in vitiligo pathogenesis through affecting Ca homeostasis and activation of
proinflammatory cascade with release of IL-1B and IL-6. It is elevated in vitiligo due to
melanocyte cytotoxicity.
S100B is a calcium binding protein and berrant calcium homeostasis has been
found in vitiligo and defective calcium (Ca2+) transport has been shown in melanocyte
cultures established from NSV. Also increased S100B resulted in an enhanced release
of proinflammatory cytokines such as IL- 1β and IL-6 that share in vitiligo
pathogenesis. Both are Th17cell related cytokines which have a role in local
depigmentation in autoimmune vitiligo.
In the current study there was a significant correlation between serum level of
S100B and both activity of the disease(assessed by VIDA score) (p=0.007) and severity
of the disease (assessed by VASI score) (p=0.05) Therefore, lowering elevated S 100 in
vitiligo patients especially those with active and severe disease may be beneficial. It was
found that low amount of S100B protects the melanocyte by inhibiting p53, and
subsequently the apoptosis process, through stimulation of the PI3K/ AKT pathway. S0
we recommend further studies on larger scales to confirm and validate current findings,
further molecular studies to investigate the mechanism of S100 induced apoptosis of
melanocytes and its role in the treatment of vitiligo.