INTRODUCTION
Vitiligo can be a psychologically devastating disease, especially
in darker skinned individuals. Vitiligo is a heritable
condition. Although the inheritance pattern has
not been fully established, up to 30% of patients report vitiligo
in another family member, and up to 21% of first-generation
family members may be affected. Offspring are at greatest risk,
followed by siblings, parents, and grandparents. Vitiligo has
been observed in monozygotic twins; the age of onset, extent,
and course may be similar. Vitiligo affecting only 1 twin has
also been reported.1 Vitiligo appears to be equally prevalent
among men and women, with no difference in occurrence rates
among skin type or race.
Vitiligo appears to be transmitted genetically in a polygenic/
multifactorial manner. The actual pathogenesis is under debate.
2 Human leukocyte antigen (HLA) complex is composed
of several closely linked loci, each containing several alleles;
it is the most gene-dense, polymorphic region of the human
genome and is known to contain over 224 identified gene
loci. Its inheritable nature and its frequent association with
autoimmune diseases have prompted studies on the association
of HLA with vitiligo. The associations of several HLA
class I and class II antigens susceptible to the development
of vitiligo have been investigated in different ethnic populations.
Using linkage disequilibrium analysis in familial
vitiligo, a study suggested that a major determinant of vitiligo
might be located in HLA.3
The increased frequencies of HLA-A2, HLA-A30, HLA-Bw60, HLACw4,
HLA-Cw6, HLA-Cw7, HLA-DR1, and HLA-DR4 in patients
with vitiligo have been reported by several investigators.4,5,6,7,8
The aim of this work was to assess the association of HLA-Cw
with vitiligo among the Egyptian population because to the best
of our knowledge there is no published molecular study on the
HLA antigens associated with vitiligo in this population.
SUBJECTS AND METHODS
Forty unrelated patients with nonsegmental vitiligo were
selected and subjected to a full history and clinical examination,
including the type and site of vitiliginous lesions. Twenty
matched controls were selected randomly from disease-free,
unrelated, apparently healthy donors.
HLA DNA Typing
DNA extraction was carried out with the classical phenol chloroform
method from fresh whole blood samples that were
anticoagulated by ethylenediaminetetraacetic acid (EDTA). A
polymerase chain reaction sequence specific primer (PCR-SSP)
method was used to determine HLA DNA typing. A dried primer
stock solution consisting of an HLA-specific primer mix, ie, allele,
and group specific was aliquoted in 0.2 mL PCR tubes.
The PCR master mix contained: 0.4 U/μL Taq Polymerase, 200
μM dNTPs, 50 mM KCI, 1.5 mM MgCl2, 10 mM Tris-HCI, pH 8.3,
0.001% w/v gelatin, 5% glycerol, and 100 μg/mL Cresol Red dye
