BASIC/CLINICAL SCIENCE

Vitiligo and Associated Autoimmune Disease: Retrospective

Review of 300 Patients
Jakub Sawicki, Sanjay Siddha, and Cheryl Rosen
Background: Vitiligo, the most common cutaneous depigmentation disorder, has reported associations with other autoimmune
diseases. However, literature on the strengths of the associations is conflicting, and no data on the subject exist from a Canadian
population.
Objective: To determine autoimmune disease associations with vitiligo and which, if any, screening bloodwork is appropriate in
vitiligo patients.
Methods: A retrospective review of vitiligo patients admitted to the Toronto Western Hospital phototherapy unit was conducted
from January 1, 2000, to August 30, 2009. Data regarding patient characteristics, vitiligo clinical features (family history, age at onset,
type, extent), associated diseases in the patient and family, and admission bloodwork (hemoglobin, vitamin B
12
, thyroid-stimulating
hormone [TSH], antinuclear antibody) were recorded and compared, using the Fisher exact test where applicable.
Results: A total of 300 patient charts were reviewed (average age 41.5 6 15.5 years; 47% male, 53% female). Hypothyroidism was
present in 12.0% and pernicious anemia in 1.3% of patientssignificant increases over the population prevalence. No other
differences in prevalence were seen compared to the general population. TSH was increased in 3.7% of patients without a history of
hypothyroidism. Hemoglobin and vitamin B
12
were decreased in 0.3% of vitiligo patients without a history of pernicious anemia.
Conclusion: We found a significantly higher prevalence of hypothyroidism and pernicious anemia in vitiligo patients.
Renseignements de base: Des e tudes ante rieures ont montre lexistence dassociations entre le vitiligo, la maladie de
de pigmentation cutane e la plus courante, et dautres maladies auto-immunes. Cependant, la documentation sur la solidite des
associations est contradictoire, et aucune donne e sur le sujet nexiste pour la la population canadienne.
Objectif: De terminer les associations pouvant exister entre les maladies auto-immunes et le vitiligo et, sil y a lieu, identifier les
tests sanguins de de pistage approprie s que devraient subir les patients atteints de vitiligo.
Me thodes: E

tude re trospective des patients atteints de vitiligo admis a` lunite de photothe rapie de lho pital Toronto Western
Hospital du 1er janvier 2000 au 30 aou t 2009. Les donne es des caracte ristiques des patients, les caracte ristiques cliniques du vitiligo
(ante ce dents familiaux, a ge dapparition, type, e tendue), les maladies associe es identifie es chez le patient et chez sa famille, et le
bilan sanguin au moment de ladmission (he moglobine, vitamine B
12
, TSH, ANA) ont e te enregistre s et compare s, en utilisant la
me thode exacte de Fisher, sil y a lieu.
Re sultats: Au total, 300 dossiers de patients ont e te examine s (a ge moyen 41,5 6 15,5 ans; 47 % dhommes, 53 % de femmes).
Lhypothyro die e tait pre sente chez 12,0 % des patients et lane mie de Biermer, chez 1,3 % des patients, des augmentations
importantes de la pre valence dans la population. Aucune autre diffe rence au niveau de la pre valence na e te observe e par rapport a` la
population ge ne rale. Une augmentation du TSH a e te observe e chez 3,7 % des patients sans ante ce dents dhypothyro die. Une
diminution de lhe moglobine et de la vitamine B
12
a e te observe e chez 0,3 % des patients souffrant de vitiligo ne pre sentant aucun
ante ce dent dane mie de Biermer.
Conclusion: Nous avons trouve une pre valence significativement plus e leve e dhypothyro die et dane mie de Biermer chez les
patients atteints de vitiligo.
V
ITILIGO is an idiopathic disorder characterized by
destruction of cutaneous melanocytes, resulting in
depigmented macules and patches on the skin. The
prevalence of vitiligo in the general population is estimated
to be 0.4%, although it may be higher.
1,2
Many theories
have been put forth to explain the condition. One
hypothesis suggests that melanocytes are destroyed by an
autoimmune mechanism.
3
The biochemical hypothesis
From the Departments of Medicine and Dermatology, University of
Toronto, Toronto, ON.
Address reprint requests to: Jakub Sawicki, Toronto Western Hospital,
Dermatology Centre, 8 East Wing, 399 Bathurst Street, Toronto, ON,
M5T 2S8; e-mail:jsawicki@qmed.ca.
DOI 10.2310/7750.2011.11055
# 2012 Canadian Dermatology Association
Journal of Cutaneous Medicine and Surgery, Vol 16, No 4 (July/August), 2012: pp 261266 261
describes chemicals that are cytotoxic specifically to
melanocytes as the causative agents.
4
Another hypothesis
states that neurochemical mediators cytotoxic to melano-
cytes are released by adjacent nerve endings, destroying
melanocytes.
5
A genetic hypothesis suggests that the
involvement of multiple interacting genes is the basis of
vitiligo.
6
The melanocyte adhesion hypothesis postulates
that vitiligo is due to chronic detachment and transepi-
dermal loss of melanocytes, termed melanocytorrhagia,
with an altered melanocyte response to cutaneous
trauma.
7,8
This theory is supported by a recent study that
showed increased susceptibility to vitiligo in patients who
had specific variants of the DDR1 gene, which encodes a
collagen IV tyrosine kinase receptor that mediates adhe-
sion of melanocytes to the basement membrane.
9
An
alternate hypothesis states that oxidative stress is a
triggering event in melanocyte destruction.
10
Suscep-
tibility to vitiligo is greater in patients with a variant
of the promoter of the catalase gene, which leads to
decreased synthesis of catalase, predisposing to free radical
formation.
11
However, none of the hypotheses alone can explain
fully the pathogenesis of vitiligo, and it is likely a complex
interplay between a variety of factors that results in the
condition. Of the proposed theories, the autoimmune
hypothesis has received the most support.
12
Much
evidence exists for a role for autoimmunity in vitiligo.
3
First, vitiligo has all of the criteria for an autoimmune
disease. These are disease transfer by transfer of auto-
antibodies, spontaneous mutation and reproducibility in
experimental animal models, identification of auto-
antibodies within affected areas, lymphocyte infiltration
in the target area, statistical association with specific major
histocompatibility complex haplotypes, association with
other autoimmune diseases, and, finally, displaying a
favorable response to immunosuppression.
3,13
Moreover,
the systemic nature of vitiligo, capable of involving
melanocytes in the eye and ear as well as the skin, and
the presence of organ-specific antibodies in the sera of
certain vitiligo patients support the autoimmune nature of
the disease.
3
The association of vitiligo with other autoimmune
diseases is a well-documented phenomenon.
3
Several
studies have shown an association with various conditions,
including thyroid disease,
14
pernicious anemia,
15
type 1
diabetes,
16
alopecia areata,
17
Addison disease,
18
systemic
lupus erythematosus (SLE),
19
inflammatory bowel dis-
ease,
20
and rheumatoid arthritis.
21
Moreover, vitiligo is a
component of autoimmune polyglandular syndrome
(APS) types 1 and 2.
22
The goal of our study was to look at the prevalence of
autoimmune diseases in a group of 300 vitiligo patients.
Materials and Methods
The charts of patients at Toronto Western Hospital
undergoing phototherapy for the treatment of vitiligo,
from January 1, 2000, to August 30, 2009, were examined.
Institutional Review Board approval was obtained for this
study. A review of 300 random charts was conducted, and
information was recorded in a database for subsequent
analysis. The age, sex, presenting year and age at onset of
vitiligo, and type and extent of involvement were recorded.
Family history of vitiligo and patient and family medical
history were derived from a standardized questionnaire
administered to each new patient with vitiligo presenting
for phototherapy. Family included parents, siblings, and
children, whereas relatives were defined as all other
blood relations. Finally, the results of bloodwork done
routinely on each new patient prior to beginning
phototherapy, including thyroid-stimulating hormone
(TSH), hemoglobin, vitamin B
12
, antinuclear antibody
(ANA), calcium, and glucose, were recorded. The results
were tabulated and recorded in numerical and, where
applicable, percentage values. Statistical analysis was
conducted using the Fisher exact test, with the population
frequency as a fixed constant.
23
A condition was
considered to be identified by screening if an abnormality
was detected by laboratory investigation that was not
reported on the history. These results are presented as the
percentage of patients with the abnormality who did not
report the respective condition on the history.
Results
Patient-defining characteristics can be seen in Table 1. Of
the 300 patient charts reviewed, there were slightly more
female (53%) than male (47%) patients. Patient ages
ranged from 11 to 82 years, with an average of 41.5 years.
The clinical features of patients with vitiligo are listed
in Table 1. Thirty percent of patients had a family history
of vitiligo, with 16.3% in the immediate family. The major
patterns of disease were focal localized (45.6%) and
generalized vitiligo vulgaris (34.3%), with acrofacial
(3.7%), segmental (2%), and universal (0.3%) vitiligo
making up the minority. Regarding disease severity, 80%
of patients fell into the first quartile of body surface area
involvement, with decreasing numbers in progressively
increasing body surface area quartiles (see Table 1). This
finding is similar to that of other studies.
20,24
Autoimmune
262 Sawicki et al
disease was present in 13.2% of the first quartile, 43.5% of
the second quartile, 12.5% of the third quartile, and 37.5%
of the fourth quartile of body surface involvement. The
average age at onset of vitiligo in our study was 33 years,
ranging from 3 to 78 years. Sixty-nine percent of patients
first developed vitiligo when they were older than age 20.
In previous studies, 50% of people with vitiligo noted the
onset after age 20.
3,25
Associations between vitiligo and autoimmune disease
in the patients and their family members are listed in
Table 2. Nineteen percent of the vitiligo patients had
associated autoimmune diseases, excluding diabetes melli-
tus. No patients were found to have SLE or myasthenia
gravis or were suspected of having APS. In addition, four
single cases of other autoimmune or connective tissue
diseases not listed in the initial screen were reported:
fibromyalgia, multiple sclerosis, autoimmune thrombocy-
topenic purpura, and autoimmune hepatitis.
A history of hypothyroidism was reported by 12% of
patients, with close to twice as many females (15.1%) as
males (8.5%) reporting the disease. All values are
significantly (p , .01) higher than the respective
prevalence of thyroid disease in the general population
(see Table 2). The same is true for the prevalence of
hypothyroidism in first-degree relatives of vitiligo patients,
with a 9.0% total prevalence, with a similar prevalence in
female (8.8%) and male (9.2%) patients, although all are
significantly greater than the prevalence in the general
population. In contrast, the prevalence of hyperthyroidism
was not found to be significantly elevated compared to the
Table 1. Patient Demographics and Clinical Features
Sex, n (%)
Male 141 (47)
Female 159 (53)
Age (yr)
Mean 6 SD 41.5 6 15.5
Range 1182
Family history of vitiligo, n (%)
Total family 90 (30.0)
Immediate family 34 (11.3)
Relatives 41 (13.7)
Both 15 (5.0)
Vitiligo pattern, n (%)
Generalized vulgaris 103 (34.3)
Acrofacial 11 (3.7)
Segmental 6 (2.0)
Focal localized 137 (45.6)
Universal 1 (0.3)
No data 42 (14.0)
Vitiligo body surface area involvement, n (%)
125% 242 (80.7)
2550% 23 (7.7)
5075% 16 (5.3)
75100% 8 (2.7)
No data 11 (3.7)
Age (yr) at onset of vitiligo
, 20, n (%) 92 (30.7)
Mean 6 SD 13 6 4
Range 320
. 20, n (%) 207 (69)
Mean 6 SD 42 6 13
Range 2178
Table 2. Associated Autoimmune Diseases in Vitiligo Patients and First-Degree Relatives
Disease
Patient, n (%) First-Degree Relatives, n (%) Population Frequency (%)
Total Male Female Total Male Female Total Male Female
Hypothyroidism 36 (12.00) 12 (8.50) 24 (15.10) 27 (9.00) 13 (9.22) 14 (8.81) 3.7* 3.1* 4.2*
Hyperthyroidism 2 (0.67) 0 (0.00) 2 (1.26) 2 (0.67) 0 (0.00) 2 (1.26) 0.5* 0.1* 0.8*
Pernicious anemia 4 (1.33) 1 (0.71) 3 (1.89) 2 (0.67) 1 (0.71) 1 (0.63) 0.15
{
0.10
{
0.20
{
Diabetes 15 (5.00) 7 (4.96) 8 (5.03) 20 (6.67) 10 (7.09) 10 (6.29) 3.20
{
3.50
{
2.90
{
Rheumatoid arthritis 3 (1.00) 1 (0.71) 2 (1.26) 4 (1.33) 2 (1.42) 2 (1.26) 0.86
{
0.45
{
1.26
{
Alopecia areata 1 (0.33) 1 (0.71) 0 2 (0.67) 1 (0.71) 1 (0.63) 0.202.00
{
Psoriasis 3 (1.00) 1 (0.71) 2 (1.26) 1 (0.33) 0 1 (0.63) 0.501.60
{
Halo nevus 1 (0.33) 0 1 (0.63) 0 0 0 1.00
1
SLE 0 0 0 0 0 0 0.024
{
0.0057
{
0.041
{
Myasthenia gravis 0 0 0 0 0 0 0.0051
{
0.0027
{
0.0076
{
SLE 5 systemic lupus erythematosus.
Boldface indicates a significant association between vitiligo and the autoimmune disorder compared to the population prevalence.
*Data from Aoki Y et al.
31
{
Population data from the US census and Alkhateeb A et al.
20
{
National Population Health Survey of Canada, 19961997.
1
Data from Herd RM and Hunter JA.
32
Vitiligo and Associated Autoimmune Disease 263
general population, with 0.67% of patients and their
relatives affected.
The prevalence of pernicious anemia was also
increased, with 1.3% of vitiligo patients reporting the
disease. Although this number represents only four cases,
it was higher than the general population prevalence of
0.15%. Three people who had pernicious anemia were
women (1.9%)a significant increase over the population
prevalence in females.
There was an increased prevalence of diabetes in
patients relatives but not in the patients themselves.
However, this increased prevalence is attributed to a
recording bias as no distinction was made between type 1
diabetes, the autoimmune condition of interest, and type 2
diabetes. This would have falsely increased the prevalence
of diabetes. No significant differences from the general
population were found in the prevalence of rheumatoid
arthritis, alopecia areata, psoriasis, halo nevi, SLE, or
myasthenia gravis. Finally, the presence of APS was not
suspected in any of our patients.
The following abnormalities were detected in patients
who did not report the given conditions on the history. Of
patients who did not report thyroid disease, 3.7% had an
increased TSH and 0.33% had a decreased TSH. Of
patients without reported pernicious anemia, 8.7% were
found to have low vitamin B
12
and 5.0% a decreased
hemoglobin, but only 0.30%, a single patient, had
decreased values of both. A positive ANA was found in
19.6% of patients, of which the majority, 12.5%, had titers
of 1:40, with the rest being 1:80 or higher. However, no
patients reported SLE on the history. Twenty-six of the
positive ANA findings had a speckled pattern, 24 had a
homogeneous pattern, 2 had both a speckled and a
homogeneous pattern, and 1 had a centromere pattern.
Discussion
Vitiligo is a condition of uncertain etiology and has been
studied in various populations.
20,24,26,27
In our study, there
were almost equal numbers of men and women. Previous
studies showed either a preponderance of women
25
or
concluded that vitiligo affects men and women equally.
20
The average age at onset of vitiligo in our study is relatively
high at 33 years when considering previous evidence that
50% of vitiligo cases begin before age 20.
25
In our
population, 30.7% of patients were age 20 or younger.
One possible reason for this may be the site of patient
accrual, a phototherapy center. For a child to be treated
with phototherapy, the child must be old enough to stand
still in the phototherapy unit during the ultraviolet
radiation exposure; thus, patients may not be referred to
our center until they are old enough to be considered a
candidate for phototherapy.
An association with autoimmune disease was present in
19% of the vitiligo patients in our study. This number is
very similar to the results of a survey of over 2,500 patients
by Alkhateeb and colleagues, who found an associated
autoimmune disease in 23% of patients.
20
However, other
large studies have documented a lower prevalence of
associated autoimmune disorders.
24,26,27
In a study of
more than 6,500 Chinese vitiligo patients, an association
with autoimmune disease was found in 7.7% of patients.
24
This may be due to the lower mean age of their patient
population (24.5 years), below the peak age at onset for
many autoimmune diseases. As well, different environ-
mental and genetic factors between the Canadian and
Chinese populations may play a role.
24
Furthermore, it
should be noted that our study population could represent
a subset of vitiligo patients with more severe disease
seeking phototherapy treatment. However, this is not
overrepresentative of the prevalence of autoimmune
disease in the general vitiligo patient population. First,
the majority of patients, 80%, fell into the lowest quartile
of involvement, similar to other large population-based
studies.
20,24
Second, there was no apparent correlation in
our study between the quartile of body surface involve-
ment and autoimmune disease prevalence, and to our
knowledge, no studies show this association.
A significant increase in the prevalence of hypothy-
roidism and pernicious anemia was seen in our study. This
is in agreement with previous studies, notably in the study
by Alkhateeb and colleagues, which showed the strongest
association between vitiligo and thyroid disease as well
as pernicious anemia.
20
Thyroid disease has commonly
been found to be associated with vitiligo,
28
with reported
prevalence ranging from 5.0%
28
to up to 40%.
29
No
significant associations were found between vitiligo and the
other autoimmune diseases that were studied.
When screening for autoimmune disease in patients
with vitiligo, the only worthwhile test based on our results is
TSH. Hypothyroidism was strongly prevalent in our patient
population, with 12% of patients affected, and an additional
3.67% of patients who did not report thyroid disease had
TSH values above normal ranges. Thus, 15.7%, or 1 of 6.4,
of vitiligo patients were likely to have hypothyroidism. This,
in our opinion, merits general screening for hypothyroidism
in people with vitiligo. Guidelines published by the British
Association of Dermatologists in 2008 on the diagnosis and
management of vitiligo also recommend screening only for
thyroid disease with TSH.
30
264 Sawicki et al
All other bloodwork values had a poor correlation
with diseases reported on the history. Only a single
patient had decreases in both hemoglobin and vitamin
B
12
, which is suspect for pernicious anemia. No patients
were clinically suspected of having APS type 1, although
3% of patients had hypocalcemia. Interestingly, not a
single case of SLE was reported in patients or first-degree
relatives, despite positive ANA levels in 19.57% of
patients, with 7.12% of titers 1:80 or higher. Other
studies have reported autoantibodies, including antithy-
roglobulin, antismooth muscle, and ANA present in 2 to
70% of vitiligo patients.
28
A recent study looking at the
correlation between the presence of serum autoanti-
bodies, including ANA, and autoimmune disease, as well
as the clinical course of vitiligo, concluded that auto-
antibodies were frequently present in the absence of overt
autoimmune disease. The presence of autoantibodies was
found to be independent of the clinical course of vitiligo
and thus was determined to be of limited clinical value.
28
Thus, the detection of ANA levels in the patients with
vitiligo, in our study, with the absence of SLE in all titers
ranging from 1:40 to 1:640, is in agreement with the work
by Ingordo and colleagues.
28
Conclusion
There is an association between vitiligo and thyroid disease
and pernicious anemia in a Canadian population, with
significantly higher levels of hypothyroidism and perni-
cious anemia detected in people with vitiligo compared to
the general Canadian population. Based on our results, we
recommend screening all new patients with vitiligo for
thyroid disease with a serum TSH.
Acknowledgment
Financial disclosure of authors and reviewers: None
reported.
References
1. Kemp E, Waterman EA, Hawes BE, et al. The melanin
concentrating hormone receptor 1, a novel target of autoantibody
responses in vitiligo. J Clin Invest 2002;109:92330.
2. Jacobson DL, Gange SJ, Rose NR, Graham NM. Epidemiology and
estimated population burden of selected autoimmune diseases in
the United States. Clin Immunol Immunopathol 1997;84:22343,
doi:10.1006/clin.1997.4412.
3. Kemp EH, Waterman EA, Weetman AP. Autoimmune aspects
of vitiligo. Autoimmunity 2001;34:6577, doi:10.3109/08916930
108994127.
4. Boissy RE, Manga P. On the etiology of contact/occupational
vitiligo. Pigment Cell Res 2004;17:20814, doi:10.1111/j.1600-
0749.2004.00130.x.
5. Yu HS. Melanocyte destruction and repigmentation in vitiligo: a
model for nerve cell damage and regrowth. J Biomed Sci 2002;9(6
Pt 2):56473, doi:10.1007/BF02254984.
6. Nath SK, Majumder PP, Nordlund JJ. Genetic epidemiology of
vitiligo: multilocus recessivity cross-validated. Am J Hum Genet
1994;55:98190.
7. Gauthier Y, Cario-Andre M, Taieb A. A critical appraisal of vitiligo
etiologic theories. Is melanocyte loss a melanocytorrhagy? Pigment
Cell Res 2003;16:32232, doi:10.1034/j.1600-0749.2003.00070.x.
8. Cario-Andre M, Pain C, Gauthier Y, Taieb A. The melanocytor-
rhagic hypothesis of vitiligo tested on pigmented, stressed,
reconstructed epidermis. Pigment Cell Res 2007;20:38593.
9. Silva de Castro CC, do Nascimento LM, Walker G, et al. Genetic
variants of the DDR1 gene are associated with vitiligo in two
independent Brazilian population samples. J Invest Dermatol 2010;
130:18138, doi:10.1038/jid.2010.34.
10. Passi S, Grandinetti M, Maggio F, et al. Epidermal oxidative stress
in vitiligo. Pigment Cell Res 1998;11:815, doi:10.1111/j.1600-
0749.1998.tb00714.x.
11. Liu L, Li C, Gao J, et al. Promoter variant in the catalase gene is
associated with vitiligo in Chinese people. J Invest Dermatol 2010;
130:264753, doi:10.1038/jid.2010.192.
12. Westerhof W, dIschia M. Vitiligo puzzle: the pieces fall in place.
Pigment Cell Res 2007;20:34559.
13. Rose NR, Bona C. Defining criteria for autoimmune diseases
(Witebskys postulates revisited). Immunol Today 1993;14:4269,
doi:10.1016/0167-5699(93)90244-F.
14. Ochi Y, DeGroot LJ. Vitiligo in Graves disease. Ann Intern Med
1969;71:93540.
15. Dawber RPR. Integumentary associations of pernicious anemia.
Br J Dermatol 1969;82:2212, doi:10.1111/j.1365-2133.1970.
tb12428.x.
16. Macaron C, Winter RA, Traisman HS, et al. Vitiligo and juvenile
diabetes mellitus. Arch Dermatol 1977;113:15157, doi:10.1001/
archderm.1977.01640110035002.
17. Sharma VK, Dawn G, Kumar B. Profile of alopecia areata in
Northern India. Int J Dermatol 1996;35:227, doi:10.1111/j.1365-
4362.1996.tb01610.x.
18. Dunlop D. Eighty-six cases of Addisons disease. Br Med J 1963;2:
88791, doi:10.1136/bmj.2.5362.887.
19. Mihailova D, Grigorova R, Vassileva B, et al. Autoimmune thyroid
disease in juvenile chronic arthritis and systemic lupus erythema-
tosus. Adv Exp Med Biol 1999;455:5560, doi:10.1007/978-1-4615-
4857-7_8.
20. Alkhateeb A, Fain PR, Thody A, et al. Epidemiology of vitiligo and
associated autoimmune diseases in Caucasian probands and their
families. Pigment Cell Res 2003;16:20814, doi:10.1034/j.1600-
0749.2003.00032.x.
21. Liu JB, Li M, Yang S, et al. Clinical profiles of vitiligo in China: an
analysis of 3742 patients. Clin Exp Dermatol 2005;30:32731,
doi:10.1111/j.1365-2230.2005.01813.x.
22. Neufeld M, Maclaren NK, Blizzard RM. Two types of autoimmune
Addisons disease associated with different polyglandular auto-
immune (PGA) syndromes. Medicine 1981;60:35562, doi:10.1097/
00005792-198109000-00003.
23. Colton T. Statistics in medicine. Boston: Little Brown; 1974.
Vitiligo and Associated Autoimmune Disease 265
24. Zhang Z, Xu SX, Zhang FY, et al. The analysis of genetics and
associated autoimmune diseases in Chinese vitiligo patients.
Arch Dermatol Res 2009;301:16773, doi:10.1007/s00403-008-
0900-z.
25. Majumder PP, Nordlund JJ, Nath SK. Pattern of familial
aggregation of vitiligo. Arch Dermatol 1993;129:9948, doi:10.
1001/archderm.1993.01680290066010.
26. Handa S, Dogra S. Epidemiology of childhood vitiligo: a study of
625 patients from north India. Pediatr Dermatol 2003;20:20710,
doi:10.1046/j.1525-1470.2003.20304.x.
27. Onunu AN, Kubeyinje EP. Vitiligo in the Nigerian African: a study
of 351 patients in Benin City, Nigeria. Int J Dermatol 2003;42:800
2, doi:10.1046/j.1365-4362.2003.01908.x.
28. Ingordo V, Gentile C, Iannazzone S, et al. Vitiligo and
autoimmunity: an epidemiological study in a representative sample
of young Italian males. J Eur Acad Dermatol Venereol 2011;25:
1059, doi:10.1111/j.1468-3083.2010.03696.x.
29. Dave S, DSouza M, Thappa DM, et al. High frequency of thyroid
dysfunction in Indian patients with vitiligo. Indian J Dermatol
2003;48:6872.
30. Gawkrodger DJ, Ormerod AD, Shaw L, et al. Guideline for the
diagnosis and management of vitiligo. Br J Dermatol 2008;159:
105176, doi:10.1111/j.1365-2133.2008.08881.x.
31. Aoki Y, Belin RM, Clickner R, et al. Serum TSH and total T4 in the
United States population and their association with participant
characteristics: National Health and Nutrition Examination Survey
(NHANES 1999-2002). Thyroid 2007;17:121123, doi:10.1089/
thy.2006.0235.
32. Herd RM, Hunter JA. Familial halo naevi. Clin Exp Dermatol
1998;23:689, doi:10.1046/j.1365-2230.1998.00327.x.
266 Sawicki et al
Copyright of Journal of Cutaneous Medicine & Surgery is the property of Decker Publishing and its content
may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express
written permission. However, users may print, download, or email articles for individual use.