SA JOURNAL OF DIABETES & VASCULAR DISEASE
REVIEW
VOLUME 8 NUMBER 1 • MARCH 2011
9
APS type 1 without vitiligo and have, in some cases, preceded the
presentation. Some 63% of patients with APS type 1 and vitiligo
have antibodies against transcription factors SOX9 and SOX10.
Patients with APS types 2 and 3 more commonly have diabetes
but less commonly have vitiligo or alopecia. They do not have
chronic mucocutaneous candidiasis.
Treatment
1,3,4,11
The aim of treating vitiligo is to achieve repigmentation, but
treatment is unsatisfactory and in many cases, patients are advised
to practise cosmetic camouflage.Psychological support in the form
of explanation of the nature of the disease process and the available
therapies (and their limitations) is mandatory. Support groups and
psychological counselling may be required.
Repigmentation therapies
Narrowband UVB is safe and effective.
Psoralen plus phototherapy (PUVA) is indicated for those in whom
there is no other satisfactory option. Topical PUVA is indicated for
isolated macules, involving 1 to 2%, occasionally 5% of the body
surface, but the topical application of psoralens is hazardous and
may cause blistering of the skin due to phototoxicity. Oral PUVA is
effective but requires at least six month’s treatment and patients
need to have reasonable expectations. Although there is a 50 to
70% chance of repigmentation of the face, neck, trunk, upper
arms and legs, mucosal and acral vitiligo does not respond well.
Topical corticosteroids are effective, but patients should be
educated and monitored for side effects, such as atrophy and striae.
Topical immunosuppressants such as 0.1% tacrolimus have
resulted in repigmentation without the side effects associated with
topical steroids.
Surgical therapies, such as autologous transplantation may be
effective in vitiligo: that is stable for at least six months, that has
had an unsatisfactory response to medical therapy, in the absence
of Koebner phenomenon, that has no tendency to scar or keloid
formation, if the age of the patient is above 12 years.
Micropigmentation is the process whereby a non-allergenic
iron oxide pigment is tattooed into the skin to camouflage
depigmentation. Although the colour may not be an exact match,
the immediate results have an aesthetic advantage.
The 308-nm excimer laser is close to narrowband UVB and is
used for localised lesions. Focused microphototherapy irradiates
only the depigmented skin, but is expensive and requires trained
personnel.
Depigmentation
This may be considered in widespread disease where few normally
pigmented areas remain. It is vital that the patient realises that his/
her appearance will change dramatically and that he/she needs to
use lifelong photoprotection.
Conclusion
Vitiligo may therefore present alone or as part of a complex of
diseases (be it rarely). Therefore, when a patient presents with
vitiligo, associated conditions should be excluded. The management
of vitiligo itself does not differ when it occurs
de novo
or as
part of a spectrum of diseases, but the other conditions require
management.
The psychological impact of this disease on quality of life must
not be underestimated.
11
References
1.
Bolognia JL, Jorizzo JL, Rapini RP.
Dermatology
. 2nd edn. Spain: Mosby-Elsevier,
2008.
2.
Nordlund JJ. Not just skin deep: The complicated pathogenesis of vitiligo. http://
_
The_complicated_pathogenesis_of_vitiligo.html
3.
Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, Fitzpatrick TB.
Fitzpatrick’s Dermatology in General Medicine
. 5th edn. New York: McGraw-Hill,
1999.
4.
Burns T, Breathnach S, Cox N, Griffiths C.
Rook’s Textbook of Dermatology
. 8th
edn. Singapore: Wiley-Blackwell, 2010.
5.
Kovacs SO. Vitiligo.
J Am Acad Dermatol
1998;
38
; 647–668
6.
Basak PY, Adiloglu AK, Ceyhan AM, Tas TK Akkaya VB. The role of helper and
regulatory T cells in the pathogenesis of vitiligo.
J Am Acad Dermatol
2009;
60
;
256–260.
7.
Hann SK, Lee HJ. Segmental vitiligo: clinical findings in 208 patients
.
J Am Acad
Dermatol
1996;
35
; 671–674.
8.
Akay BN, Bozkir M, Anadolu Y, Gullu S. Epidemiology of vitiligo, associated
autoimmune diseases and audiological abnormalities: Ankara study of 80
patients in Turkey.
J Eur Acad Dermatol Venereol
2010;
24
; 1144–1150.
9.
Lerner AB, Kirkwood JM. Vitiligo and melanoma: can genetically abnormal
melanocytes result in both vitiligo and melanoma within a single family?
J Am
Acad Dermatol
1984;
11
; 696–701.
10. Betterle C, Zanchetta R. Update on autoimmune polyendocrine syndromes (APS).
Acta Bio Medica
2003;
74
: 9–33.
11. May W, Linthorst Homan MW, Spuls PI, de Korte J, Bos JD, Sprangers MA,
et al.
The burden of vitiligo: Patient characteristics associated with quality of life.
J Am
Acad Dermatol
2009;
61
; 411–420.
Figure 8.
Alopecia areata has been reported in up to 16% of vitiligo
patients.
