In contrast to albinism where melanocytes are present but unable to produce pigment, vitiligo is characterised by the loss of melanocytes, from affected areas.
- although histological and histochemical evidence point out that melanocytes are lost from the white patches, Tobin et al managed to culture some melanocytes from the white patches in people with long standing disease
- in some instances melanocytes appear to survive in hair follicles within the patches (1)
The aetiology of this condition is unknown, both environmental and genetic factors are believed to play an important role (1). Hypotheses which explain the pathogenesis of vtiligo include:
- autoimmune damage to melanocytes
- autocytotoxic - the autodestruction of melanocytes by toxic intermediates of melanin synthesis
- neurogenic dysfunction
- oxidative stress
- melanocyte detachment (5)
Of these, autoimmune hypothesis appears most likely, with anti-melanocyte antibodies being found in some patients, and the apparent association of vitiligo with autoimmune disorders including diabetes mellitus, pernicious anaemia, Addison's disease and autoimmune thyroiditis (5).
Many patients also show a positive family history. Around 20-30% of patients has first or second degree relatives with vitiligo (5)
- (1) The Vitiligo Society 2007. Vitiligo: Information for medical professionals
- (2) Silverberg NB et al. Tacrolimus ointment promotes repigmentation of vitiligo in children: a review of 57 cases. J Am Acad Dermatol. 2004 Nov;51(5):760-6
- (3) Murphy GF & Mihm MC, in Robbins Pathologic Basis of disease, ed. Cotran, Kumar & Robbins, 1989, 4th edition, Pub. WB Saunders, pg 1278-1279.
- (4) Kirby JTD, in Clinical Medicine, Ed. Kumar & Clark, 1994, 2nd edition, Pub. Balliere Tindall, pg 1045-1046.
- (5) Grimes P.E. New Insights and New Therapies in Vitiligo. JAMA 2005;293: 730-735