Review of the etiopathomechanism of vitiligo: a convergence theory.
Vitiligo is an acquired melanin pigmentary disorder manifesting itself by expanding depigmented lesions of the skin. To date, the etiopathomechanism of vitiligo has not been convincingly elucidated and a number of seemingly mutually opposed hypotheses with equal likelihood still coexist. Concurrent theories on vitiligo etiology, together with supportive evidence, are reviewed here. Due to the observed variation in clinical manifestations of the disease, it seems likely that the etiology of vitiligo may differ among patients. Therefore several theories on vitiligo etiopathogenesis have been combined to formulate a convergence theory for vitiligo, also presented in this article. This theory states that stress, accumulation of toxic compounds, infection, autoimmunity, mutations, altered cellular environment and impaired melanocyte migration and/or proliferation can all contribute to vitiligo etiopathogenesis in varying proportions.
Le Poole
I C
IC
Department of Dermatology, Amsterdam University, The Netherlands.
Das
P K
PK
van den Wijngaard
R M
RM
Bos
J D
JD
Westerhof
W
W
D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology; D002455:Cell Division; D002465:Cell Movement; D005609:Free Radicals; D006801:Humans; D007239:Infections / Q000150:complications / Q000276:immunology; D015603:Keratinocytes / Q000378:metabolism / Q000473:pathology; D008543:Melanins / Q000378:metabolism; D008544:Melanocytes / Q000276:immunology / Q000473:pathology; D008954:Models, Biological; D015995:Prevalence; D013312:Stress, Physiological / Q000150:complications; D014820:Vitiligo / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000473:pathology
D005609:Free Radicals; D008543:Melanins