Conflicts of interest None declared.
Chemical leucoderma: a clinico-aetiological study of 864 cases in the perspective of a developing country
Article first published online: 8 SEP 2008
© 2008 The Authors. Journal Compilation © 2008 British Association of Dermatologists
British Journal of Dermatology
Volume 160, Issue 1, pages 40–47, January 2009
How to Cite
Ghosh, S. and Mukhopadhyay, S. (2009), Chemical leucoderma: a clinico-aetiological study of 864 cases in the perspective of a developing country. British Journal of Dermatology, 160: 40–47. doi: 10.1111/j.1365-2133.2008.08815.x
- Issue published online: 15 DEC 2008
- Article first published online: 8 SEP 2008
- Accepted for publication 22 May 2008
- chemical leucoderma;
- contact leucoderma;
- occupational leucoderma;
Background Chemical leucoderma, often clinically mimicking idiopathic vitiligo and other congenital and acquired hypopigmentation, has been increasing rapidly in incidence in developing countries such as India.
Objectives This study attempts to detect clinical and epidemiological patterns of chemical leucoderma.
Methods Detailed history-taking, especially of exposure to contributory chemicals, clinical examination, relevant investigations, data recording and analysis were done.
Results In a total of 864 cases of chemical leucoderma, 65·6% cases started de novo and vitiligo patches were pre-existing in the remaining cases. Patches were limited to the contact area in 73·7% but had spread to remote areas in 26·3% cases. The face (41·1%) and scalp (5·9%) were the commonest and least involved sites. Confetti macules were seen in 89% and pruritus was complained of in 21·8%. Aetiological agents identified were hair dye 27·4% (21% self-use; 6·4% not self-use), deodorant and spray perfume 21·6%, detergent and cleansers 15·4%, adhesive bindi 12%, rubber chappal 9·4%, black socks and shoes 9·1%, eyeliner 8·2%, lipliner 4·8%, rubber condoms 3·5%, lipstick 3·3%, fur toys 3·1%, toothpaste 1·9%, insecticides 1·7%, ‘alta’ 1·2%, amulet string colour 0·9%. Therapeutic response was much better in ‘pure’ chemical leucoderma (73·4%) than in those with co-existing vitiligo (20·9%).
Conclusions Chemical leucoderma, a disease of mostly industrial origin in developed countries, may be induced by common domestic products in developing countries. Diagnosis and differentiation from other causes of hypopigmentation can be done confidently by following the clinical criteria as proposed. The therapeutic response of chemical leucoderma is better than that of vitiligo.