[Acquired leukomelanoderma caused by topical depigmenting agents].

Three patients applied a cream containing monobenzyl ether (MBEH) (2 cases) or monomethyl ether of hydroquinone (1 case) on acquired hyperpigmentary disorders. We observed depigmentation locally and at a distance from the treated areas. The depigmenting ability of MBEH was founding in 1939 by Oliver, at the time of an occupational accident. This happended among black workers wearing rubber gloves containing MBEH as an anti-oxydant. The depigmenting ability has been used as a treatment for acquired hyperpigmentary disorders, but adverse effects were observed--irritation and local sensitization--depigmentation locally and at a distance from the treated areas--melanoleukodermia among asiatics--no repigmentation: therefore treatment with MBEH has been used by Mosher in extensive vitiligo on the unaffected areas. As regards to the mechanism of these pigmentary disorders, knowledge is incomplete, particulary concerning depigmentation at a distance: hypothesis was: destruction by degrees of the melanocytes, as in Lerner's theory concerning vitiligo, autoimmune mechanism? Genetic predisposition? Electron microscopy shows cellular disturbances in melanosomes and degeneration of intracytoplasmic membrane thus killing cell. The physiopathology was the work of Riley: he has shown that MBEH is selectively incorporated into cultured melanocytes. Evidence of free radical formation has been obtained in guinea-pig skin treated with this agent. Cultured melanocytes are irreversibly damaged by exposure to low concentrations. Riley postulates that these compounds diffuse into melanosomes of the pigment cell where they are oxidized by tyrosinase to produce free radicals; the latter bring about lipid peroxidation of cell membrane lipids, thus killing the cell.