About: Leukoderma is a research topic. Over the lifetime, 386 publications have been published within this topic receiving 4288 citations. The topic is also known as: hypomelanosis & Hypopigmentation.
TL;DR: The data suggests that tyrosinase-related protein-1, rather than tyOSinase, facilitates toxicity, possibly by catalytic conversion of the compounds, which results in the generation of radical oxygen species.
Abstract: Vitiligo is an acquired depigmentary disorder of the skin that results from the selective destruction of melanocytes, generally during the second decade of life and affecting approximately 1% of the population worldwide. Loss of cutaneous pigment appears to render the skin susceptible to premature aging and cancer. In addition this disease can be socially devastating for afflicted individuals. The etiology of vitiligo is poorly understood. The present dogma suggests that genetic factors render the melanocyte fragile thus predisposing individuals to developing vitiligo. When subjected to instigating factors, these susceptible, fragile melanocytes undergo apoptosis. Autoimmune factors then perpetuate the removal of the melanocyte component from the skin. In the majority of cases the instigating factors are not known (idiopathic vitiligo), however a small sub-set of individuals develop contact/occupational vitiligo following exposure to particular chemicals. Many of these chemicals have been implicated in both contact/occupational vitiligo and chemical leukoderma. Both conditions present with well-defined, depigmented skin lesions that develop following exposure. Only in the case of vitiligo does the depigmentation spread beyond the areas of contact, probably via an immune-mediated mechanism. The largest class of chemicals known to trigger contact/occupational vitiligo is the phenolic/catecholic derivatives. Many have been demonstrated to be preferentially cytotoxic to melanocytes, with high-dose exposure resulting in the initiation of apoptosis. Phenolic/catecholic derivatives are structurally similar to the melanin precursor tyrosine, and therefore tyrosinase was originally implicated as a mediator of cytotoxicity. However, our data suggests that tyrosinase-related protein-1, rather than tyrosinase, facilitates toxicity, possibly by catalytic conversion of the compounds, which results in the generation of radical oxygen species. The ensuing oxidative stress then triggers activation of cellular free radical scavenging pathways to prevent cell death. Genetic inability of melanocytes to tolerate and/or respond to the oxidative stress may underlie the etiology of contact/occupational vitiligo.
TL;DR: Autologous minigrafting is suggested as an alternative for treating localized vitiligo, particularly when other medical therapeutic attempts have failed in repigmenting this often refractory condition.
Abstract: • Autologous minigrafting has been reported as an effective method for repigmenting diverse types of stable leukoderma A group of 22 patients with localized vitiligo, 17 segmental and five focal, who are under treatment with this method, are described Thirteen patients attained a 90% to 100% repigmentation, two others achieved a partial improvement, and five patients had a positive test area indicating the possibility of repigmentation by means of this procedure Only two patients had a negative test with minigrafts and, consequently, they were left untreated Autologous minigrafting is suggested as an alternative for treating localized vitiligo, particularly when other medical therapeutic attempts have failed in repigmenting this often refractory condition (Arch Dermatol1988;124:1649-1655)
TL;DR: The technique known as autologous minigrafting has proven useful and reliable for repigmenting diverse types of leukoderma and a few refinements of this technique are described as discussed by the authors.
Abstract: The technique known as autologous minigrafting is reviewed. This procedure has proven useful and reliable for repigmenting diverse types of leukoderma. A few refinements of this technique are described. These refinements were used in six patients who were successfully repigmented. Causes of pigment loss in these cases included thermal burns, contact with monobenzyl ether of hydroquinone, chronic discoid lupus erythematosus, and segmental vitiligo.
TL;DR: Some of the methods currently available and the potential use of newer technologies for repigmenting vitiligo and other types of stable leukoderma are reviewed.
Abstract: When these trials fail, surgical methods for repigmenting leukoderma should be considered such as placing a new source of pigment cells to reinitiate melanogenesis within the affected areas. This article will review some of the methods currently available and the potential use of newer technologies for repigmenting vitiligo and other types of stable leukoderma
TL;DR: In a Negro woman with long-standing leukoderma that followed a chemical burn, nine 1- and 2-mm diameter normal-skin autografts were transplanted into the leukodermic site and the grafts retained their pigment-forming capacity and showed temporary hyperpigmentation.
Abstract: In a Negro woman with long-standing leukoderma that followed a chemical burn, nine 1- and 2-mm diameter normal-skin autografts were transplanted into the leukodermic site. The grafts retained their pigment-forming capacity and showed temporary hyperpigmentation. The "pigment spread phenomenon" was evidenced by 1-mm wide zones of melanosis that developed around each autograft in the leukodermic skin. The melanotic annulus about the first autograft has thus far persisted for two years. The observations indicate donor autograft dominance in leukoderma in contradistinction to recipient site dominance in vitiligo.