Raccoon-like periorbital leukoderma from contact with swim goggles

A 12-year-old girl developed a periorbital leukoderma from contact with swim goggles. She had worn the same goggles the preceding year and re-used them after the leukoderma had cleared without any ill effects. The hypopigmentation was believed to be caused by the leakage of breakdown products in the neoprene rubber or glue. These breakdown products may have caused a toxic rather than an allergic reaction on skin contact, inhibiting melanin production possibly by competitive inhibition of tyrosine oxidation. These chemical compounds probably leaked from the goggles and were eventually exhausted. This possibility may explain why the leukoderma did not recur after re-use of the goggles.     

Chemical Leukoderma Improved by Low-dose Steroid Pulse Therapy

Chemical leukoderma occurs due to the toxic effect of a specific chemical preceding allergic contact dermatitis. The mechanism is either destruction or inhibition of melanocytes by the offending substance. Clinicohistopathologically, no absolute criteria can differentiate chemical leukoderma from vitiligo. However, chemical leukoderma can be diagnosed clinically by a history of repeated exposure to a known or suspected depigmenting agent at the primary site. There is no agreed treatment guideline for chemical leukoderma. We report a healthy 51-year-old man who had multiple hypopigmented macules and patches on his face, neck, arms and legs after exposure to occupationally related chemicals. The lesions were recalcitrant to topical corticosteroids, but they showed much improvement after 3 cycles of systemic steroid pulse therapy. We suggest this therapy may be a good treatment option for chemical leukoderma.     

Spontaneous Contraction of Leukodermic Patches in Waardenburg Syndrome

Waardenburg Syndrome is an autosomal dominantly inherited disorder with variable penetrance (1–5). It is a rare disorder with an estimated frequency of 1:20,000 in Kenya (East Africa) and 1:40,000, in the Netherlands presenting with or without deafness. The frequency with deafness is lower, estimated at 1:50,000 to 1:212,000 (1, 2). The major characteristic features are as follows, with reported incidences in parenthesis: 1) Dystopia canthorum (99%); 2) synophrys (17%–69%); 3) broad nasal root (78%); 4) depigmentation of hair, skin, or both (17%–58% with white forelock); 5) heterochromic or hypochromic irides (greater than 20%); 6) congenital deafness (9%–38%) (1–7). Genetic heterogeneity has led to classification of affected families as type I, with dystopia canthorum, or type II, without dystopia canthorum (2, 6). Piebaldism and Woolf's Syndrome can present with pigmentary changes which are similar to Waardenburg Syndrome (2, 3, 8). Woolf's Syndrome also includes deafness (9). However, the distinguishing structural ophthomologic abnormalities of dystopia canthorum, broad nasal root, and synophrys are not found in either piebaldism or Woolf's Syndrome (2, 3, 8, 9). The congenital patterns of leukoderma in both piebaldism and Waardenburg Syndrome has been believed to be stable throughout the lifetime of the affected individuals (2, 10). We report an otherwise typical family with Waardenburg Syndrome, type I, in which 2 members atypically demonstrate spontaneous pigmentation and contraction of congenital leukodermic patches. To our knowledge, this has not been previously reported in Waardenburg Syndrome (1, 2, 6, 10).     

Frontiers and controversies in the pathobiology of vitiligo: separating the wheat from the chaff

Abstract:  The pathogenesis of vitiligo is complex and not well understood. Genes play a role in all aspects of vitiligo pathogenesis, and studies are ongoing to identify these genes and understand their biology. There is a body of interlocking, compelling evidence supporting an autoimmune basis for most or all cases of generalized vitiligo. The development of an autoimmune disease generally involves three components; the immune system, environmental triggers and other exogenous precipitating factors, and the target tissue. In vitiligo, precipitating factors could induce melanocyte damage in genetically susceptible individuals and consequent cell death, loss of tolerance, and induction of melanocyte-directed autoimmunity. Future research will more precisely define the multiple biological events that regulate development of vitiligo.     

Chronic White Plaque of the Vulva in Postmenopausal Women

We report 13 cases of white lesions of the vulva in postmenopausal women. Nine cases had clinical and histological features typical of lichen sclerosus et atrophicus (LSA). Two cases exhibited mild histological changes suggestive of LSA. Two cases had normal-appearing histology without significant histological changes. Considering the relatively short duration of the disease and relatively small lesions in the last two cases, they may be considered to represent the initial stage of LSA.     

Postburn leukoderma successfully treated with topical daylight psoralen UVA therapy

Postburn leukoderma is challenging to treat with different surgical and nonsurgical treatments resulting in variable outcomes. We report a case of a 56‐year‐old female with postburn leukoderma treated successfully with topical daylight psoralen UVA therapy for 6 months. The treatment was well tolerated and showed excellent improvement. In conclusion, we report the successful use of topical daylight PUVA for postburn leukoderma with almost complete repigmentation. This is a simple, convenient, and cheap nonsurgical treatment option.     

Vitiligo-like manifestations of graft-versus-host disease in a pediatric population

Vitiligo-like changes are an uncommon cutaneous manifestation of graft-versus-host disease (GVHD). We report three cases and review the literature of pediatric patients with vitiligo-like changes associated with GVHD. Improved characterization of this phenomenon may lend insight into the biologic pathways that underlie both vitiligo and GVHD.     

Contact Leukoderma of the Scalp or an Unusual Variant of Vitiligo?

Contact leukoderma due to hair dyes is strongly suspected in patients presenting with depigmented patches sharply localized to the scalp. We describe three patients with a striking pattern of depigmentation, which stopped abruptly at the hair margins. However, no definite correlation with the use of hair dyes could be made in any of them. Our cases represent an unusual pattern of vitiligo of the scalp, which seems to have been previously attributed mainly to hair colorants. Careful examination of the lesions on the scalp may reveal more cases with this pattern.     

Different effects of five depigmentary compounds,rhododendrol, raspberry ketone,monobenzone, rucinol and AP736 on melanogenesis and viability of human epidermal melanocytes

Numerous medications are used to treat hyperpigmentation. However, several reports have indicated that repeated application of some agents, such as rhododendrol (RD), raspberry ketone (RK) and monobenzone (MB), can be toxic to melanocytes. Although these agents had severe side effects in human trials, no current in vitro methods can predict the safety of such drugs. This study assessed the in vitro effects of five depigmentary compounds including leukoderma‐inducing agents. In particular, we determined the effects of different concentrations and exposure times of different depigmentary agents on cell viability and melanogenesis in the presence and absence of ultraviolet B (UVB) radiation. Concentrations of RD, RK and MB that inhibit melanogenesis are similar to concentrations that are cytotoxic; however, concentrations of rucinol (RC) and AP736 that inhibit melanogenesis are much lower than concentrations that are cytotoxic. Furthermore, the concentrations that cause toxic effects depend on exposure duration, and prolonged exposure to RD, RK and MB had more cytotoxic effects than prolonged exposure to RC and AP736. The cytotoxic effects of RD and RK appear to be mediated by apoptosis due to increased expression of caspase‐3 and caspase‐8; UVB radiation increased the cytotoxicity of these agents and also increased caspase activity. Our results indicate that different leukoderma‐inducing compounds have different effects on the viability of normal epidermal melanocytes and suggest that the in vitro assay used here can be used to predict whether an investigational compound that induces leukoderma may lead to adverse effects in human trials.     

Expression of discoidin domain receptor 1 and E-cadherin in epidermis affects melanocyte behavior in rhododendrol-induced leukoderma mouse model

Vitiligo is a depigmentation disease characterized by gradual loss of melanin and melanocytes from the epidermis. The mechanism of melanocyte loss is not yet known. In this report, we showed that the expression of discoidin domain receptor 1 and E-cadherin, known adhesion molecules, was variable or absent in the epidermis of rhododendrol-induced leukoderma (RDIL) mice during the depigmentation process. Our findings suggest that melanocyte damage by rhododendrol promotes reduction of adhesion molecules not only in melanocytes but also in keratinocytes, and this is associated with the detachment of melanocytes from the basal layer.     

威灵仙致接触性皮炎后色素异常

报告1例威灵仙致接触性白斑和色素性接触性皮炎。患者男，34岁。外敷威灵仙5个月后左腕关节屈侧皮肤出现色素减退斑、周围不规则色素沉着斑8个月。皮肤科检查：左腕关节屈侧皮肤见面积约4cm×4cm大不规则白斑，其周围有宽度不同、颜色均一的色素沉着斑，边界清楚。其他部位皮肤未见白斑或色素沉着斑。行威灵仙乙醇和水提物斑贴试验均为阳性。诊断：威灵仙致接触性白斑和色素性接触性皮炎。     

伊藤痣上继发色素减退斑1例

报告1例伊藤痣上继发色素减退斑。患者女,43岁。7个月前原左颈肩区先天性蓝色斑片中开始出现色素改变：自后体表正中线向左,呈瓷白色、天蓝色及黄蓝色逐渐改变。天蓝色皮损组织病理检查示：表皮基底层黑素细胞消失．真皮浅层及中层少量梭形黑素细胞及较多形态各异的载色素细胞。表皮轻度海绵形成、角化不全、角质形成细胞局灶性坏死及基底层空泡变性。表、真皮交界处淋巴细胞浸润。诊断为继发于伊藤痣上的晕痣（halonevus）和晕皮炎（halo dermatitis）。