The treatment of postburn hypopigmentation was primarily surgical before the advent of new technologies. Medical devices and therapies are emerging to manage scar sequelae that can be disfiguring and associated with severe psychosocial impact. These innovations have been poorly investigated for hypopigmentation, but they represent a real hope. We reviewed all articles published on Pubmed up to June 2022. Included studies had to specifically focus on treating postburn hypopigmented scars. All articles evaluating transient solutions such as make-up, and articles describing inflammation-linked hypopigmentation with no etiological details or no burn injury history were excluded. Through this review, we have highlighted 6 different types of nonsurgical treatments reported in postburn leukoderma potentially allowing definitive results. Electrophoto-biomodulation or E light (combining intensive pulsed light, radiofrequency, and cooling), topical daylight psoralen UVA therapy, and lasers (fractional lasers using pulse energies or CO2FL devices, lasers-assisted drug delivery as local bimatoprost and tretinoin or pimecrolimus) have been explored with encouraging results in hypopigmented burns. Finally, other promising medical strategies include using FK506, a nonsteroidal anti-inflammatory drug, to induce melanogenesis or using melanocyte-stimulating hormones with fractional laser-assisted drug deliveries, which are expected to emerge soon.

BACKGROUND: Metabolic syndrome (MetS) has been associated with various skin conditions including vitiligo. However, the association between these 2 conditions has yet to be determined by quantitative meta-analysis.
OBJECTIVE: The aim of this paper was to determine the association between vitiligo and metabolic syndrome via systematic review and meta-analysis.
METHODS: A systematic literature search of Pubmed, Embase, Cochrane, and Web of Science was performed for all published literature prior to August 16, 2020. Case control and prospective cross-sectional studies analyzing the association between vitiligo and MetS were included in this review. The primary outcome measures include the type of vitiligo, diagnostic criteria for MetS, components of MetS (waist circumference, blood pressure, triglycerides, fasting glycemic index, and high-density lipoprotein cholesterol), low-density lipoprotein cholesterol levels, and BMI. A meta-analysis was performed to evaluate the prevalence and association of MetS in patients with vitiligo.
RESULTS: A total of 6 studies (n=734 participants) meeting eligibility criteria were included for systematic review and meta-analysis. The pooled prevalence of MetS in patients with vitiligo was (0.296, 95% CI 0.206, 0.386; P<.001). Patients with vitiligo were no more likely to develop MetS compared to control patients (odds ratio 1.66, 95% CI 0.83, 3.33; P=.01). A leave-one-out sensitivity analysis showed a significant association between MetS and vitiligo (P<.001). Significant elevations in fasting glycemic index (mean difference 5.35, 95% CI 2.77, 7.93; P<.001) and diastolic blood pressure (mean difference 1.97, 95% CI 0.02, 3.92; P=.05) were observed in patients with vitiligo compared to control patients.
CONCLUSIONS: The association between vitiligo and metabolic syndrome carries important clinical implications. Dermatologists and other multidisciplinary team members should remain vigilant when treating this patient population in order to prevent serious cardiovascular complications that may arise as a result of metabolic disease.

BACKGROUND: The autologous noncultured melanocyte keratinocyte transplant procedure (MKTP) has emerged as a popular grafting technique with proven efficacy for achieving repigmentation. However, there remains no consensus regarding the optimal recipient-to-donor (RD) ratio required to achieve acceptable repigmentation. In this retrospective cohort study of 120 patients, we sought to examine whether expansion ratios impact the repigmentation success rates following MKTP.
RESULTS: A total of 69 patients (mean [SD] age was 32.4 [14.3] years, mean follow-up was 30.4 [22.5] months, 63.8% were male; 55% were dark-skinned individuals [Fitzpatrick IV-VI]) were included. The mean percent change in the Vitiligo Area Scoring Index (VASI) was 80.2 (±23.7; RD of 7.3) in patients with focal/segmental vitiligo (SV), 58.3 (±33.0; RD of 8.2) in those with non-segmental vitiligo (NSV), and 51.8 (±33.6; RD of 3.7) in those with leukoderma and piebaldism. Focal/SV was positively associated with a higher percent change in VASI (parameter estimate: 22.6, p value <0.005). In the SV/focal group, non-white patients had a higher RD ratio compared to White individuals (8.2 ± 3.4 vs. 6.0 ± 3.1, respectively, p value = 0.035).
CONCLUSIONS: In our study, we found that patients with SV were significantly more likely to achieve higher repigmentation rates compared to those with NSV. Although repigmentation rates were higher in the low expansion ratio group than in the high expansion ratio group, we did not observe a significant difference between the two groups.
CONCLUSIONS: MKTP is an effective therapy for restoring repigmentation in patients with stable vitiligo. Therapeutic response of vitiligo to MKTP appears to be influenced by the type of vitiligo, rather than a specific RD ratio.

Oxidative metabolism of rhododendrol (RD), a skin-whitening ingredient, by tyrosinase has caused leukoderma in a certain population of Japanese consumers. Toxic RD metabolites and reactive oxygen species are proposed causes for the melanocyte death. However, the mechanism by which reactive oxygen species are produced during RD metabolism remains elusive. Some phenolic compounds are known to act as suicide substrates for tyrosinase, resulting in release of a copper atom and hydrogen peroxide during its inactivation. We hypothesized that RD may be a suicide substrate for tyrosinase and that the released copper atom may be responsible for the melanocyte death through hydroxyl radical production. In line with this hypothesis, human melanocytes incubated with RD showed an irreversible decrease in tyrosinase activity and underwent cell death. A copper chelator, d-penicillamine, markedly suppressed the RD-dependent cell death without significantly affecting the tyrosinase activity. Peroxide levels in RD-treated cells were not affected by d-penicillamine. Given the unique enzymatic properties of tyrosinase, we conclude that RD acted as a suicide substrate and resulted in release of a copper atom and hydrogen peroxide, which would collectively impair melanocyte viability. These observations further imply that copper chelation may alleviate chemical leukoderma caused by other compounds.

Vitiligo patients may desire laser hair removal, skin rejuvenation, vascular treatments, and other laser or intense pulsed light (IPL) assisted treatments. However, there is a risk of inducing new depigmented patches (Koebner phenomenon). In absence of guidelines on the safe use of laser or IPL in vitiligo patients, dermatologists tend to be reluctant to administer these treatments. The aim of this survey study was to provide an estimation of the occurrence and related risk factors of laser/IPL-induced leukoderma or vitiligo. A cross-sectional survey study was performed among 15 vitiligo experts from 11 countries, with 14 questions about affected patients, involved laser/IPL treatments and the physicians\' approach. In a total of 11,300 vitiligo patients, laser/IPL-induced leukoderma or vitiligo was reported in 30 patients (0.27%). Of these, 12 (40%) patients had a medical history of vitiligo and seven (58%) of these patients had stable (> 12 months) vitiligo before the treatment. Most frequently reported were hair removal procedures and localization of the face and legs. Side effects like blistering, crusting, and erosions occurred in 56.7% of the cases. These vitiligo experts based their advice on the risk of the laser treatment on stability of the vitiligo (43%) and activity signs (50%), and 50% discuss the risks before starting a laser treatment. Relevant activity signs are the Koebner phenomenon (57.1%), confetti-like lesions (57.1%) and hypochromic borders (50%). Laser-induced leukoderma or vitiligo is an uncommon phenomenon. Remarkably, a minority had a medical history of vitiligo of which 58% were stable. Consequently, most cases could not have been prevented by not treating vitiligo patients. However, a majority had laser/IPL-induced skin damage. Therefore, caution is advised with aggressive settings and test-spots prior to the treatment are recommended. This study showed significant variation in the current recommendations and approach of vitiligo experts regarding laser/IPL-induced leukoderma or vitiligo.

BACKGROUND: The tyrosinase inhibitor rhododendrol (RD), used as a skin whitening agent, reportedly has the potential to induce leukoderma.
OBJECTIVE: Although an immune response toward melanocytes was demonstrated to be involved in leukoderma, the molecular mechanism is not fully understood.
METHODS: We hypothesized that if RD is a pro-hapten and tyrosinase-oxidized RD metabolites are melanocyte-specific sensitizers, the sensitizing process could be reproduced by the human cell line activation test (h-CLAT) cocultured with melanocytes (h-CLATw/M) composed of human DC THP-1 cells and melanoma SK-MEL-37 cells. Cell surface expression, ROS generation and ATP release, mRNA expression, and the effects of several inhibitors were examined.
RESULTS: When RD was added to the h-CLATw/M, the expression of cell-surface CD86 and IL-12 mRNA was greatly enhanced in THP-1 cells compared with those in the h-CLAT. The rapid death of melanoma cells was induced, with ROS generation and ATP release subsequently being greatly enhanced, resulting in the cooperative upregulation of CD86 and IL-12. Consistent with those observations, an ROS inhibitor, ATP receptor P2X7 antagonist, or PERK inhibitor antagonized the upregulation. CD86 upregulation was similarly observed with another leukoderma-inducible tyrosinase inhibitor, raspberry ketone, but not with the leukoderma noninducible skin-whitening agents ascorbic acid and tranexamic acid.
CONCLUSIONS: RD is a pro-hapten sensitizer dependent on tyrosinase that induces ROS generation and ATP release from melanocytes for CD86 and IL-12 upregulation in DCs, possibly leading to the generation of tyrosinase-specific cytotoxic T lymphocytes. The coculture system h-CLATw/M may be useful for predicting the sensitizing potential to induce leukoderma.

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Melanocyte cell death can lead to various melanocyte-related skin diseases including vitiligo and leukoderma. Melanocytotoxic chemicals are one of the most well-known causes of nongenetic melanocyte-related diseases, which induce melanocyte cell death through apoptosis. Various chemicals used in cosmetics, medicine, industry and food additives are known to induce melanocyte cell death, which poses a significant risk to the health of consumers and industrial workers. This review summarizes recently reported melanocytotoxic chemicals and their mechanisms of toxicity in an effort to provide insight into the development of safer chemicals.

Leukoderma, or hypomelanosis of the skin, can occur in response to various chemical and pharmacologic substances ranging from topical medications to optic preparations and systemic medications. In this case report, we present a 78-year-old man with a history of restless leg syndrome (RLS) who had been using rotigotine transdermal patches once daily for 1 year and developed leukoderma on the bilateral anterior shoulders in the area of patch application. Histopathologic examination showed an absence of melanocytes at the dermal-epidermal junction confirmed by Melan A stain. While the patient was not bothered by the depigmentation and elected to continue the rotigotine patch for his RLS, this case highlights leukoderma as a potential side effect of dopamine transdermal patches and offers insight into the potential mechanism of hypopigmentation in response to dopamine agonism.

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.