白癜风氧化应激机制及抗氧化治疗进展

白癜风是一种常见的色素脱失性疾病,临床上以表皮黑素细胞破坏缺失而出现色素脱失斑为主要特征.其发病机制不明.近年来发现,通过体内外各种因素,引起白癜风患者体内的氧化-抗氧化系统平衡失调,导致体内的活性氧簇或活性氮簇增加,引起氧化应激,造成黑素细胞损伤.随着研究的深入,一些人工或天然抗氧化剂应用于白癜风的临床治疗,如槲皮素、胎盘制剂、银杏叶提取液等.     

下颌部白癜风和斑秃并发1例

白癜风是一种后天性色素脱失性皮肤病,可并发银屑病、扁平苔藓等[1-3] .但白癜风与斑秃同患一处者较少见,现报告1例.患者男,34岁.因下颌部色素脱失斑中胡须脱落1个月,于2005年2月就诊.患者约半年前下颌须部出现色素脱失斑,后色素脱失斑处毛发也逐渐变白.     

白癜风与黑素瘤关系的研究进展

白癜风是以皮肤黑素细胞破坏导致的获得性色素脱失性疾病;黑素瘤是皮肤、黏膜黑素细胞异常增生导致的一种恶性肿瘤。近年来研究发现黑素瘤患者的白癜风发生率远远高出正常人群,这一现象的发生可能是机体抗黑素瘤的细胞及体液免疫应答作用于正常黑素细胞的结果。     

白癜风的药物及外科治疗进展

正白癜风(Vitiligo)是一种常见的色素脱失性皮肤病,表现为皮肤出现局限性或泛发性色素脱失斑。本病损害外观容貌,严重影响患者的生活质量。所以研究白癜风的治疗具有十分深远的意义。近些年随着对白癜风发病机制的深入研究,治疗上也出现了许多新药物及新技术,在一定程度上为白癜风患者带来了新的曙光。本文对于近些年白癜风的药     

白癜风相关细胞因子在黑素细胞自噬中的作用

白癜风是后天性黑素细胞特发性损伤和功能异常进而色素脱失的全身性皮肤疾病，白癜风的确切发病机制至今尚未清楚。细胞因子是由多种组织细胞（主要为免疫细胞）合成和分泌的小分子多肽或糖蛋白，主要参与调节免疫应答、免疫细胞分化及介导炎症反应等，在白癜风中发挥重要作用，机体免疫调节异常可导致炎性介质过度表达，炎性反应扩大，损伤皮肤黑素细胞导致皮肤色素脱失，白斑形成。几个与白癜风相关的细胞因子在黑素细胞自噬中起重要作用。     

细胞黏附分子与白癜风

白癜风是一种色素脱失性疾病，临床上表现为以皮肤黑素细胞破坏缺失而出现色素脱失斑为特征。导致白癜风黑素细胞破坏的分子机制目前尚未阐明。近年来有关细胞黏附分子在白癜风发病中的作用研究日益增多。研究细胞黏附分子与白癜风发病的相互关系，可以对白癜风的发病机制进行更深入的探讨。     

中草药黄酮类提取物对白癜风抗氧化应激作用机制的研究进展

白癜风是一种获得性皮肤黏膜色素脱失性皮肤病,氧化应激在白癜风发生和发展中扮演了重要角色。中草药黄酮类提取物在皮肤细胞中具有强效抗氧化应激作用,其机制主要包括直接清除活性氧簇(ROS)、鳌合金属离子和调节抗氧化系统;具有潜在的白癜风临床治疗价值。本文主要综述中草药黄酮类提取物在皮肤细胞中抗氧化应激作用机制。     

白癜风患者心理研究进展

白癜风是一种色素脱失性疾病，累及皮肤、黏膜和毛发，临床表现为白色的斑片和白发，影响外观。尤其是暴露部位的白癜风，对患者的心理产生很大的影响。     

蕈样肉芽肿合并白癜风2例报告

目的：探讨蕈样肉芽肿（MF）合并白癜风的机制。方法：对2例MF色素脱失处和色素正常处皮肤活检，进行HE和Fontans染色，检查黑素细胞的分布情况。结果：2例患者的皮肤色素脱失处基底层均未见黑素颗粒，符合白癜风的病理改变；色素正常处皮肤的表皮基底层有较多黑素颗粒存在，真皮上部有黑素颗粒滴落和散在噬黑素细胞。2例患者色素脱失与色素正常处真皮内淋巴细胞浸润和分布情况不一致。结论：MF患者皮肤黑素细胞的缺失可能与其被淋巴细胞的破坏有关，而物理治疗可能促进了这种变化。     

白驳丸治疗白癜风的疗效观察

白癜风是由于皮肤黑素细胞减少或缺失而引起的色素脱失斑。易诊断，难治疗^[1]。本病虽对身体并无大碍，但给患者造成的精神及思想压力很大，影响工作、学习及社会交往。我们使用本院制剂白驳丸内服治疗白癜风，取得了一定的疗效，现报告如下。     

Animal models of vitiligo: Matching the model to the question

Vitiligo is an autoimmune disease of the skin that is characterized by patchy depigmentation (i.e., white spots) and results from the loss of melanocytes, which are pigment-producing cells. The pathogenesis of human vitiligo consists of an interaction between intrinsic melanocyte defects, environmental factors, and autoimmune mechanisms that target these cells for destruction. Human clinical and translational studies have outlined pathways that are important in human disease; however, combining human correlative studies with mechanistic studies in representative preclinical animal models is a powerful approach to study disease pathogenesis and develop new treatments. Because of the complex pathogenesis of vitiligo, it is unlikely that any one single animal model will adequately reflect all factors implicated in the initiation, progression, and maintenance of the disease. Therefore, vitiligo is best modeled by multiple systems—each with its strengths and weaknesses—that allow insight into specific components of vitiligo pathogenesis. In this paper, we describe some of the available animal models that have been developed to study vitiligo.     

白癜风皮损中非黑素细胞进展

白癜风的发病机制尚未完全明了.其发病除黑素细胞异常外,还涉及非黑素细胞的变化,近年来非黑素细胞在白癜风中的研究逐渐增多.研究表明,一些皮肤非黑素细胞如角质形成细胞、朗格汉斯细胞、成纤维细胞等与黑素细胞关系密切,这些细胞影响黑素细胞的迁移、增殖、分化等功能.白癜风皮损中非黑素细胞超微结构的异常和分泌细胞因子的变化可影响黑素细胞的活性及凋亡,影响皮肤色素生成,从而参与白癜风发病.     

白癜风动物模型研究进展

白癜风的病因和发病机制尚未完全阐明,遗传、自身免疫、氧化应激和环境等多种因素参与了白癜风的发病, 建立适宜的白癜风动物模型可为研究其发病机制和开发新疗法奠定基础。相较自发性白癜风模型,诱导性模型能更好的模拟白癜风发病的病理过程及影响因素。本文着重综述了诱导性白癜风动物模型的最新进展。     

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.     

Generalized Vitiligo Preceded by a Generalized Figurate Erythematosquamous Eruption

The pathogenesis of vitiligo is still unknown. We saw a patient with vitiligo who may support an immunological pathogenesis for this disease. A 77-year-old man developed sharply demarcated, irregularly shaped, figurate, erythematosquamous plaques on most of the areas of his body. Histologically, lymphocytic cells invaded the lower epidermis. The lesions were gradually replaced by vitiliginous macules of the same configuration. Histologically, there were no active malanocytes in the vitiliginous lesions. We believe that the present patient presents an extraordinary example of inflammatory vitiligo and may provide an indication of an immunological pathogenesis for vitiligo.     

Vitiligo pathogenesis: autoimmune disease,genetic defect,excessive reactive oxygen species,calcium imbalance,or what else?

Abstract: The pathobiology of vitiligo has been hotly disputed for as long as one remembers, and has been a magnet for endless speculation. Evidently, the different schools of thought – ranging, e.g. from the concept that vitiligo essentially is a free‐radical disorder to that of vitiligo being a primary autoimmune disease – imply very different consequences for the best therapeutic strategies that one should adopt. As a more effective therapy for this common, often disfiguring pigmentary disorder is direly needed, we must strive harder to settle the pathogenesis debate definitively – on the basis of sound experimental evidence, rather than by a war of dogmatic theories. Recognizing, however, that it is theories which tend to guide our experimental designs and choice of study parameters, the various pathogenesis theories on the market deserve to be critically, yet unemotionally re‐evaluated. This Controversies feature invites you to do so, and to ask yourself: Is there something important or worthwhile exploring in other pathogenesis scenarios than those already favoured by you that may help you improve your own study design, next time you have a fresh look at vitiligo? Vitiligo provides a superb model for the study of many fundamental problems in skin biology and pathology. Therefore, even if it later turns out that, as far as your own vitiligo pathogenesis concept is concerned, you have barked‐up the wrong tree most of the time, chances are that you shall anyway have generated priceless new insights into skin function along the way.     

Public perceptions and attitudes toward vitiligo

Background:Previous studies have discussed attitudes of vitiligo patients toward their disease. However, no studies have addressed this issue from the public's point of view.Objective:To explore the perceptions, attitudes, and misconceptions of the public toward vitiligo.Methods:A self-administered questionnaire was distributed to attendees of primary health care centers in Riyadh, Saudi Arabia, between January and August 2010.Results:Overall, 924 of the 1,000 distributed questionnaires were returned, and 429 were males (46.8%). Moreover, 33.1% (303 of 916) believed that vitiligo is contagious or did not know that it is not. The cause of vitiligo was thought to be infectious by 20.4% of respondents (182 of 894), inherited by 40.5% (365 of 902), autoimmune by 41.2% (370 of 899), and due to a lack of hygiene by 22.5% (199 of 883). Unmarried individuals and those with less education were more likely to state that vitiligo is caused by an infection (. = .02, . = .03, respectively). Younger individuals and those with less education were more likely to think that vitiligo is caused by a lack of hygiene (. = .01, . = .001, respectively). More than half of the participants (56.1%, 504 of 898) would be unwilling to marry a vitiligo patient. Younger individuals and males were less likely to marry a vitiligo patient (. = .01, . = .05, respectively), whereas those of lower income were more likely to accept it (. = .002).Conclusions:Various misconceptions and negative attitudes about vitiligo among the public are prevalent. Educating the public about vitiligo could ultimately lead to better psychosocial well-being of vitiligo patients.     

Clinical and histopathologic characteristics of trichrome vitiligo

BACKGROUND: The term trichrome vitiligo describes lesions that have a tan zone of varying width between normal and totally depigmented skin, which exhibits an intermediate hue. However, the pathogenesis and the histopathologic characteristics of trichrome vitiligo are unknown. OBJECTIVE: Our purpose was to investigate the clinical and histopathologic characteristics and the pathogenesis of trichrome vitiligo. METHODS: Four punch biopsy specimens were taken from 21 patients with trichrome vitiligo; they were from vitiliginous skin, light brown skin, perilesional normal skin, and normal skin as far as 5 cm from the nearest vitiligo spot. The sections were stained with hematoxylin-eosin; in selected cases, we performed immunohistochemical staining with S-100 protein and CD1a. RESULTS: Trichrome vitiligo occurred most frequently on the trunk in active vitiligo vulgaris. Focal vacuolar degeneration of the basal cell layer and mild inflammatory cell infiltration of the epidermis and dermis were more prominent in light brown skin and perilesional normal skin than in vitiliginous skin and normal skin. The number of melanocytes was decreased in light brown skin compared with perilesional normal skin (P <.05) and in vitiliginous skin compared with light brown skin (P <.05); a few melanocytes were observed even in skin affected by trichrome vitiligo. The number of Langerhans cells was increased in the epidermis of light brown skin and perilesional normal skin compared with vitiliginous and normal skin (P <.05). PUVA therapy yielded excellent repigmentation. CONCLUSION: Trichrome vitiligo is a variant of active vitiligo. The changes of melanocytes, keratinocytes, and Langerhans cells may be involved in the pathogenesis of depigmentation in trichrome vitiligo.     

Vitiligo antibodies are not directed to tyrosinase

BACKGROUND: Patients with vitiligo have a markedly increased incidence of antibodies to melanocytes, referred to as vitiligo antibodies. Antibodies to tyrosinase have been reported in some patients with vitiligo, suggesting that vitiligo antibodies may be directed to this enzyme. However, there is considerable controversy as to the frequency with which these antibodies occur, and, hence, about their relevance to the pathogenesis of vitiligo. The frequency with which antityrosinase antibodies occur in vitiligo is critical to evaluate their potential role in the pathogenesis of this disease. OBJECTIVE: To examine the prevalence of antibodies to tyrosinase in a large group of patients with vitiligo. DESIGN: We examined the incidence of antibodies to enzymatically and immunologically active tyrosinase in patients with and without vitiligo. SETTING: Outpatient clinic in referral center. PATIENTS: The study was conducted on serum samples obtained from 54 patients with active (n = 40) and inactive (n = 14) uncomplicated vitiligo and from 52 age- and sex-matched individuals without vitiligo. MAIN OUTCOME MEASURE: Presence in the serum of antibodies to enzymatically and/or immunologically active tyrosinase. RESULTS: By immunoblotting, 20 patients (50%) with active vitiligo, 9 of those (64.3%) with inactive vitiligo, and 29 control individuals (55.8%) had antibodies to an antigen that comigrated with tyrosinase. However, by immunoprecipitation DOPA stain and by sandwich enzyme-linked immunosorbent assay, none of the vitiligo or control individuals had antibodies to tyrosinase, even though both assays easily detected control antityrosinase antibodies. CONCLUSION: These results indicate that while antibodies to an antigen(s) that comigrates with tyrosinase are common in patients with or without vitiligo, vitiligo antibodies are not directed to tyrosinase.