Huang Carol L, Nordlund James J, Boissy Raymond
Department of Dermatology, University of Cincinnati, Pavilion A, Ohio 45267-0523, USA.
Am J Clin Dermatol. 2002;3(5):301-8. doi: 10.2165/00128071-200203050-00001.
Vitiligo is a common cutaneous disorder that has significant biological and social consequences for those affected. It is characterized by a loss of melanocytes from the epidermis, which results in the absence of melanin, i.e. depigmentation. There are numerous hypotheses about the etiology of vitiligo, but no data to definitively prove one theory over another. It is likely that there are numerous causes for the loss of these melanocytes. One way to approach the identification of the etiology is to determine the mechanism by which the melanocytes are destroyed. The two known mechanisms for the destruction of cells are necrosis and apoptosis. One purpose of this paper is to review the extant data that might suggest which of the two mechanisms is operative against melanocytes in patients with vitiligo. The histological data, and some laboratory data, support apoptosis, rather than necrosis, as the mechanism for removal of melanocytes. Apoptosis can be induced by a variety of factors, including immune cytokines, some environmental chemicals (for example substituted hydroquinones such as monobenzone) or other molecular mechanisms. Current therapies, such as corticosteroids and ultraviolet light, do affect apoptosis in a variety of ways. Confirmation of apoptosis as a mechanism, and identification of how apoptosis is initiated to produce vitiligo, can serve as a basis for devising medications that might stop the progression of the disorder. The problem of vitiligo would be essentially solved if there was a medication that is well tolerated in children, adults and pregnant women, and that would halt the progression of the depigmentation. The study of apoptosis, mechanisms of its induction, and the ways to block apoptosis, is one possible way to find both the causes of depigmentation and medications to prevent its progression.
白癜风是一种常见的皮肤疾病，对患者有着重大的生物学和社会影响。其特征是表皮黑素细胞缺失，导致黑色素缺乏，即色素脱失。关于白癜风的病因有众多假说，但尚无数据能明确证实某一种理论优于其他理论。这些黑素细胞缺失可能有多种原因。确定病因的一种方法是确定黑素细胞被破坏的机制。已知的细胞破坏机制有坏死和凋亡。本文的一个目的是回顾现有数据，以提示在白癜风患者中这两种机制中哪一种对黑素细胞起作用。组织学数据以及一些实验室数据支持凋亡而非坏死是黑素细胞清除的机制。凋亡可由多种因素诱导，包括免疫细胞因子、一些环境化学物质（例如单苯醚等取代对苯二酚）或其他分子机制。目前的治疗方法，如皮质类固醇和紫外线，确实以多种方式影响凋亡。确认凋亡为一种机制，并确定凋亡如何引发白癜风，可为设计可能阻止疾病进展的药物提供依据。如果有一种药物在儿童、成人和孕妇中耐受性良好且能阻止色素脱失的进展，白癜风问题将基本得到解决。对凋亡、其诱导机制以及阻断凋亡方法的研究，是找到色素脱失原因和预防其进展药物的一种可能途径。
