Cutaneous sarcoidosis associated with cosmetic fillers

Cutaneous sarcoidosis associated with cosmetic fillers
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与化妆品填充剂相关的皮肤结节病

DOI:
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发表时间:
2009
影响因子:
9.2
通讯作者:
L. Izikson
L. Izikson
中科院分区:
医学2区
文献类型:
--
作者:
L. Izikson

文献摘要

被引文献

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讨论黑素细胞为什么以及如何消失而诱发白癜风病变尚未完全清楚。白癜风的发病机制主要有三种假说:(i)神经假说认为神经化学物质减少黑色素的产生,黑色素细胞可能被神经末梢产生和释放的毒素破坏;(ii)复杂的生化失衡和自由基防御缺陷可能影响黑色素的产生;(iii)自身免疫假说。最流行的假说是自身免疫假说。在文献中,在白癜风患者中检测到针对黑素细胞的循环抗体。此外,循环黑素细胞特异性细胞毒性T细胞已被检测到在白癜风患者的高频率。白癜风和自身免疫性疾病的关联间接支持了白癜风的自身免疫发病机制的想法。催乳素主要由脑下垂体前叶产生,但也由T淋巴细胞、B淋巴细胞和人绒毛膜产生。催乳素是淋巴细胞的生长因子,具有在多个水平刺激免疫应答的潜力,并作为细胞因子发挥作用。催乳素刺激Th 1应答所需的干扰素调节因子-1,并可调节Th 1细胞因子,如干扰素-c和白细胞介素-15。在SLE、RA、银屑病关节炎、多发性硬化症、赖特综合征、原发性干燥综合征、银屑病和葡萄膜炎患者中发现催乳素水平升高。我们的研究是第一个调查白癜风患者催乳素水平的研究。我们没有发现患者和对照组的催乳素水平有显著差异。泌乳素水平与患者的年龄、性别、病程、家族史及白癜风的扩大程度均无相关性。我们的研究结果表明,催乳素不发挥作用,白癜风的发病机制。
Discussion Why and how melanocytes disappear to induce the vitiligo lesions is not fully understood. There are three major hypotheses for pathogenesis of vitiligo: (i) neural hypothesis suggests that neurochemical substance decreases melanin production and the melanocytes could be damaged by a toxin produced and released from the nerve endings; (ii) a complex biochemical imbalance and defective free-radical defence could affect production of melanin; (iii) autoimmune hypothesis. The most popular hypothesis is the autoimmune hypothesis. In literature, circulating antibodies to melanocytes was detected in vitiligo patients. Also, circulating melanocyte-specific cytotoxic T cells have been detected in high frequencies in the patients with vitiligo. The association of vitiligo and autoimmune disorders indirectly supports the idea of an autoimmune pathogenesis of the disease. Prolactin is made mainly in the anterior pituitary gland; however it is also produced in T lymphocytes, B lymphocytes, and human chorion. Prolactin is a growth factor for lymphocytes with the potential to stimulate immune responses at many levels and affect as a cytokine. Prolactin stimulates interferon regulatory factor-1 that is required for Th1 responses and can regulate Th1 cytokines such as interferon-c and interleukin-15. Elevated levels of prolactin have been found in patients with SLE, RA, psoriatic arthritis, multiple sclerosis, Reiter’s syndrome, primary Sjögren’s syndrome, psoriasis and uveitis. Our study is the first study that investigated prolactin levels in vitiligo patients. We could not found significant difference in prolactin levels in the patient and control groups. Also, no correlation was found between prolactin levels and age and sex of the patients, duration of the disease, family history and expansion of the vitiligo. Our results suggest that prolactin does not play a role in the pathogenesis of vitiligo.