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首页> 外文期刊>Journal of the European Academy of Dermatology and Venereology: JEADV >Ultrastructural findings in progressive macular hypomelanosis indicate decreased melanin production.
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Ultrastructural findings in progressive macular hypomelanosis indicate decreased melanin production.

机译:进行性黄斑黑色素减少症的超微结构发现表明黑色素生成减少。

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BACKGROUND: The pathogenesis of progressive macular hypomelanosis (PMH) is unknown. Recently, Westerhof et al. (Arch Dermatol 2004; 140: 210-214) hypothesized that Propionibacterium acnes produces a depigmenting factor that interferes with melanogenesis in the skin, resulting in hypopigmented spots. The purpose of the study is to gain an insight into the pathogenesis of PMH. MATERIALS AND METHODS: We took a biopsy of 2-mm diameter from normal and lesional skin in eight PMH patients. Using electron microscopy, we compared melanization of melanosomes, melanosome transfer and amount of epidermal melanin in normal and lesional skin. RESULT: Compared to non-lesional skin, we observed a decrease of epidermal melanin and less melanized melanosomes in lesional skin of all patients. When comparing normal and lesional skin of patients with skin type V and VI, we observed a difference in melanosome size and maturation and a switch of transferred melanosomes from single stage IV transferred melanosomes to aggregated stage I, II and III transferred melanosomes, as seen in healthy skin of skin type I to IV. CONCLUSION: Hypopigmentation in PMH seems to be the result of an altered melanogenesis based on a decrease in melanin formation and a change in the distribution of melanosomes. In lesional skin of PMH patients with skin type V and VI less melanized, aggregated melanosomes in stead of single, mature melanosomes are transferred from melanocytes to keratinocytes. This results in a decrease of epidermal melanin. Further investigations are needed to determine the precise role of Propionibacterium acnes in this alteration of melanogenesis.
机译:背景:进行性黄斑部黑色素瘤病(PMH)的发病机制尚不清楚。最近,韦斯特霍夫等。 (Arch Dermatol 2004; 140:210-214)假设痤疮丙酸杆菌会产生色素沉着因子,该色素沉着因子干扰皮肤黑色素生成,导致色素沉着斑。该研究的目的是深入了解PMH的发病机理。材料与方法:我们对8例PMH患者的正常和病变皮肤进行了2毫米直径的活检。使用电子显微镜,我们比较了正常和病变皮肤中黑素体的黑色素化,黑素体转移和表皮黑色素的量。结果:与非病变皮肤相比,我们观察到所有患者的病变皮肤中表皮黑色素减少,黑色素体含量降低。比较具有V型和VI型皮肤的患者的正常皮肤和病变皮肤时,我们观察到黑素体大小和成熟度的差异,并且已将转移的黑素体从单阶段IV转移的黑素体转变为聚集的I,II和III转移的黑素体。 I至IV型皮肤的健康皮肤。结论:PMH色素沉着似乎是基于黑色素形成减少和黑素体分布变化而改变的黑色素生成的结果。在具有V型和VI型皮肤的PMH患者的病灶皮肤中,黑色素少,聚集的黑素体代替单个成熟的黑素体从黑素细胞转移到角质形成细胞。这导致表皮黑色素的减少。需要进一步的研究以确定痤疮丙酸杆菌在这种黑色素生成变化中的确切作用。

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