无色素痣的临床、组织学和超微结构观察

目的 探讨无色素痣的临床和组织学特征。方法 分析85例无色素痣患者的发病年龄、类型和皮损特点,并对部分患者行皮肤色素测定和反射式共聚焦显微镜（RCM）观察。对其中17例患者的皮损区和正常区皮肤组织进行组织病理检查,透射电镜观察皮损区超微结构。免疫组化法检测皮损区和正常皮肤处酪氨酸酶（TYR）、HMB45、酪氨酸酶相关蛋白1（TRP-1）、TRP-2和CD117表达。结果 85例无色素痣患者中,23例（27.1%）出生时发现皮损,21例（24.7%）出现于3岁以后,最大发病年龄为29岁。皮损分布于躯干部25例（29.4%）,颈部13例（15.3%）;72例（84.7%）皮损边缘不规则,54例（63.5 %）仅有1处皮损。19例无色素痣患者患处的黑素指数（186.56 ± 52.86）和相对黑素指数（80 ± 11）低于正常人皮肤（分别为223.88 ± 63.19和100）,高于12例白癜风患者皮损处（分别为128.57 ± 64.31和60 ± 20）,差异均具有统计学意义（P < 0.01）。反射式共聚焦显微镜示,无色素痣皮损中含黑素细胞数量减少,亮度减低,黑素分布均匀,皮损区与正常皮肤分界区常不清晰。皮损区Fontana-Masson染色示皮损区黑素强度为1810.12 ± 327.96,较正常区（2064.24 ± 260.41）明显减弱。电镜下发现黑素细胞数量减少,黑素小体减少,黑素细胞胞质和树突以及角质形成细胞中可见Ⅱ、Ⅲ期未成熟的黑素小体,角质形成细胞中可见聚集成团的黑素小体。17例患者正常区TYR表达水平为1827.35 ± 307.09,TRP-1为6102.54 ± 1642.64,而皮损区TYR（1477.35 ± 224.05）和TRP-1（5322.33 ± 1565.26）表达下降,正常区与皮损区比较,P均 < 0.01;HMB45、TRP-2、CD117表达两处比较差异均无统计学意义。 结论 无色素痣是一种早期发病、非家族聚集性、稳定的不规则色素减退性疾病,其皮损中黑素细胞和黑素小体数量均减少,可见未成熟黑素小体。相对黑素指数和反射式共聚焦显微镜检查可作为诊断无色素痣的无创性检测方法。     

进行性斑状色素减少症一例

患者男,28岁.因躯干色素减退斑8年就诊.皮疹为色素减退性斑片,大小不一,境界不清,表面无鳞屑,色减斑片在躯干近中线处融合.真菌学直接镜检阴性.Wood灯检查显示皮损区域毛囊性红色荧光.组织病理学仅提示基底层见色素减少,皮肤电镜提示皮损处黑素小体数目较临近正常处皮肤减少,且以Ⅰ～Ⅲ期为主,周围正常皮肤处黑素小体以Ⅳ期为主.根据患者临床表现、Wood灯检查及组织病理、皮肤电镜结果,确诊为进行性班状色素减少症.窄谱UVB治疗有效.     

体外培养节段型白癜风样无色素痣皮损黑素细胞及其临床意义

【摘要】 目的 评价负压吸疱表皮黑素细胞培养对节段型白癜风样无色素痣的辅助诊断价值。方法 收集2019年6月至2020年3月于杭州市第三人民医院皮肤科依据Coupe标准临床诊断的8例节段型白癜风样无色素痣患者,进行伍德灯、反射式共聚焦显微镜（RCM）检查,308 nm准分子激光试验,负压吸疱获取表皮黑素细胞并培养,记录结果。结果 8例患者中,6例皮损伍德灯下可见荧光,4例RCM下可见色素环完整性缺失,5例经308 nm准分子激光照射试验后未见复色反应。8例患者体外培养的皮损黑素细胞硫酸亚铁染色均阳性,经消化离心后沉淀呈黄白色,电镜下黑素细胞胞质内可见Ⅰ~ Ⅲ期黑素小体;皮损对侧同一解剖部位正常皮肤黑素细胞沉淀则呈黑色,电镜下黑素细胞胞质内可见Ⅰ~ Ⅳ期黑素小体。结论 负压吸疱表皮黑素细胞培养有助于诊断节段型白癜风样无色素痣。     

白癜风复色区黑素细胞特异性抗原表达的研究

目的：研究白癜风复色区黑素细胞分布及gp100、酪氨酸酶（TYR）等抗原的表达。方法：对白癜风患者复色区皮肤活检的组织标本以免疫组化染色识别gp100、TYR、酪氨酸酶相关蛋白（TRP）-1和TRP-2,以HPIAS-1000彩色病理图文报告系统定量分析阳性表达的强弱。结果：色素脱失斑处未见活性黑素细胞,复色区黑素细胞数目与正常人皮肤比较差异无统计学意义（P〉0．05）。色素脱失斑内岛状复色区皮肤,近毛囊部位黑素细胞数目较多,远离毛囊部位数目较少;色素脱失斑边缘复色区内,黑素细胞在表皮及毛囊的基底层中分布较均匀。复色区黑素细胞树突短粗、数目变少。复色区阳性细胞gp100和TRP-2图像灰度值与正常皮肤比较差异无统计学意义（P〉0．05）,TYR低于正常皮肤（P〈0．05）,而TRP-1明显低于正常皮肤（P〈0．01）。结论：色素脱失斑处有功能黑素细胞缺失。复色区内可见黑素细胞,其结构、功能皆完整,数目与正常人无明显差别。复色区黑素细胞可能来源于毛囊组织．亦可能来源于色素脱失斑边缘正常黑素细胞。TRP-1的高表达可能导致复色区黑素细胞的形态异常。     

银屑病患者皮肤中T细胞与黑素细胞的检测及临床意义

目的 研究银屑病患者皮肤中CD4+和CD8+ T细胞与黑素细胞的关系和临床意义。 方法 取29例进行期银屑病患者皮损和非皮损、5例消退期患者皮损和非皮损及6例健康人皮肤。免疫组化检测CD4+ T细胞和CD8+ T细胞的数量和分布,并对比基底层黑素细胞和色素颗粒情况。采用SPSS18.0软件进行统计分析,多组间比较采用单因素方差分析（ANOVA）,两组间比较采用最小显著差异法（LSD）,相关性分析采用Pearson检验。 结果 银屑病患者皮损中每个高倍（× 200）视野CD4+ T细胞平均数（表皮5.29 ± 4.66,真皮77.50 ± 43.66）明显高于非皮损（表皮为0,真皮9.67 ± 7.73）,皮损与非皮损比较,均P ＜ 0.05;而CD8+ T细胞的数量（表皮7.83 ± 6.27,真皮46.08 ± 34.26）亦明显高于非皮损（表皮0.71 ± 1.20,真皮5.54 ± 4.43）,皮损与非皮损比较,均P ＜ 0.05。与健康对照皮肤相比,银屑病患者皮损中CD4+ T细胞和CD8+ T细胞均明显增多,差异有统计学意义（均P ＜ 0.05）。银屑病皮损处基底层黑素细胞数量（103.45 ± 16.96）明显高于非皮损（43.62 ± 14.20,P ＜ 0.05）及健康人皮肤（P ＜ 0.05）,但色素颗粒阳性细胞比例（7.45% ± 3.86%）明显低于非皮损（43.10% ± 14.91%,P ＜ 0.05）及健康人皮肤（P ＜ 0.05）。非皮损处CD8+ T细胞、CD4+ T细胞、黑素细胞数量及色素颗粒阳性细胞比例与健康人比较差异均无统计学意义。消退期皮损黑素细胞数量高于消退后白斑（P ＜ 0.05）,色素颗粒阳性细胞比例略低于消退后白斑,但差异无统计学意义;与健康人比较,消退期皮损黑素细胞数量高,而色素颗粒阳性细胞比例低,均有统计学差异（均P ＜ 0.05）,消退后白斑的黑素细胞数量与健康人比较差异无统计学意义,而色素颗粒阳性细胞比例降低（P ＜ 0.05）。进行期患者皮损中CD4+、CD8+ T细胞数与黑素细胞数及色素颗粒阳性细胞比例均无相关性（均P > 0.05）,而非皮损中CD4+、CD8+ T细胞数与黑素细胞数呈正相关（r值分别为0.46和0.56,均P ＜ 0.05）,但与色素颗粒阳性细胞比例无明显相关性（P > 0.05）。 结论 在银屑病进行期皮损中,CD4+ T细胞和CD8+ T细胞明显增多,基底层黑素细胞数量增加,但色素颗粒明显减少;皮损消退后,黑素细胞数量及色素颗粒逐渐接近健康人水平。     

硬皮病:皮肤黑素障碍的超微结构研究

作者对6例系统性,2例限局性硬皮病患者作活检,多巴染色,并作了电镜检查,测定黑素体的大小,以研究其皮肤黑素障碍的特征.结果:色素过多的皮肤中,黑素细胞数目正常或仅稍增加,其分布不如正常皮肤规则,其大小、树突数及其长度普遍增加,多巴氧化酶活性较周围正常皮肤为高.在色素脱失的皮肤中,其皮损边缘的黑素细胞较正常的大(3或4倍),且分布不规则,其中一些呈星形或长梭形,其余的呈圆形,无树突.有时其多巴氧化酶较色素过多皮肤还高.皮损中央:未见多巴阳性的黑素细胞.在色素减退的皮肤中,黑素细胞数增加,分布不规则,其细胞大小、树突数     

黑素细胞和噬黑素细胞在瑞尔黑变病中的结构与分布

目的探讨瑞尔黑变病的黑素细胞和噬黑素细胞的组织病理特点。方法收集瑞尔黑变病皮损标本50例,正常皮肤标本20例,所有病理切片标本均进行Fontana-Masson染色、多巴染色、CD68染色、C-Kit(CD117)染色,用图像分析软件Image-proplus6.0分析各组标本中平均光密度值。并通过透射电镜观察4例黑变病皮损的超微结构。结果①特殊染色:Fontana-Masson染色、多巴染色中黑变病组平均光密度值均高于正常组。②电镜:角质形成细胞内的黑素颗粒比正常皮肤中的少,基底层中黑素细胞的大小、形态与正常皮肤相比无明显变化,但基底层黑素细胞内线粒体、高尔基体、粗面内质网丰富,Ⅲ,Ⅳ期黑素小体明显增加;真皮浅层可见较多噬黑素细胞,其内有大量的被溶酶体吞噬的黑素颗粒,呈团块状分布。③免疫组化:黑变病组真皮内存在CD68阳性细胞;C-Kit在黑变病组表达较正常组高。结论瑞尔黑变病皮肤中黑素细胞合成黑素的功能活跃;真皮浅层内含有大量的噬黑素细胞;C-Kit受体在黑变病色素沉着中可能起到调控作用。     

葛根素促进黑素细胞黑素合成及其机制的初步探讨

目的 探讨葛根素对正常人黑素细胞黑素合成的影响和可能机制。 方法 用噻唑蓝（MTT）法、NaOH裂解法观察葛根素对黑素细胞增殖及黑素合成作用,RT-PCR及Western印迹法检测葛根素对黑素细胞小眼畸形相关转录因子（MITF）、酪氨酸酶（TYR）、酪氨酸酶相关蛋白1（TRP-1）基因转录和蛋白表达水平的影响。 结果 1 ~ 40 μmol/L浓度范围内葛根素对体外培养的黑素细胞增殖影响与正常对照组相比,差异无统计学意义（P > 0.05）。与正常对照组相比,40 μmol/L葛根素可显著促进黑素细胞的黑素合成（P < 0.05）,并可显著增加MITF、TYR、TRP-1 mRNA及蛋白的表达（P < 0.05）。40 μmol/L葛根素使MITF、TYR、TRP-1的蛋白表达量分别比正常对照组增加8.69%,10.28%和10.58%（P < 0.05）;并使MITF、TYR、TRP-1的mRNA表达量分别比正常对照组增加2.48倍,1.91倍和1.63倍（P < 0.05）。 结论 葛根素能增加MITF、TYR、TRP-1 mRNA及蛋白的表达水平,促进黑素合成。     

人毛囊无色素黑素细胞培养方法的改良及色素生成相关酶表达的研究

目的进一步改良人毛囊无色素黑素细胞（amelanotic melanocytes，AMMC）培养的方法，并研究了AMMC内黑素生成相关酶的表达：酪氨酸酶（tyrosinase,TYR）、酪氨酸酶相关蛋白-1（tyrosinase related protein-1，TRP—1）和酪氨酸酶相关蛋白-2（tyrosinase related protein-1，TRP-2）。方法采用1％分离酶（dispase）消化分离毛囊，选用含干细胞因子（stem cell factor，SCF）、内皮素-3（endothelin-3，ET-3）、碱性成纤维细胞生长因子（basic fibroblast grow factor，bFGF）和霍乱毒素（cholera toxin，CT）的成黑素细胞培养基培养AMMC，同时培养表皮黑素细胞（melanocytes，MC）作为对照，采用免疫组化、多巴染色和透射电镜对细胞进行鉴定，蛋白印记法分析TYR、TRP-1和TRP-2的表达。结果1％分离酶消化24h可以容易获得游离的毛囊，结合我们所用的培养基完全排除了成纤维细胞的污染。所用成黑素细胞培养基促AMMC增殖明显，细胞可传5代以上。免疫组化结果显示，AMMC表达gp100、酪氨酸酶（tyrosinase，TYR）、酪氨酸酶相关蛋白-1（tyrosinase related proteifl-1，TRP-1）和酪氨酸酶相关蛋白-2（tyrosinase related protein-1，TRP-2），证明培养的细胞为黑素细胞。AMMC的多巴染色呈阴性，并且透射电镜发现AMMC胞质中仅含大量的Ⅰ期、Ⅱ期黑素小体，未见Ⅲ、Ⅳ期黑素小体，因此说明AMMC处于未分化状态。TYR和TRP-1在MC中的表达明显强于AMMC。TRP-2的表达在两种细胞间没有明显差别，进一步说明AMMC与MC具有异质性。结论我们成功培养了完全纯化、快速增殖的AMMC，并且培养的细胞不能生成黑素，生物学性状更接近活体中的状态，其与表皮黑素细胞具有异质性。     

色素障碍性皮肤病

970359 寻常型进行期白癜风的超微结构变化/杜娟…//中华皮肤科杂志。-1996,29（4）。-240 用透射电镜观察了10例寻常型进行期白癜风患者白斑、白斑边缘及远离白斑对应侧正常皮肤的超微结构变化。结果显示:9例白斑区黑素细胞及黑素小体缺乏,1例残留一黑素细胞,但明显退化。白斑边缘显示多种异常,黑素细胞内粗面内质网高度扩张,数量增多,远离白斑处临床正常皮肤已经出现病理改变。本研究表明皮损处表皮三种主要细胞即角朊细胞、黑素细胞及郎格罕细胞均有异常。表1参4（贾泰元）970360 两种类型白癜风患者郎格罕细胞电镜观察/石得仁…//临床皮肤科杂志。-1996,25（3）。-129 对皮节型和泛发型白癜风患者皮肤内郎格罕细胞进行了电镜比较观察。结果表明,两型白癜风患者皮肤内郎格罕细胞均存在着不同程度的形态学改变,以皮节型皮损区更为明显。作者认为白癜风皮肤郎格罕细胞可能受累,但这些改变主要见于皮节型白癜风皮损区。目前还难以肯定郎格罕细胞在白癜风发病机制中的作用。表1参4（原文摘要）     

Clinical, pathologic, and ultrastructural studies of progressive macular hypomelanosis

Background Progressive macular hypomelanosis (PMH), a condition of uncertain etiology, is characterized by asymptomatic hypopigmented macules, predominantly located on the trunk. To date, the study of this disease has been sporadic and there are still no clinical diagnostic criteria. The aim of this study was to investigate the histopathologic and ultrastructural characteristics of PMH, and propose the clinical diagnostic criteria of PMH. Methods The Wood’s lamp and Confocal Laser Scanning Microscopy were used to observe the lesions’ features. Skinbiopsies were used for hematoxylin and eosin staining, melanin staining, antibodies staining of S‐100 protein, tyrosinase‐related protein‐1(TRP‐1) and tyrosinase (T311), and also for ultra‐structural study. Melanocytes were isolated and cultured from the lesions. Results Under Wood’s lamp examination, the lesions of PMH showed punctiform red fluorescence. Confocal Laser Scanning Microscopy observation of the lesion showed that its “pigmented ring” around the dermal papillae was intact, but its melanin content was decreased compared with the surrounding normal skin. Ferrous sulfate staining showed that melanin content in the lesion of PMH was significantly decreased compared with the normal skin (P < 0.05). S‐100 staining showed that the number of positive cells in the basal layer had no statistical significance (P > 0.05) between the lesion areas (8.25 ± 0.96) and the surrounding normal skin (8.75 ± 1.71). TRP‐1 staining showed no significant difference between lesion areas (4.25 ± 0.96) and the surrounding normal skin (4.50 ± 1.29) (P > 0.05), and T311 staining also showed no difference between lesion areas (4.01 ± 0.87) and the surrounding normal skin (4.30 ± 1.05) (P > 0.05). Ultra‐structural studies revealed a large reduction in the number of mature melanosome from PMH lesions. There were many membrane‐bound groups in PMH lesions with normal appearance the margin, which contained a number of smaller type II–IV melanosomes, which were distributed in clusters. No degradation of melanosomes was present in the lysosomal compartments of PMH lesions. When melanocytes from the PMH lesions were cultured in vitro, the morphology of those melanocytes showed no difference compared with normal melanocytes. Conclusion As a result of the above findings, we discussed and summarized the PMH’s clinical diagnostic criteria.     

Ultrastructural findings in progressive macular hypomelanosis indicate decreased melanin production

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.     

Hypermelanocytic guttate and macular segmental hypomelanosis

We report two sisters, 27 and 30 years of age, with a cutaneous pigmentary anomaly, which seems to be a new entity. At the age of 26 years the elder sister developed an asymptomatic and persistent rash consisting of discrete, grouped, round to oval, guttate and nummular, hypopigmented macules, 0.2-5 cm in diameter. The distribution of the lesions was unilateral. They were located on the right side of the thorax with a moderately sharp demarcation in the mid-line and ran in a segmental distribution over the right arm, hand and fingers. Microscopic examination of lesional skin scrapings was negative for fungi. Examination with Wood's light accentuated the lesions from the surrounding normal skin. The younger sister had experienced identical, mostly guttate, skin lesions for many years, which at examination were distributed on all extremities and buttocks, and to a lesser degree on the trunk, but here in a segmental distribution. Histological examination (Masson-Fontana staining) of lesional skin of both sisters was identical. A slightly thinned epidermis and a marked decrease in pigmentation of the epidermal basal layer was seen. Electron microscopic examination of lesional skin showed an overall linear increase of morphologically and cytologically normal melanocytes just above the epidermal basal membrane. At many places the density of melanocytes was so high that the keratinocytes were displaced from the basal layer. The melanocytic dendrites extended into the suprabasal layer. The keratinocytes of lesional skin showed a decreased number of melanosomes. It is paradoxical that a hypomelanotic macule shows a histological picture of an increase in normal functioning melanocytes. In all probability a deficient melanosome transfer is responsible for this unexpected phenomenon.     

Progressive macular hypomelanosis in Singapore: a clinico-pathological study

INTRODUCTION: Progressive macular hypomelanosis (PMH), a condition of uncertain etiology, is characterized by asymptomatic hypopigmented macules predominantly located on the trunk. To date, there are no reports from South-East Asia concerning this condition. We sought to record the clinical features of PMH in Asian patients, identify etiologic factors, and study the structural and ultrastructural features of melanocytes in this disorder. METHODS: Patients who presented to the National Skin Center with acquired, hypopigmented macules on the trunk, without a history of inflammation or infection, were recruited. Erythrocyte sedimentation rate (ESR), complete blood count, fasting blood glucose, liver function tests, skin scrapings for fungi, and skin biopsy specimens (from lesional and normal skin) were obtained. Biopsies were stained with hematoxylin and eosin (H&E), Fontana Masson, an immunohistochemical panel for identification of melanocyte differentiation antibodies (HMB 45, Melan A, and S100) and CD 68. Electron microscopy (EM) was also performed. The patients were evaluated every 3 months. RESULTS: During a 9 month period, eight patients (all Chinese) presented with hypopigmented, ill-defined, confluent macules involving the lower aspect of the trunk. There were four men and four women, and the mean age was 25.9 years (range 19-45 years). Skin scrapings were negative for fungi and laboratory tests were normal. Microscopic evaluation of skin biopsy specimens showed reduced pigmentation of lesional as compared with normal appearing skin, but H&E-stained sections revealed only minimal histologic differences between lesional and normal skin. EM demonstrated a statistically significant (P = 0.047, Wilcoxon Signed Rank Test, Wilcoxon 95% CI 0.02-0.62) higher ratio of stage IV and late stage III (dark) melanosomes in normal vs. lesional skin. CONCLUSIONS: PMH may occur among young adults in Singapore. Its etiology is uncertain. The melanin content of lesional skin appears to be less than that in normal sites. EM shows a higher ratio of immature melanosomes in lesional vs. normal skin.     

Clinical, histopathological and ultrastructural characteristics of naevus depigmentosus

Background.  Naevus depigmentosus (ND) is a congenital, nonfamilial, well-circumscribed, uniformly hypopigmented macule, the relative size and distribution of which is stable throughout life. The aetiopathogenesis of ND is not yet fully understood, and reports about the clinical and histopathological characteristics of ND are few.
Objective.  To investigate the clinical and histopathological characteristics of ND, and to make it easier to diagnose ND clinically.
Methods.  A clinical survey on 38 patients with ND was performed according to the diagnostic criteria proposed by Coupe. Wood's lamp examination was used to distinguish the different appearance of ND and vitiligo. Skin-biopsy specimens were stained with haematoxylin and eosin, silver, antibodies to S-100 protein, tyrosinase-related protein-1 and tyrosinase, then used for ultrastructural study. Melanocytes were also cultured.
Results.  Leucoderma was present at birth in 13 patients (34.2%), and appeared during the first 3 years of life in 15 patients. The trunk was the most commonly affected site, and the lesions usually had serrated, irregular borders. Under Wood's lamp, lesions had an off-white accentuation without fluorescence. Immunohistochemistry showed that the melanin content of ND lesions was decreased compared with perilesional normal skin, but there was no change in the number of melanocytes. Ultrastructural study showed that some aggregated melanosomes were present in the affected keratinocytes.
Conclusion.  As a result of the above findings, we suggest changes to Coupe's criteria for ND.     

白癜风皮损边缘黑素细胞线粒体超微结构的电镜观察

【摘要】 目的 探讨白癜风患者皮损边缘黑素细胞线粒体结构的变化。方法 在透射电镜下观察健康对照、进展期白癜风及稳定期白癜风患者皮损边缘黑素细胞形态,体视学方法测量线粒体体密度（Vv）、表面积密度（Sv）、数密度（Nv）等参数。结果 健康对照组黑素细胞可见大量黑素小体（28.57 ± 3.21）,以Ⅲ、Ⅳ期为主,线粒体规则分布在细胞内,结构正常、嵴密集,部分细胞胞质内可见自噬小体。进展期和稳定期白癜风黑素细胞内黑素小体数量减少,单位细胞内黑素小体数量分别为22 ± 6.16和17.43 ± 6.24,其中,Ⅲ期黑素小体显著减少,线粒体大小不一、形态多样,大部分线粒体明显肿胀,嵴模糊、排列紊乱甚至断裂,呈空泡状改变,未见线粒体自噬现象。线粒体形态结构定量研究显示,健康对照组Nv、Vv、Sv分别为（7.194 ± 1.434） μm－3、（4.8 ± 1.2）%、（2.42 ± 0.86） μm－1;进展期白癜风组Nv、Vv、Sv分别为（4.055 ± 0.906） μm－3、（7.4 ± 2.1）%、（3.58 ± 1.15） μm－1;稳定期白癜风组Nv、Vv、Sv分别为（5.311 ± 0.873） μm－3、（6.5 ± 1.4）%和（2.82 ± 0.94） μm－1,组间差异有统计学意义（P ＜ 0.05）。结论 白癜风皮损边缘黑素细胞线粒体受损,且进展期损伤程度大于稳定期。 【关键词】 白癜风; 黑素细胞; 线粒体; 显微镜检查,电子,透射     

Confetti‐like lesions with hyperkeratosis: a novel ultraviolet‐induced hypomelanotic disorder?

Confetti leucoderma can occur in a variety of unrelated skin disorders and is often a diagnostic challenge. We describe a 33-year-old man with a history of mycosis fungoides and vitiligo. He developed disseminated 1-2-mm round-shaped leucodermic lesions 6 months after psoralen photochemotherapy and 12 months after systemic therapy with interferon. The skin lesions had a discrete hyperkeratotic scale. Multiple skin biopsies and immunohistochemical studies showed lamellar orthohyperkeratosis, papillomatosis, hypomelanotic keratinocytes but a normal number of melanocytes. Langerhans cells, in contrast, were reduced in lesional skin. Electron microscopy disclosed only a few type I and II melanosomes in lesional melanocytes, while keratinocytes were largely devoid of any melanosomes. This constellation of clinical, immunohistochemical and ultrastructural findings has not been reported before and distinguishes our case from leucoderma punctatum, idiopathic guttate hypomelanosis and disseminated hypopigmented keratoses. We suggest that the skin lesions observed in our patient represent an unusual response to ultraviolet damage to melanocytes followed by reactive epidermal hyperkeratosis.     

Wood灯在皮肤浅表真菌感染诊断中应用价值评估

目的 评估Wood灯在皮肤常见浅表真菌感染诊断中的应用价值.方法 对129例根据临床病史及体征初步诊断为皮肤浅表真菌感染患者进行Wood灯和真菌实验室检查.结果 花斑糠疹、马拉色菌毛囊炎患者Wood灯检查的阳性率分别为84%、85.7%,同时阳性病例的真菌培养或镜检的阳性率达92.9%、87.5%,两者有高度的一致性.而临床诊断手足癣和体股癣者其荧光阳性率只有8.3%.真菌总检出率却高达85.4%(41/48),两者不具有一致性.结论 Wood灯在花斑糠疹、马拉色菌毛囊炎的检查上有较高的特异性和敏感性,临床诊断上有应用价值,而对手足癣和体股癣诊断则无意义.

Abstract：

Objective To estimate the performance of Wood's lamp examination in the diagnosis of superficial cutaneous fungal infections. Methods Totally, 129 patients, who were diagnosed with superficial cutaneous fungal infections according to clinical medical history and signs, were enrolled in this study. Wood's lamp examination of lesions was carried out. Cutaneous samples were obtained from the patients and subjected to microscopic examination and fungal culture. Results Wood's lamp examination was positive in 84% and 85.7% of patients with tinea versicolor and malassezia folliculitis, respectively; among these patients positive for Wood's lamp examination, 92.9% were positive for fungal culture, and 87.5% for microscopic examination. In patients clinically diagnosed with tinea manus and pedis, tinea corporis or tinea cruris, 8.3% were positive for Wood's lamp examination, while 85.4% were positive for fungal examination. There was a high consistency between Wood's lamp examination and fungal examination in patients with tinea versicolor and malassezia folliculitis, but not in those with tinea manus and pedis, tinea corporis or tinea cruris. Conclusions Wood's lamp examination shows a high specificity and sensitivity and is useful in the diagnosis of tinea versicolor and malassezia folliculitis, but seems unapplicable for the diagnosis of tinea manus and pedis, tinea corporis or tinea cruris.