A case of amyloidosis cutis dyschromica

报告1例色素异常性皮肤淀粉样变性.患者男,17岁.全身色素沉着伴有色素脱失斑2年,不痛不痒.色素沉着由躯干逐渐蔓延至四肢及面部.皮损组织病理检查:(色素增加处)表皮大致正常,真皮乳头处有淀粉样物质沉积及噬黑素细胞增多.刚果红染色:(色素脱失处)见真皮乳头处有粉红色的阳性物质沉积.诊断:色素异常性皮肤淀粉样变性.     

老年皮肤的变化

老年皮肤的表皮与真皮变薄,表真皮交界处界面变平，黑素细胞和朗格汉斯细胞减少，真皮体积可减少205左右，皮肤附属器结构和功能发生改变和减退，致使表皮更替速率、修复速率变慢，对损伤的反应、屏障功能、清除化学物质速率、感觉功能、血管反应性、体温调节能力均有所下降，因此老年人易患皮肤干燥、瘙痒、色素改变（增加或减退）、大疱性类天疱疮以及各种增生性疾病等。     

皱褶部位色素异常性皮肤淀粉样变一例

56岁女性患者,颈部色素沉着及色素减退斑3年.皮损组织病理示:表皮角化过度,真皮乳头可见团块状均质淡红染物质,真皮浅层少量炎性细胞浸润,并可见噬色素细胞;甲紫染色和刚果红染色均阳性.诊断:色素异常性皮肤淀粉样变.     

色素异常性皮肤淀粉样变1例

报告1例色素异常性皮肤淀粉样变。患者男,22岁,四肢及项部色素减退斑21年。查体:项部、四肢弥漫性黑褐色斑,其上有较多色素减退斑,大小不一,少数融合,对称分布。皮损病理检查:表皮灶性角化过度,表皮下裂隙,真皮乳头见嗜伊红均质物沉积,可见较多色素滴落及噬黑素细胞,血管周围少许淋巴细胞。甲基紫染色阳性。根据临床表现及皮肤组织病理,诊断为色素异常性皮肤淀粉样变。     

基底细胞癌伴显著皮肤纤维增生1例

患者女,40岁。左下肢黑色丘疹30年。皮肤科情况:左大腿后部见一黄豆大黑色丘疹,表面粗糙,质硬,界清。丘疹中央无明显糜烂、渗出。皮肤组织病理示:表皮棘层肥厚,基底层色素增加,可见基底细胞样瘤细胞自表皮呈蕾芽状突入真皮浅层,瘤团周边细胞呈栅栏样排列,并可见收缩间隙。真皮浅层胶原纤维显著增生,排列成漩涡状、车轮状。诊断:基底细胞癌伴显著皮肤纤维增生。     

色素异常性皮肤淀粉样变病一家系报道

患者,男,61岁。全身皮肤出现色素沉着及减退斑10年余。其父、兄与其有相同的皮疹特征。皮损组织病理示：表皮角化过度,部分上皮脚融合,棘层轻度增生,真皮浅层小血管可见淋巴细胞浸润,部分真皮乳头层可见嗜伊红团块状物质,其间可见裂隙。真皮乳头层团块状物质刚果红染色阳性。结合临床及实验室检查,诊断为色素异常性皮肤淀粉样变病。     

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。     

皮肤组织工程研究现状

人们将组织工程的技术和原理运用于皮肤再造已经成功的研制出了各种类型的皮肤替代物。组织工程化皮肤大致可分为:表皮替代物,真皮替代物,具有表皮真皮双层结构的复合皮肤替代物三种类型。本文就各种皮肤替代物的研制方法和应用,皮肤组织工程的发展和展望做了简要的论述。     

色素异常性皮肤淀粉样变

报告3例色素异常性皮肤淀粉样变.3例患者临床表现为四肢和(或)躯干、面部弥漫色素沉着伴色素减退斑,毛细血管扩张及表皮萎缩不明显,一般手足未累及.自觉症状不明显.本病易被误诊为白癜风、血管萎缩性皮肤异色病等,组织病理诊断及特殊染色有助于鉴别.对其中1例使用共聚焦激光扫描显微镜观察皮损,在真皮乳头处可观察到折光较强的物质沉积,伴有部分真皮乳头毛细血管扩张,皮损基底层有黑素帽增多的现象.     

节段性皮肤僵硬综合征一例

患儿,男,8岁。因右侧股部、臀部及腰部皮肤触之僵硬8年就诊。患者皮损呈单侧分布,伴有轻度多毛和色素沉着。病理活检示表皮过度角化,基底层色素增加,真皮中层胶原纤维增粗、致密,呈均质化,无炎症细胞浸润,附属器未见异常。阿新蓝染色呈阳性。综上诊断为节段性皮肤僵硬综合征。     

Pigment‐independent cAMP‐mediated epidermal thickening protects against cutaneous UV injury by keratinocyte proliferation

The epidermis increases pigmentation and epidermal thickness in response to ultraviolet exposure to protect against UV‐associated carcinogenesis; however, the contribution of epidermal thickness has been debated. In a humanized skin mouse model that maintains interfollicular epidermal melanocytes, we found that forskolin, a small molecule that directly activates adenylyl cyclase and promotes cAMP generation, up‐regulated epidermal eumelanin accumulation in fair‐skinned melanocortin‐1‐receptor (Mc1r)‐defective animals. Forskolin‐induced pigmentation was associated with a reproducible expansion of epidermal thickness irrespective of melanization or the presence of epidermal melanocytes. Rather, forskolin‐enhanced epidermal thickening was mediated through increased keratinocyte proliferation, indirectly through secreted factor(s) from cutaneous fibroblasts. We identified keratinocyte growth factor (Kgf) as a forskolin‐induced fibroblast‐derived cytokine that promoted keratinocyte proliferation, as forskolin induced Kgf expression both in the skin and in primary fibroblasts. Lastly, we found that even in the absence of pigmentation, forskolin‐induced epidermal thickening significantly diminished the amount of UV‐A and UV‐B that passed through whole skin and reduced the amount of UV‐B‐associated epidermal sunburn cells. These findings suggest the possibility of pharmacologic‐induced epidermal thickening as a novel UV‐protective therapeutic intervention, particularly for individuals with defects in pigmentation and adaptive melanization.     

Factors influencing sunless tanning with dihydroxyacetone

BACKGROUND: Sunless tanning preparations have been used for more than 50 years and are still very popular because they provide temporary pigmentation resembling an ultraviolet-induced tan. The pigment is the product of reactions between dihydroxyacetone (DHA) and amino acids in the stratum corneum. OBJECTIVES: To understand the factors that influence the reactions of DHA with amino acids in the stratum corneum with the ultimate goal of producing pigmentation with greater photoprotection. METHODS: The influence of hydration and/or oxygen on the development of DHA-induced pigment was assessed in vivo using an occlusive dressing and ex vitro on human epidermal preparations. Two spectroscopic techniques, diffuse reflectance and fluorescence emission, were used to monitor the extent of pigment development. The optimal relative humidity for DHA-induced pigmentation was assessed on the epidermal preparations. The formation of products from reactions between DHA and nine amino acids was studied in solutions buffered at pH 5 and 7. RESULTS: Development of DHA-induced pigmentation was inhibited by a 24-h occlusive dressing but appeared after its removal, indicating that DHA was still present. High hydration but not the absence of oxygen inhibited coloration of occluded skin. The extent of pigmentation did not vary in a simple manner with hydration, as pigment formation was positively correlated with humidity from 0 to 75% but negatively correlated from 75 to 100%. Lysine, glycine and histidine reacted most rapidly with DHA, with reaction rates greater at pH 7 than at pH 5. The products absorbed with maxima at wavelengths up to 340 nm. CONCLUSIONS: These results indicate that extent of hydration, pH and availability of certain amino acids influence the development of DHA-induced pigmentation in the stratum corneum and suggest that manipulation of these factors might produce pigmentation with greater photoprotection.     

Postinflammatory hyperpigmentation

The epidermis provides a barrier against environmental toxins. The epidermal inflammatory response (dermatitis) causes the release of many peptides, chemical agents that alter the activity of both immune cells and pigment cells. Postinflammatory pigmentation may be an indicator that the melanocytes are part of the epidermal inflammatory system. Programs for treatment of postinflammatory pigmentation have been outlined.     

表皮移植联合叶酸及腺苷钴胺治疗白癜风临床疗效观察

目的：探索以表皮磨削 负压吸疱自体表皮移植术联合叶酸及腺苷钴胺治疗白癜风的效果。方法：36例稳定期白癜风患者在采用表皮磨削 负压吸疱自体表皮移植术的基础上联合服用叶酸及腺苷钴胺，并与35例单纯接受手术者进行了比较；观察术后复色开始出现的时间及第8周被移植区出现色素情况。结果：两组相比，复色开始出现的时间及第8周受区复色面积／实际覆盖皮片面积之比均有显著性差异。结论：叶酸及腺苷钴胺用于表皮磨削 负压吸疱自体表皮移植术，可使受区复色时间提前并克服了色素生长欠均匀之缺陷。     

Epidermal thickness,skin pigmentation and constitutive photosensitivity

The important factors for UV sensitivity in humans are considered to be the skin pigmentation and the epidermal thickness. In this study on 73 Caucasians (age 20–85 years), we investigated in UV unexposed buttock skin the relationship between the UV sensitivity and constitutive skin pigmentation and thickness of the stratum corneum and the cellular part of the epidermis, in 34 normal people and in 39 skin cancer patients (20 patients with cutaneous malignant melanoma and 19 patients with basal cell carcinoma of the skin). Skin pigmentation was measured by skin reflectance spectroscopy, and UV sensitivity by phototest with a solar simulator. Thicknesses of the stratum corneum and the cellular part of the epidermis were determined by light microscopic evaluation of skin biopsies from the phototest areas. We found that epidermal thickness was independent of skin type and was not correlated to constitutive skin pigmentation. Thickness of the stratum corneum was statistically not different in normal persons and in skin cancer patients (P=0.4l) and was independent of gender (P=0.61) and age (P=0.56), while thickness of the cellular epidermis decreased with age (P<0.01). Stratum corneum thickness was found to be of minor importance for the constitutive UV sensitivity (accounting for on average 11% of the total photoprotection), which was mainly determined by the constitutive skin pigmentation (goodness-of-fit for correlation r=0.83). A theoretical model for the relationship of UV dose to induction of clinical erythema grade and skin pigmentation and thickness of the stratum corneum was developed. Objective measurements of skin pigmentation in UV unexposed skin by skin reflectance spectroscopy in Caucasians, normal people and people with cutaneous malignant melanoma and basal cell carcinoma of the skin predicts the constitutive UV sensitivity with a high degree of precision.     

Cholesterol regulates melanogenesis in human epidermal melanocytes and melanoma cells

Abstract:  Cholesterol is important for membrane stability and is the key substrate for the synthesis of steroid hormones and vitamin D. Furthermore, it is a major component of the lipid barrier in the stratum corneum of the human epidermis. Considering that steroid hormone synthesis is taking place in epidermal melanocytes, we tested whether downstream oestrogen receptor/cAMP signalling via MITF/tyrosine hydroxylase/tyrosinase/pigmentation could be possibly modulated by cholesterol. For this purpose, we utilized human primary melanocyte cell cultures and human melanoma cells with different pigmentation capacity applying immunofluorescence, RT-PCR, Western blotting and determination of melanin content. Our in situ and in vitro results demonstrated that melanocytes can synthesize cholesterol via HMG-CoA reductase and transport cholesterol via LDL/Apo-B100/LDLR. Moreover, we show that cholesterol increases melanogenesis in these cells and in human melanoma cells of intermediate pigmentation (FM55) in a time- and dose-dependent manner. Cellular cholesterol levels in melanoma cells with different pigmentation patterns, epidermal melanocytes and keratinocytes do not differ except in the amelanotic (FM3) melanoma cell line. This result is in agreement with decreasing cholesterol content versus increasing pigmentation in melanosomes. Cholesterol induces cAMP in a biphasic manner i.e. after 30 min and later after 6 and 24 h, meanwhile protein expression of oestrogen receptor β, CREB, MITF, tyrosine hydroxylase and tyrosinase is induced after 72 h. Taken together, we show that human epidermal melanocytes have the capacity of cholesterol signalling via LDL/Apo-B100/LDL receptor and that cholesterol under in vitro conditions increases melanogenesis.     

Localization of melanin pigmentation in the skin with Wood's lamp

Examination of the skin or hair with Wood's lamp has long been used to aid in the clinical diagnosis of some cutaneous disorders. A new observation reported here illustrates that Wood's light can be used to determine the depth of melanin pigmentation in the skin: contrast in epidermal pigmentation is increased while contrast in dermal pigmentation is decreased under Wood's lamp illumination compared to ambient visible light. The principles underlying this phenomenon are discussed. Use of the Wood's lamp to localize abnormal melanin pigmentation in the skin can be a guide to clinical diagnosis of hypermelanosis.     

An extract of <Emphasis Type="Italic">Melia toosendan</Emphasis> attenuates endothelin-1-stimulated pigmentation in human epidermal equivalents through the interruption of PKC activity within melanocytes

To elucidate the effects of redox balance regulation on epidermal pigmentation, we used an antioxidant-rich extract of the herb Melia toosendan (dried mature fruits) to assess its effect on endothelin-1 (EDN1)-stimulated pigmentation in human epidermal equivalents and analyzed its biological mechanism of action. Addition of the Melia toosendan extract elicited a marked depigmenting effect on EDN1-stimulated pigmentation after 14 days of treatment, which was accompanied by a significant decrease in eumelanin content. Real-time RT-PCR and Western blotting revealed that the EDN1-stimulated expression of melanocyte-specific proteins (including tyrosinase) was significantly suppressed at the gene and protein levels by the extract. Signaling analysis with specific inhibitors and immunoblots revealed that in melanoma cells treated with the extract, there was a marked deficiency in the EDN1-stimulated phosphorylation of Raf-1, MEK, ERK, MITF and CREB. Since all those proteins are downstream phosphorylation targets of PKC activity, these findings indicate that the Melia toosendan extract attenuates the EDN1-stimulated pigmentation by preferentially inhibiting PKC activity within melanocytes.     

Pigmented hairy epidermal nevus (Becker).

The pigmented hairy epidermal nevus (Becker) is a variety of epidermal nevus in which epidermal thickening may be minimal and hairiness and pigmentation obvious. Characteristically it is a unilateral lesion of the shoulder in males but it may affect other sites, be multiple and bilateral, and be found in women and Negroes. Histological examination may show no epidermal thickening. Nevus cells are not seen in the dermis.     

黄褐斑：表皮屏障与黑素屏障失衡

黄褐斑是一种面部获得性色素增加性皮肤病，发病机制尚不清，概述黄褐斑的表皮屏障及黑素屏障的变化，以及真皮血管的变化。在此基础上推测黄褐斑的可能发病机制为紫外线、化妆品、避孕药等不良刺激导致表皮屏障功能障碍，代偿性引起黑素细胞功能活跃，黑素屏障增强，形成临床上表现为色素沉着为主的皮肤病。进一步导致真皮毛细血管扩张，血管内皮生长因子表达增加，促进色素沉着发生。