网状色素性扁平苔藓

报告1例网状色素性扁平苔藓.患者女,50岁.颈部、躯干及四肢对称分布大片网状棕褐色斑,及褐色斑基础上密集大小不等紫红色多角形扁平丘疹,表面有蜡样光泽,可见Wickham纹.皮损组织病理检查示表皮局限性萎缩,颗粒层增厚,基底细胞液化变性,真皮浅层带状炎性细胞浸润,可见噬黑素细胞.结合临床表现及皮损组织病理改变诊断为色素性扁平苔藓.     

色素性扁平苔藓1例

报告1例色素性扁平苔藓。患者女68岁。胸背部、腋下起黑褐色斑疹半年余,无自觉症状。皮肤科检查见躯干及腑下米粒至蚕豆大黑褐色斑,呈圆形或椭圆形,躯干部皮损主要是向心性分布。组织病理改变符合色素性扁平苔藓。     

色素性扁平苔藓1例

患者男，58岁。面部、颈、躯干、四肢散在分布直径0．1－3．0cm黑褐色班或斑片，无瘙痒。颈及双腋下皮损类似固定性药疹，右颊黏膜可见白色细纹和糜烂。组织病理显示色素性扁平苔藓的改变。     

色素性扁平苔藓1例

患者男,27岁。全身皮肤起褐色皮疹3月余。查体见四肢、躯干散在米粒至绿豆大小圆形或椭圆形紫褐色斑,界清,中央略凹陷,表面有蜡样光泽,可见wickham纹。皮损组织病理:表皮角化过度,基底层及真皮浅层色素增多,基底细胞灶性液化变性,真皮浅层水肿,真皮浅层及血管周围淋巴细胞呈带状浸润。诊断:色素性扁平苔藓。     

光线性角化病伴多发鳞状细胞癌一例

患者男，38岁。因躯干起结节、溃疡，伴有臭味3个月于1991年来我院。20年前发现躯干、四肢散在豆大褐色斑疹。无不适痔状，本人木在意。褐色斑疹逐渐增多，并逐渐在双手掌、双手背、双足跖、足背及蚁肘仲侧出现高粱粒至黄豆大小角化件丘疹，同时伴有毛细血管扩张及皮肤萎缩，末行治疗。近3个月，躯干、四肢出现10余个蚕豆大小结宵，此结节均发生于原褐色斑疹上，伴有微痒，部分形成溃疡，有臭味。     

色素性玫瑰疹1例

色素性玫瑰疹是一种原因不明的色素性皮肤病，无特效疗法。现将报道1例如下。 临床资料 患者男，18岁。因全身发生斑疹3年于2009年6月就诊。自诉3年前无明显诱因于胸部发生红斑，自觉瘙痒，在当地诊所打“抗过敏针”无效，半月后皮损颜色逐渐变为褐色，不再瘙痒。1年内皮损蔓延至全身，部分融合成斑片。在省级医院诊断为“扁平苔藓”，给予阿维A治疗1个月（具体用量不详），无明显效果，遂来我院就诊。     

包素性玫瑰糠疹1例

临床资料 患者，女23岁。躯干，四肢泛发褐色色素斑半年余。患者约半年前无明显诱因于胸前，背部散发大小不一玫瑰红色斑块，无明显痒痛。皮损逐渐扩展至颈、四肢伸侧及整个躯干。数月后皮疹变成灰褐色，曾在外院以色素性荨麻疹诊治（）具体治疗不详，无明显改善。     

成人型色素性荨麻疹1例

色素性荨麻疹又称斑丘疹性皮肤肥大细胞增生症,多在幼儿和青春期发病,成人发病不常见.c-kit基因突变是多数肥大细胞增生症的病因,1本文报道临床所见1例典型成人色素性荨麻疹. 临床资料患者男,56岁,因全身褐色斑丘疹5年就诊,5年前患者躯干出现数处淡红色圆形斑疹,缓慢增多,颜色逐渐转变为红褐色,后蔓延至颜面和四肢.皮损不能自行消失,无明显自觉症状.     

色素性扁平苔藓并发大疱性扁平苔癣1例

患者男,60 岁,躯干泛发灰蓝色斑片1个月余.皮肤科情况:躯干弥漫性灰蓝色斑片,四肢可见散在紫红色扁平斑丘疹,下肢部分皮损伴发水疱,直径约1 cm,疱液清亮,尼氏征阴性.病理检查示表皮萎缩,基底细胞液化形成表皮下疱,真皮浅层血管周围散在中等量淋巴细胞及嗜黑素细胞浸润.诊断:色素性扁平苔藓(LPP)并发大疱性扁平苔癣(B...     

大疱性扁平苔藓

报告1例大疱性扁平苔藓。患者男,51岁。躯干及四肢红斑、丘疹及水疱2个月余。皮肤科检查:躯干、四肢散在较多紫红色扁平丘疹、水疱,呈圆形、椭圆形或多角形,大小不等,界清,部分皮损上覆少许鳞屑。皮损组织病理检查:表皮角化过度,表皮下水疱,疱周基底细胞液化变性,真皮上部较多淋巴细胞呈带状浸润。诊断:大疱性扁平苔藓。     

膜联蛋白A2在银屑病中的表达及意义

目的探讨银屑病患者外周血单个核细胞(PBMC)及皮损处膜联蛋白A2(annexin A2)的表达及其在银屑病发病中的意义。方法流式细胞术检测annexin A2在21例寻常型、5例脓疱型、5例关节病型、12例红皮病型银屑病患者及10例正常人PBMC上的表达;免疫荧光染色检测annexin A2在7例寻常型银屑病患者皮损和4例正常人皮肤处表达。结果 annexin A2在寻常型银屑病患者PBMC及皮损部位中表达均较正常对照增高(P<0.05),关节病型银屑病患者PBMC中annexin A2表达也增高(P<0.05),而红皮病型银屑病患者PBMC中annexinA2表达低于正常对照(P<0.01)。结论 annexin A2在寻常型银屑病患者PBMC和皮损处高表达,在关节病型银屑病PBMC中也高表达,而在红皮病型银屑病患者PBMC中低表达。     

CYP17基因多态性与痤疮中医分型的相关性

目的探讨CYP17基因多态性与痤疮中医分型的相关性。方法提取肝郁气滞型、湿热内蕴型痤疮患者和正常对照者的血DNA标本。设计引物通过PCR技术扩增出包括CYP17基因多态位点的片段,用限制性内切酶Ms- pA1Ⅰ进行酶切,产物在2%琼脂糖凝胶上电泳,确定出CYP17基因的3种基因型(A1A1、A1A2、A2A2),并经测序证实。结果肝郁气滞型组基因型A1A2频率、湿热内蕴型组基因型A1A2频率间及分别与正常对照组基因型A1A2频率比较,差异无显著性意义(P>0.05);肝郁气滞型组基因型A2A2频率和正常对照组基因型A2A2频率比较,差异无显著性意义(P>0.05);湿热内蕴型组基因型A2A2频率分别与肝郁气滞型组基因型A2A2频率和正常对照组基因型A2A2频率比较,差异有显著性意义(P<0.05)。结论CYP17基因-34bp处T→C碱基的置换存在与痤疮湿热内蕴型有关。     

寻常型银屑病患者及正常人S100A6、S100A8、S100A9基因的研究

目的：通过测定家族性寻常型银屑病患者和正常人中S100A6、S100A8和S100A9基因的外显子编码区序列，探索其与银屑病发病的关系。方法：从家族性寻常型银屑病患者和正常人的外周血中提取基因组DNA，用自动测序法测定S100A6、S100A8和S100A9基因的外显子编码区序列。结果：患者和正常对照组的S100A6、S100A8、S100A9基因外显子编码区序列均相同，未发现基因多态性。结论：S100A6、S100A8、S100A9基因的外显子编码区序列与家族性寻常型银屑病发病无相关性。     

携带HPV11基因组的HaCaT细胞APOBEC3s表达及α干扰素的调控

目的 探讨携带HPV11基因组的HaCaT细胞(HPV11.HaCaT)中载脂蛋白B信使RNA编辑酶催化多肽样蛋白3家族(APOBEC3s,A3s)mRNA表达、主要A3蛋白在细胞内的表达、分布,以及外源性α干扰素对其调节.方法 qRT-PCR检测HPV11.HaCaT细胞中A3A、A3B、A3C和A3H mRNA的基础表达水平,并与正常HaCaT细胞作比较;分别用不同浓度的重组人IFN-α2b (rhIFN-α2b)作用于HaCaT、HPV11.HaCaT、Hela细胞6、24、48 h后,qRT-PCR检测A3A、A3B、A3C和A3H mRNA表达水平.细胞免疫荧光染色法观察rhIFN-d2b刺激6h时,A3A蛋白在3种细胞中的表达和分布情况.结果 HPV 11.HaCaT细胞内A3A、A3B、A3C mRNA表达量均明显高于正常HaCaT细胞(P＜0.05).在不同浓度rhIFN-α2b刺激下,3种细胞4种A3成员mRNA表达趋势存在差异,其中A3A升高最为明显.与各自正常对照组相比,106 IU/ml rhIFN-α2b刺激6h时3种细胞的A3A mRNA表达明显升高,差异有统计学意义(HaCaT细胞35.77±5.01比1.00±0.05,P＜ 0.05;HPV11.HaCaT细胞15.34±2.14比0.99±0.01,P＜0.05;Hela 24.60±5.45比0.97±0.03,P＜0.05),而A3B、A3C和A3HmRNA相对表达量均低于10倍.经106 IU/ml rhIFN-α2b处理6h后,3种细胞胞质和胞核中均可见到A3A蛋白的阳性染色增加.结论 HPV11进入HaCaT细胞后,可激活A3s(尤其是A3A)免疫系统.α干扰素诱导A3A的高表达可能是其发挥免疫调控功能的机制之一.     

寻常型银屑病患者皮损中白介素-22和S100A7,A8,A9mRNA的表达及关系

目的研究白介素-22(IL-22)和S100A7,A8,A9mRNA在寻常型银屑病皮损中的表达及关系。方法采用逆转录聚合酶链反应(RT-PCR)技术对35例寻常型银屑病患者皮损和16例正常人皮肤中IL-22,S100A7,A8,A9mR-NA进行检测。结果①IL-22和S100A8,A9mRNA在寻常型银屑病皮损中呈阳性表达,而在正常皮肤中为阴性;S100A7mRNA在寻常型银屑病皮损中的表达水平为1.133±0.0403,较正常对照组0.744±0.0371明显升高,差异有显著性(P<0.01)。②IL-22mRNA与S100A7,A8,A9mRNA的表达呈显著正相关r1=0.543,r2=0.774,r3=0.621,P均<0.01。结论IL-22和S100A7,A8,A9与银屑病的发生和发展中明确相关,可能成为银屑病治疗新的靶位点。     

The CDKN2A p.A148T variant is associated with cutaneous melanoma in Southern Brazil

Several germline mutations and sequence variants in cancer predisposition genes have been described. Among these, the CDKN2A p.A148T variant appears to be frequent in patients with melanoma, at least in certain ethnic groups. In this case-control study, we evaluated 127 patients with cutaneous melanoma and 128 controls from Southern Brazil, the region with the highest melanoma incidence rates in the country. Using PCR-RFLP, we demonstrate that CDKN2A p.A148T variant was significantly more frequent in patients with melanoma than in controls (12.6% vs 3.9%; P=0.009). There was no association between presence of the polymorphism and tumor thickness, site of the primary tumor, melanoma subtype, age at diagnosis, quantitative and qualitative number of nevi. Patients with a positive family of history for other cancers were particularly prone to carry the CDKN2A p.A148T allele. All patients with p.A148T-positive melanoma reported European ancestry, especially German, and this was confirmed using a panel of ancestry-informative INDELs. Our data suggest that CDKN2A p.A148T is a melanoma susceptibility allele in Southern Brazil and is particularly common in patients with melanoma of predominantly European ancestry.     

Vitamin A in acne vulgaris

Thirty-five patients with acne vulgaris were studied regarding vitamin A and E status, and the safety and efficacy of vitamin A supplementation over a 6-week period. The patients studied had significantly lower plasma vitamin A levels than normal controls and a lower frequency of consumption of foods rich in vitamin A. Vitamin E status in the patients was similar to that of normal controls. Vitamin A supplementation had no significant effect on plasma vitamin A levels during the study, but the patients had significantly (P<0.005) higher levels at 6 weeks post-supplementation when compared with pre-supplementation values. Furthermore, vitamin A supplementation was associated with a significant and progressive increase in plasma retinol ester concentration. Vitamin A at the dose administered was ineffective in the treatment of acne and was associated with symptoms compatible with hypervitaminosis A only in a small percentage of patients.     

TNFα‐ and IL‐17A‐mediated S100A8 expression is regulated by p38 MAPK

The antimicrobial peptide S100A8 is known to be upregulated in lesional psoriatic skin compared with non‐lesional psoriatic skin and is believed to play a role in the pathogenesis of psoriasis. However, little is known about the signalling pathways involved in the regulation of S100A8 expression. Using quantitative real‐time RT‐PCR analysis, we demonstrated that stimulation with TNFα and IL‐17A in combination resulted in a significant and synergistic induction of S100A8 mRNA in human keratinocytes. TNFα and IL‐17A also induced the S100A8 promoter activity synergistically. This was demonstrated by a gene reporter assay in cells transfected with a luciferase plasmid construct, consisting of 3502 base pairs of the human S100A8 promoter. The TNFα‐ and IL‐17A‐mediated induction of S100A8 mRNA and protein was mediated by a p38 MAPK‐dependent mechanism, as demonstrated by the use of a p38 MAPK inhibitor. Finally, adalimumab treatment for patients with psoriasis significantly decreased S100A8 mRNA at day fourteen after start of treatment, but not at day four. Taken together, this study demonstrates that the p38 MAPK signalling pathway plays a key role in the TNFα‐ and IL‐17A‐induced expression of S100A8 in cultured human keratinocytes.     

Elevated serum levels of calcium-binding S100 proteins A8 and A9 reflect disease activity and abnormal differentiation of keratinocytes in psoriasis

BACKGROUND: The expression of calcium-binding S100 molecules organized within the epidermal differentiation complex on chromosome 1q21 is disturbed in hyperproliferative skin diseases such as psoriasis. OBJECTIVES: We studied whether serum levels of S100 proteins A8 (S100A8) and A9 (S100A9) are elevated in psoriasis, correlated their amounts with disease activity and identified potential cellular sources. METHODS: Serum obtained from psoriasis patients or from healthy individuals was studied for S100A8 and S100A9 levels by enzyme-linked immunosorbent assay. Data were correlated to disease activity as reflected by the Psoriasis Area and Severity Index (PASI). Cellular sources of S100A8 and S100A9 were identified by in situ hybridization and immunohistochemistry of lesional psoriatic and nonlesional, nonpsoriatic skin. RESULTS: A significant increase of S100A8/S100A9 serum levels was found in patients with psoriasis compared with healthy controls. Grading the patients into two groups of severity, individuals with a PASI of <15 showed serum levels of 705+/-120 ng mL-1 (mean+/-SEM, n=18), those with a PASI of >or=15 showed levels of 1315+/-150 ng mL-1 (n=32) while controls presented with 365+/-50 ng mL-1. Performing in situ hybridization of lesional psoriatic skin we detected a dramatic induction of both S100A8 and S100A9 mRNA and protein primarily in the suprabasal layers of the epidermis while expression was negligible in nonlesional, nonpsoriatic interfollicular epidermis. CONCLUSIONS: Our data demonstrate that hyperproliferation and abnormal differentiation of psoriatic skin is associated with a massive upregulation and secretion of S100A8 and S100A9, suggesting not only a prominent role of these molecules during intracellular calcium-dependent signalling but also implying distinct extracellular functions.