72例银屑病患者生活质量调查及影响因素研究

目的：探讨银屑病对患者生活质量的影响状况及对生活质量主要影响因素的分析。方法：采用皮肤病生活质量指数（dermatology life quality index,DLQI）和银屑病无能指数（psoriasis disability index,PDI）量表调查72例银屑病患者,记录患者的一般情况;同时采用银屑病面积和严重程度指数（psoriasis area and severity index,PASI）评分评判患者病情的严重程度,采用方差分析比较不同病情严重程度患者间生活质量的差异。结果：DLQI与PDI调查结果均显示银屑病患者在工作学习方面的分值（DLQI：1．69±1．31,PDI：2．92±2．61）最高,受到影响最大;PDI量表显示男性患者总分平均值高于女性患者,差异有统计学意义（t=2．73,P〈0．05）,DLQI与PDI量表均显示重度（PASI〉10）患者的总分平均值高于轻度（0〈PASI≤5）患者,差异有统计学意义（DLOQ：t=0．72;PDI：t=1．45,P值均〈0．05）。结论：银屑病为一种身心性疾病,患者在工作学习方面受到的影响较明显;与患者生活质量最为相关的是病情的严重程度,病情严重程度越高的患者生活质量受到的影响越大。     

大麻素2型受体在寻常性银屑病皮损组织中的表达

目的 探讨大麻素2型受体在寻常性银屑病皮损组织中的表达及其意义。 方法 实时荧光定量聚合酶链反应（RT-PCR）、免疫组化技术检测20例寻常性银屑病患者皮损组织及皮损周围组织、10例非银屑病患者的正常皮肤组织中大麻素2型受体在mRNA和蛋白不同水平的表达情况。 结果 寻常性银屑病皮损组织、皮损周围组织及正常皮肤中均有大麻素2型受体mRNA表达,寻常性银屑病组表达明显高于皮损周围组及正常对照组（P < 0.05）;三组皮损组织均有大麻素2型受体蛋白表达,且寻常性银屑病组表达明显高于皮损周围组、正常对照组,差异有统计学意义（P < 0.05）。 结论 寻常性银屑病皮损组织中大麻素2型受体在基因及蛋白水平表达均升高,提示大麻素2型受体可能与寻常性银屑病的发生发展有关联。     

白细胞介素33/转硫酶同系物2信号通路与皮肤相关性疾病的研究进展

白细胞介素33/转硫酶同系物2信号通路是一条促炎症通路,通过增加T淋巴细胞介导的炎症反应刺激Th2细胞因子的分泌,促进肥大细胞和嗜酸性粒细胞脱颗粒,及诱导Th2细胞和中性粒细胞趋化,在银屑病、白癜风、特应性皮炎和鳞状细胞癌等多种皮肤炎症性疾病的免疫反应和肿瘤的免疫应答中发挥作用。研究表明,转硫酶同系物2基因存在单核苷酸多态性及编码变异,因此,白细胞介素33/转硫酶同系物2通路在疾病的发病机制中也表现了一定的遗传背景。转硫酶同系物2基因多态性可能提高了患者的患病风险。免疫组化可以指导治疗方案的选择和预后的判断,而白细胞介素33和（或）转硫酶同系物2水平的降低则有利于炎症性疾病的治疗。     

The risk of organ-based comorbidities in psoriasis: a systematic review and meta-analysis

BackgroundThe close relationship between psoriasis and concomitant diseases is widely accepted. However, a comprehensive analysis of organ-based comorbidities in psoriasis is still lacking.ObjectiveThe authors aimed to present the risk of organ-based comorbidities in psoriasis by comparing the general population.MethodsThe authors retrieved a search of Pubmed, EMBASE, and Cochrane databases for studies reporting organ-based comorbidities in psoriasis versus the general population. Observational studies that met the following criteria were assessed: 1) Psoriasis diagnosis; 2) Cardiovascular or kidney or liver or respiratory or cerebrovascular outcomes; 3) Comparison group of individuals without psoriasis. Pooled Relative Risks (pRRs) and 95% Confidence Intervals (CIs) were calculated by using the random-effect model.ResultsFifteen observational studies with 216,348 psoriatic patients and 9,896,962 individuals from the general population were included. Psoriasis showed a greater risk of organ-based comorbidities. Compared to the general population, pRR for all organ-based comorbidities was 1.20 (95% CI 1.11?1.31) in psoriasis, and pRR was lower in mild 0.61 (95% CI 0.46?0.81) than in moderate/severe patients. pRR was 1.20 (95% CI 1.11?1.30) for cardiovascular, 1.56 (95% CI 1.20?2.04), and 1.75 (95% CI 1.33?2.29) for cerebrovascular and liver diseases, respectively. pRR for coexisting renal and cardiovascular events was 1.09 (95% CI 1.01?1.18). pRR for coexisting renal and cerebrovascular events was 1.28 (95% CI 0.99?1.66). pRR for coexisting renal and liver diseases was 1.46 (95% CI 1.10?1.94). pRR for coexisting cardiovascular and liver diseases was 1.41 (95% CI 1.11?1.80).Study limitationsThere is heterogeneity.ConclusionPsoriasis has a higher risk of single and multiple organ-based comorbidities than the general population. The present study will further improve attention to psoriasis as a systemic inflammatory disease.     

Are psoriasis and psoriatic arthritis the same disease? The IL-23/IL-17 axis data

Psoriatic arthritis (PsA) is a psoriasis (Ps)-associated inflammatory joint disease that affects peripheral joints, entheses, spine, and eyes. PsA and Ps are likely to be the same disease. PsA develops in nearly 70% of patients with Ps, and the hallmark of the disease is bone erosions and bone formation. Both innate and adaptive immunity appear to contribute to pathogenesis of PsA and Ps. Trauma may be a trigger factor for both PsA and Ps. The same T cell clones were reported to be present in both synovial tissues and skin lesions suggesting that a common antigen drives T cell immune response in the joints and skin lesions of patients with PsA. The IL-23/IL-17 axis plays a critical pathogenic role for both PsA and Ps, and biologics neutralizing IL-17A or IL-23/IL-12 are effective therapies for PsA and Ps. The differential expression of Th17 cytokines IL-17 and IL-22 at various sites could explain the different manifestations of the disease. IL-17 is highly expressed in peripheral joints and skin lesions and causes bone erosions. IL-22 is highly expressed in skin lesions and entheses, not peripheral joints, and cause bone formation. Finally, mannan from baker's yeast caused PsA-like arthritis and Ps-like skin lesions that were blocked by IL-17 treatment. These data suggest that PsA and Ps are likely to be the same disease exhibiting different manifestations depending on the local cytokine production.     

银屑病生物治疗研究进展

 当前医学界一致认为，银屑病是一种 T 细胞引发并维持的自身免疫性疾病，病人机体免疫系统紊乱，健康细胞受到攻击，造成临床上典型的皮肤鳞屑性炎症病变^[1]。这种慢性炎症性疾病的病理过程包括T细胞浸润、真皮血管的改变、表皮角质细胞过度增生和异常分化 。其中参与银屑病发病的 T 细胞大致经历3个阶段的变化：T细胞（CD45RO+）的初始活化；T 细胞迁移至病变皮肤；活化T 细胞释放细胞因子发挥促增殖功能。真皮内的 CD4+ T细胞及其产生的细胞因子是银屑病发病的中心环节，角质细胞与血管内皮细胞的变化只是继发于细胞免疫机制异常的一种改变^[2]。随着对银屑病发病机制及免疫学机制研究的不断深入，人们陆续开发出多种生物制剂。这些生物制剂与传统的化学制药制造出来的具有严格化学分子式的小分子药品完全不同，它们都是蛋白质大分子，可以特异性作用于T细胞活化过程中不同的信号转导分子及途径，从而阻断疾病进程。此类生物制剂均通过生物工程技术获得，按性质大致可以划分为重组单克隆抗体（单抗）、重组抗体融合蛋白、重组细胞因子或生长因子等 3 大类；根据作用于 T 细胞活化靶点的不同，又可以分为针对原发性刺激、阻断共刺激分子作用、抑制T细胞增殖、抑制有炎症介导活性细胞因子和平衡有免疫调节活性的细胞因子等 5 大类^[3-4]。生物制剂的出现，为银屑病治疗提供了新的选择，正逐步改变着皮肤科医师治疗银屑病的传统模式。本文就近几年来银屑病生物治疗方面的最新研究进展做一综述。......     

银屑病发病机制研究进展

银屑病（psoriasis）是多种免疫细胞共同参与的慢性复发性炎症性皮肤病,它具有明显的鳞屑性红斑和不同程度的自觉症状,严重影响患者的生活质量。该病的发病机制探讨多集中在遗传、感染、免疫等方面。目前,越来越多的研究证明了IL-23和CD4阳性辅助性T淋巴细胞17（CD4＋Thelper17,Thl7）在银屑病病理机制中起到了关键作用。本文就银屑病发病机制的进展作一综述。     

HIF-1α mRNA在寻常型银屑病及脂溢角化病皮损表皮中的表达及意义

[目的]研究低氧诱导因子-1α（HIF-1α） mRNA在寻常型银屑病及脂溢性角化病皮损表皮中的表达,探讨其在银屑病及脂溢性角化病中的作用机制.[方法]应用原位杂交法检测HIF-1α mRNA在寻常型银屑病、脂溢性角化病及正常皮肤组织各25例皮损表皮中的表达和分布.[结果]在25例寻常型银屑病皮损表皮的中下层可见HIF-1α mRNA阳性表达,在25例脂溢性角化病皮损表皮的全层可见HIF-1α mRNA阳性表达,在正常皮肤的表皮未见HIF-1α mRNA的表达;银屑病、脂溢性角化病皮损表皮中HIF-1α mRNA的表达阳性率均为100%（25/25）,均显著高于正常对照组,其差异有统计学意义（P〈0.01）.[结论]HIF-1α mRNA在寻常型银屑病及脂溢性角化病皮损的表皮中表达均增高.