银屑病伴瘙痒的临床特点、发病机制及治疗研究进展

以往认为银屑病属于非瘙痒性皮肤病, 近年来, 人们逐渐认识到瘙痒是加重银屑病患者疾病负担的因素之一。本文主要阐述瘙痒在银屑病中的临床特点, 关注神经源性炎症中神经肽异常表达和神经末梢异常分布在瘙痒发病机制中作用, 介绍治疗银屑病对瘙痒症状缓解的影响。     

银屑病瘙痒机制的研究进展

瘙瘁是银屑病患者常见的临床症状,易造成患者的痛苦,降低患者生活质量.除神经系统、免疫系统、血管系统以及皮肤之间的相互作用外,其他相关因子也可能参与了银屑病瘙痒机制.深入探索银屑病瘙痒机制,能为银屑病瘙瘁的治疗提供新的思路和方法,从而更加针对性地治疗银屑病患者的瘙痒症状.     

银屑病的瘙痒机制及其临床意义

瘙痒是银屑病患者常见且影响最大的症状,严重影响患者的身心健康,其发病机制复杂,涉及神经免疫及炎症等多方面。目前的治疗方案多针对银屑病皮损,可以一定程度缓解瘙痒,但针对瘙痒的治疗方法选择有限。该文对银屑病瘙痒的流行病学、机制、临床表现及治疗的相关研究进展作一综述。     

瘙痒发生机制的研究进展

瘙痒是一种常见的皮肤感觉，神经生理学研究已经证实，有特异性的神经传导通路参与瘙痒的发生。基于对外周性瘙痒(致痒因子感受性瘙痒)和中枢性瘙痒(神经源性瘙痒和神经性瘙痒)的认识．综述与瘙痒发生有关的外周机制和中枢机制．为临床治疗提供理论依据。     

银屑病瘙痒机制及治疗研究进展

瘙痒是银屑病患者的一种常见症状,严重影响患者的生活质量.但其瘙痒的机制尚不清楚,许多常规治疗瘙痒的药物并不能有效缓解银屑病的瘙痒.目前认为,银屑病皮损中神经分布异常增多和敏感性增加,炎症细胞在病灶中聚集、活化并释放炎症介质是银屑病瘙痒的主要原因.抗组胺药不能有效控制银屑病瘙痒,而神经肽受体拮抗剂、免疫抑制剂及光疗等为治疗银屑病瘙痒的有效方法.

Abstract：

Pruritus is an important symptom of psoriasis.It seriously affects the quality of life of psoriatic patients,but its pathogenesis remains unanswered.Many routine treatments cannot relieve the pruritus in psoriasis effectively.It has been demonstrated that the pruritus in psoriasis is mainly attributed to the abnormally increased innervation and sensitivity of sensory nerves,as well as the aggregation,activation of and release of inflammatory mediators by inflammatory cells.Antihistamine drugs are usually ineffective for the treatment of pruritus in psoriasis,while antagonists of neuropeptide receptors,immunosuppressants and phototherapy have shown favorable efficacy.     

银屑病的瘙痒特征及相关因素分析

目的调查银屑病患者中瘙痒发生率、瘙痒程度等临床特征及其影响瘙痒的相关因素。方法采用问卷调查的形式调查了112例银屑病患者,评价其瘙痒特征及影响瘙痒的相关因素。结果 112例银屑病患者中83%存在不同程度瘙痒,相关分析显示:患者瘙痒与否与年龄、疾病活动度呈显著相关(P0.05),而与患者性别、病程、家族史、吸烟、饮酒及身体质量指数(BMI)无相关性,瘙痒程度与银屑病皮损面积及严重程度指数(PASI)评分、浸润程度呈显著相关(P0.05),而与红斑、鳞屑无相关性。结论大多数银屑病患者存在不同程度的瘙痒症状,年纪越大、皮损越广泛、浸润程度越高以及处在进展期的银屑病患者瘙痒越剧烈。     

银屑病发病机制的研究进展

银屑病是一种与多种因素相关的慢性炎症性皮肤疾病.在过去10年研究人员提出了该病发病机制可能涉及的因素,但未能建立一个包含所有致病因素的模型.伴随分子生物学技术的进步,现将银屑病发病机制的研究进展综述如下.     

银屑病发病机制的现代概念

近十年来银屑病的发病机制的研究有了显著的进展，其中有关免疫－炎症病理生理机制的研究已获较多实验资料，发病机制概念的更新为银屑病药物治疗的实验和临床研究提供了新线索。     

脂肪因子在银屑病发病机制中的研究进展

银屑病是一种慢性炎症性皮肤病,患者多伴有系统性代谢性疾病。脂肪组织作为内分泌器官可分泌多种脂肪因子参与多种代谢性疾病和炎症性疾病的发病。目前的研究证实一些脂肪因子可能参与银屑病的发病过程,并且为将来的诊断治疗提供新的生物学标志。     

IL-33在银屑病发病机制中的研究进展

银屑病是一种炎症性皮肤病,其发病与多种细胞因子有关。白细胞介素(IL)-33是IL-1细胞因子超家族的成员,与多种疾病关系密切,尤其是在急、慢性炎症的发生与发展中发挥着重要的作用。近年来,越来越多的研究发现IL-33在银屑病的发病中起着重要的作用,基于IL-33的治疗也取得了一定的进展。本文就IL-33在银屑病中的研究进展作一综述。     

Eosinophils, pruritus and psoriasis: effects of treatment with etretinate or cyclosporin-A

Background The antipsoriatic drugs cyclosporin A (CyA) and etretinate have been found to influence proinflammatory eosinophilic leukocytes and pruritus.
Aim We compared the number of Wood eosinophils, concentration of serum eosinophil cationic protein (ECP), and pruritus in patients with psoriasis treated with either CyA or etretinate.
Study design Patients with psoriasis vulgaris were randomly assigned to treatment for 10 weeks with either CyA ( n = 21) or etretinate ( n = 10). The psoriasis area-and-severity index (PASI-score) and pruritus (according to a 0–3 scale) served as clinical parameters, the blood esosinophil counts (Coulter Counter) and the serum ECP (RIA, Pharmacia) as laboratory parameters.
Results After CyA treatment the PASI-score amounted to 24 ± 4%, after etretinate to 56 ± 6% of the initial values (mean ± SEM). One week after CyA treatment, esosinophils dropped from 190 ± 21 to 137 ± 16/μ ( P = 0.038, Wilcoxon test), after 10 weeks to 127 ± 18/μ ( P = 0.006). By contrast, under etretinate blood eosinophil counts only changed marginally. Before treatment, ECP concentrations of 15.71 ± 1.30 (CyA) and 15.3 ± 5.53 μg/1 (etretinate) were measured (normal range 3–16 /μg/1), ECP remained constant under both CyA and etretinate or tended to increase after 10 weeks; about 50% of the patients exhibited elevated ECP concentrations. Pruritus diminished more with CyA than etretinate therapy. PASI-scores and pruritus were directly proportional.
Outcome We conclude that treatment of psoriasis with CyA leads to a rapid drop of blood eosinophils and that the activation state of eosinophils does not decrease after antipsoriatic treatment. Pruritus in psoriasis is coupled to disease severity. The underlying antipsoriatic mechanisms of CyA may be linked to lowering the number of blood eosinophils.     

银屑病患者的心理压力、神经内分泌系统与肥大细胞研究现状

银屑病中有相当比例的患者因心理压力而使病情恶化,但其机制尚不明确.心理压力能激活下丘脑-垂体-肾上腺轴和皮肤感觉神经,导致内分泌激素和神经介质释放.多种激素和神经介质能活化肥大细胞产生和释放一系列的炎症介质和细胞因子.银屑病患者中,一些激素、神经肽、感觉神经纤维和肥大细胞在表达水平和数量上增高.心理压力影响银屑病病情的机制之一可能与应激介质通过肥大细胞的作用有关.     

银屑病发病机制中免疫学研究进展

银屑病的发病机制与免疫关系密切,近几年研究倾向于银屑病是Th1/Th17混合途径的免疫性疾病.银屑病的发病中除了有树突细胞、T细胞、角质形成细胞以及Tb1型的细胞因子如白介素12、白介素18等参与外,还有Th17型细胞因子,如白介素23及白介素22等的参与,Th17型免疫反应可能在银屑病发病中起到重要的作用.     

Characteristics of Pruritus according to Morphological Phenotype of Psoriasis and Association with Neuropeptides and Interleukin-31

BackgroundPruritus is a common symptom in psoriasis. However, few studies have assessed the characteristics of pruritus according to morphological phenotypes of psoriasis.ObjectiveTo investigate the characteristics of pruritus according to morphological phenotypes of psoriasis and to assess the association with inflammatory mediators related to pruritus.MethodsPsoriasis patients were divided into 2 groups according to clinical phenotype: eruptive inflammatory (EI) and chronic stable (CS). Clinical data of pruritus were assessed by an itch questionnaire. Serum neuropeptides and cytokines including substance P, histamine, vasoactive intestinal peptide, neuropeptide Y, calcitonin gene-related peptide and interleukin-31 (IL-31) were quantitatively measured.ResultsIn total, 50 patients with psoriasis (30 male, 20 female; mean age, 45.7 years) were studied (EI, n=15 and CS, n=35). Pruritus was reported by 80% of EI and CS patients. There were no significant differences in prevalence of pruritus, pruritus intensity, severity of psoriasis, serum neuropeptides, or IL-31 between the 2 groups.ConclusionThe morphological phenotype does not seem to be an important factor affecting the prevalence and characteristics of pruritus in psoriasis.     

降钙素基因相关肽在银屑病发病机制中的研究进展

银屑病发病机理目前尚不完全清楚,研究人员在对皮损的组织病理研究中发现,银屑病的组织病理表现及皮肤内神经纤维的过度增生均与皮损内高水平的神经介质相关,基于相关研究确立了银屑病神经源性炎症发病机制的概念［１］……     

Clinical Characteristics of Pruritus in Patients with Scalp Psoriasis and Their Relation with Intraepidermal Nerve Fiber Density

Background

The scalp is frequently affected in psoriasis patients, and pruritus can adversely affect the quality of life of affected patients. Few studies have assessed pruritus in scalp psoriasis.

Objective

To determine the correlation among the clinical characteristics of pruritus, psoriasis scalp severity index (PSSI), and intraepidermal nerve fiber (IENF) density in psoriatic scalp lesions.

Methods

Eighty patients (53 men, 27 women; mean age, 46.4 years; mean PSSI, 19.9) with scalp psoriasis were evaluated by using the PSSI and the Leuven itch scale. Biopsies were obtained from the lesional and nonlesional skin of 19 patients (10 men, 9 women; mean age, 37.8 years; mean PSSI, 25.8). Immunofluorescence staining of protein gene product 9.5 was performed to determine the IENF density.

Results

Sixty-four patients (80%) complained of pruritus associated with scalp psoriasis, which negatively affected their quality of life to varying degrees. A moderate positive relation between PSSI score and pruritus intensity was identified (r=0.225 and p=0.044). The IENF density in psoriatic lesions was significantly higher than that in the nonlesional scalp (6.2±1.2 vs. 4.2±1.6, p<0.001). However, the correlations between IENF density and PSSI score, and IENF density and pruritus intensity were insignificant.

Conclusion

These results indicate that pruritus prevalence is high in patients with scalp psoriasis, and pruritus considerably influences the patients'' daily lives and quality of life. In addition, high IENF density in psoriatic scalp lesions may play a role in the development of pruritus in scalp psoriasis.     

趋化因子在银屑病发病机制中的研究进展

银屑病是一种常见的慢性炎症增生性皮肤病,其皮损的产生和维持需要多种细胞共同作用,在这个过程中,免疫细胞浸润到皮肤,引起表皮角质形成细胞及血管内皮细胞改变.趋化因子是一类控制细胞定向移动的细胞因子,可分为4个亚族,在炎症和感染皮肤的生理反应中,趋化T细胞及其他细胞迁移及定植到皮肤,在银屑病的发病过程中起到了重要的作用.