慢性荨麻疹患者负性情绪与血清神经生长因子水平的相关性研究

为探讨慢性荨麻疹(CU)患者负性情绪(焦虑/抑郁)与血清神经生长因子(NGF)水平变化的关系,应用焦虑自评量表(SAS)和抑郁自评量表(SDS)对慢性荨麻疹患者进行问卷测评;双抗夹心酶联免疫吸附法测定其血清NGF水平,并与正常对照人群比较。CU患者血清NGF水平高于正常对照人群,且CU患者中负性情绪的程度与血清NGF水平呈正相关。CU患者负性情绪对病情活动的影响与血清NGF的变化之间可能存在关联。     

多形性日光疹患者负性情绪与神经生长因子和P物质水平的相关性

目的探讨多形性日光疹(PLE)患者焦虑和抑郁负性情绪与血清神经生长因子(NGF)和P物质(SP)水平的关系。方法应用焦虑自评量表(SAS)和抑郁自评量表(SDS)对多形性日光疹患者进行问卷测评,双抗夹心酶联免疫吸附法测定其血清中NGF和SP水平,并与正常人作比较。结果 PLE患者焦虑和抑郁评分高于正常人,且与血清NGF和SP水平呈正相关。结论 PLE患者焦虑和抑郁负性情绪对病情影响与血清NGF和SP水平变化可能有关联。     

物理性皮肤病

20130746多形性日光疹患者负性情绪与神经生长因子和P物质水平的相关性/王刚(青海大学附属医院皮肤科),燕华玲,冶娟…∥中国皮肤性病学杂志.-2012,26(2).-112～113应用焦虑自评量表(SAS)和抑郁自评量表(SDS)对多形性日光疹患者进行问卷测评,双抗夹心酶联免疫吸附法测定其血清中神经生长因子(NGF)和P物质(SP)水平,并与正常人作比较。结果 :多形性日光疹     

银屑病患者P物质、神经生长因子水平与焦虑、抑郁的相关性研究

正银屑病是一种常见、易复发的慢性炎症性皮肤病,其发病机制目前尚不明确。国外的研究[1]表明银屑病是典型的心身疾病,心理因素如焦虑及抑郁等负性情绪可诱发或加重银屑病,有相当比例的银屑病是由精神紧张而触发或加重。近年来,有研究发现血清P物质(SP)和神经生长因子(NGF)可能是焦虑及抑郁情绪影响某些心身性皮肤病如银屑病病情活动程度的相关物质[2],但目前有关心理因素、SP及NGF与银屑病发病的报道国内很少见。本研究通过检测银屑病患者血清SP和NGF的水平,并对患者进行焦虑及抑郁的心理测试评估,探讨银屑病患者精神因素与血清中SP、NGF的相关性。     

物理性皮肤病

20130078多形性日光疹患者负性情绪与神经生长因子和P物质水平的相关性/王刚(青海大学附院皮肤科),燕华玲,冶娟…∥中国皮肤性病学杂志.-2012,26(2).-112～113应用焦虑自评量表(SAS)和抑郁自评量表(SDS)对多形性日光疹患者进行问卷测评,双抗夹心酶联免     

寻常性银屑病患者瘙痒与无瘙痒皮损中神经生长因子及其受体TrkA的表达

瘙痒为银屑病患者中常见的症状,据报道约80%银屑病患者伴有瘙痒[1],为所有症状中令患者最痛苦的,占81.8%[2].我们通过检测瘙痒与无瘙痒的寻常性银屑病患者皮损处神经生长因子(NGF)及其高亲和力p140受体(即Trk A)表达分布情况.探讨NGF和TrkA是否在银屑病瘙痒发生过程中发挥作用.     

银屑病患者认知功能障碍分析

目的:明确银屑病患者认知功能特点及影响因素。方法:对43例银屑病患者、30名健康对照采用蒙特利尔认知功能评估量表(MoC A)进行认知功能的评估,同时使用贝克抑郁自评量表(BDI)及贝克焦虑自评量表(BAI)进行抑郁及焦虑情绪的评估,并对可能影响银屑病患者认知功能的因素进行分析。结果:银屑病患者的认知功能障碍发生率为30.2%。银屑病认知障碍组视空间功能及执行功能得分分别为1.69±1.25和2.46±0.87,显著低于银屑病认知正常组(3.03±0.80,3.33±0.88)及对照组(3.30±0.75,3.57±0.56),差异均有统计学意义(均P0.05)。经多元回归分析发现,银屑病患者的年龄、病程及BDI评分是影响认知功能的消极因素(P0.05)。结论:银屑病患者的部分认知域功能较正常人群减退,主要累及视空间功能及执行功能。影响银屑病患者认知功能的因素包括年龄、病程与抑郁情绪。     

心理护理对银屑病患者心理状态的影响

目的探讨银屑病患者的心理特点及心理护理措施。方法采用焦虑自评量表(SAS)、抑郁自评量表(SDS)和症状自评量表(SCL-90)对160例银屑病患者的心理状况进行调查评估,定时定期对患者进行心理干预。结果 56.25%银屑病患者有抑郁症状,28.75%有焦虑症状;经心理护理干预后,抑郁患者的比例降至15.63%,焦虑患者降至4.55%。结论有效的心理护理措施能够显著降低银屑病患者焦虑和抑郁的比例,有利于患者身心的恢复。     

银屑病患者抑郁和焦虑的调查及其对共患病的影响

目的：研究银屑病患者抑郁和焦虑的状况及其对共患病的影响。方法：采用一般情况问卷（自行设计）及抑郁自评量表(SDS)、焦虑自评量表(SAS)对来我院就诊的184例银屑病患者进行调查及评定。结果：184例患者中,合并抑郁或焦虑的银屑病患者113例（61.41%）。合并抑郁或焦虑的银屑病患者与不合并抑郁或焦虑相比发生心血管疾病、脑血管疾病、糖尿病、高血压和高脂血症的比例更高。结论：抑郁或焦虑是银屑病患者发生心血管疾病、脑血管疾病、糖尿病、高血压、高脂血症的独立危险因素。     

心理护理对寻常型银屑病患者病情恢复影响评价

1 资料和方法 1.1 临床资料病例来源2007年1月至2008年12月在本院住院的寻常型银屑病患者.纳入标准:①符合赵辨<临床皮肤病学>寻常型银屑病的诊断标准,处于进行期或静止期的病人.②治疗前3个月内未用治疗本病的药物及方法.③应用焦虑自评量表(SAS)和抑郁自评量表(SDS)1评定患者情绪状态,阳性者入选.     

神经生长因子受体P75和P140trkAmRNA在寻常型银屑病患者皮损中的表达

目的研究神经生长因子(nerve growth factor,NGF)受体P75和P140trkA在寻常型银屑病发病机制中的作用.方法应用原位杂交技术检测了33例寻常型银屑病患者(18例为进展期,15例为静止期)和10例正常人皮肤组织中两受体(P75和P140trkA)mRNA的表达情况.结果与正常人皮肤比较,寻常型银屑病皮损及非皮损中P75和P140trkA受体mRNA的表达明显上调,且皮损中的表达明显高于非皮损区(P＜0.01);进展期患者皮损与非皮损中P75和P140trkA受体mRNA的表达分别高于静止期患者的皮损与非皮损区(P＜0.01).结论神经生长因子及其两受体可能是参与银屑病病理机制的重要因子.     

Decreased cutaneous expression of stem cell factor and of the p75NGF receptor in urticaria

BACKGROUND: Mast cells, the main effector cells in urticaria, have been reported to be increased in number in lesional and nonlesional skin of urticaria patients, but the underlying mechanisms have so far not been studied. Serum NGF has however, been reported to be increased in urticaria. OBJECTIVES: We have therefore explored the potential involvement of known mast cell growth modulating factors in urticaria. METHODS: Tissue sections from patients with different types of urticaria and healthy controls were studied for the immunohistochemical expression of known mast cell growth factors (stem cell factor, SCF; nerve growth factor, NGF), of the inhibitory granulocyte-macrophage colony-stimulating factor (GM-CSF), and of the corresponding receptors, using the alkaline phosphatase-antialkaline phosphatase technique. RESULTS: Compared to skin of normal controls, staining for SCF, but not for NGF and GM-CSF, was significantly decreased in epidermis, endothelium and perivascular cells in lesional and nonlesional skin of all urticarias. On separate analysis of urticaria subtypes, decreased expression reached significance only in delayed pressure urticaria. Expression of the p75NGF receptor (p75NGFR) was also significantly decreased on endothelium and on perivascular cells of lesional and nonlesional skin in all urticarias. On evaluation of serial sections, p75NGFR expression was also decreased on c-Kit positive dermal mast cells. In contrast, expression of the NGF receptor tyrosine kinase and of the SCF and GM-CSF receptors was unchanged. CONCLUSIONS: These findings show that SCF and p75NGFR are selectively and systemically down-regulated in the skin of urticaria patients and may represent a negative feedback to increased mast cell reactivity and proliferation.     

Desmoplastic and spindle cell melanomas express protein markers of the neural crest but not of later committed stages of Schwann cell differentiation

BACKGROUND: The rare desmoplastic and spindle cell variants of malignant melanoma exhibit histological and biochemical features suggestive of early Schwann cell differentiation. These features include a spindle-shaped morphology, neurotropism, and the expression of the low affinity nerve growth factor receptor (p75NGFR). METHODS: We evaluated by immunohistochemistry (using formalin-fixed, paraffin-embedded tissues) nine desmoplastic and three spindle cell melanomas for the expression of peripherin, p75NGFR, neural cell adhesion molecule (CD56/N-CAM), and growth-associated phosphoprotein-43 (GAP-43). Peripherin is expressed in the neural crest and in neurons, but not in cells committed to the Schwann cell lineage. p75NGFR and CD56/N-CAM also are expressed in early neural crest cells, but persist in unmyelinated and early premyelinating Schwann cells. GAP-43 is expressed in unmyelinated Schwann cells, but is downregulated in the later premyelinating to promyelinating stages of cells committed to the Schwann cell lineage. RESULTS: Peripherin was expressed in 7/12 (58%), p75NGFR in 4/12 (33%), and CD56/N-CAM in 6/12 (50%) of the desmoplastic and spindle cell melanomas. GAP-43 was not expressed (0%) in any of the 12 melanomas (chi2, p = 0.05). CONCLUSIONS: Desmoplastic and spindle cell melanomas express protein markers common to cells of the neural crest and to neurons similar to the immunophenotype previously reported for epithelioid cell melanomas. The expression of peripherin and the lack of expression of GAP-43 further define that these rare subtypes of melanoma do not recapitulate the later committed stages of Schwann cell differentiation.     

Low‐affinity nerve growth factor receptor (P75 NGFR) as a marker of perineural invasion in malignant melanomas

Background: Perineural invasion (PNI) is a well‐recognized route of tumor extension in cutaneous neoplasms. Despite an established association with increased local recurrences and metastases, the mechanisms responsible for PNI have yet to be elucidated. We hypothesize that P75 NGFR, a nerve growth factor receptor, may be implicated in the pathogenesis of PNI in these tumors. Methods: P75 NGFR immunohistochemical staining was performed on 47 skin tumors with PNI including invasive squamous cell carcinomas (SCCs = 29), basal cell carcinomas (BCCs = 8) and malignant melanomas (MMs = 10). These were compared with similar lesions without PNI (SCCs = 7, BCCs = 7 and MMs = 9). Results: P75 NGFR staining was absent in all invasive SCCs irrespective of the presence of PNI (n = 0/36). Two BCCs with PNI (n = 2/8) and three without PNI (n = 3/7) showed focal P75 NGFR staining. Interestingly, 8 of 10 invasive MMs with PNI had positive P75 NGFR expression (80%), in contrast to only 1 of 9 without PNI (11%). Conclusions: P75 NGFR may play a mechanistic role in invasive MMs demonstrating PNI. Furthermore, its expression may serve as a marker of PNI in those tumors that lack histological evidence of nerve involvement at the time of excision. Chan MM, Tahan SR. Low‐affinity nerve growth factor receptor (P75 NGFR) as a marker of perineural invasion in malignant melanomas.     

The expression of retrovirus-like particles in psoriasis

Retrovirus-like particles have been isolated from patients with psoriasis. Antigens crossreacting with the major internal protein, pso p27, of these particles have been demonstrated in the wall of dermal vessels and in a subfraction of cells in psoriatic lesions. The antigen has also been observed in blood lymphocytes from psoriatic patients. Pso p27 antigen and anti-pso p27 antibodies are present as complement-activating immune complexes in psoriatic scale and in the blood of patients with psoriasis and psoriatic arthritis. The potential contribution of the circulating immune complexes to the inflammatory process in psoriasis is discussed.     

Increased nerve growth factor and its receptors in atopic dermatitis: an immunohistochemical study

Evidence suggests that neurotrophins may regulate certain immune functions and inflammation. In the present study, the localization and distribution of nerve growth factor (NGF) and its receptors were explored using immunohistochemical methods, with the aim of detecting the cause of the neurohyperplasia in early lesions of atopic dermatitis (AD). In AD involved skin, strong NGF-immunoreactive (IR) cells were observed in the epidermis. In some cases, a huge number of infiltrating cells with stronger NGF immunoreactivity was seen mainly in the dermal papillae. Some trkA immunoreactivity was observed in the outer membrane of cells in the basal and spinal layers of the epidermis. In the papillary dermis, a larger number of cells demonstrated strong trkA immunoreactivity. The p75 NGFr-IR nerve fibre profiles were increased (900 per mm²; p<0.001) compared to normal [the involved skin also differed from the uninvolved skin (p<0.05)] in the dermal papillae. These nerve fibres were larger, coarser and branched, some of them terminated at p75 NGFr-IR basal cells, and also revealed a stronger fluorescence staining than the controls or the uninvolved skin. In normal healthy volunteers and AD uninvolved skin, the NGF immunoreactivity was weak in the basal layer of epidermis. Only a few trkA positive cells were seen in the basal layer of the epidermis and upper dermis. The IR epidermal basal cells revealed a striking patchy arrangement with strong p75 NGFr immunostaining in the peripheral part of the cells, and short and thick NGFr-IR nerve fibre profiles appeared as smooth endings scattered in the dermis including the cutaneous accessory organs. Using NGF and p75 NGFr double staining, both immunoreactivities showed a weak staining in the epidermis and dermis in normal and uninvolved skin. In the involved dermis of AD, the intensity of p75 NGFr-IR nerves was stronger in areas where there were also increased numbers of NGF-IR cells. These findings indicate that NGF and its receptors may contribute to the neurohyperplasia of AD.     

NGFR (p75) expression in cutaneous scars; Further evidence for a potential pitfall in evaluation of reexcision scars of cutaneous neoplasms, in particular desmoplastic melanoma

Desmoplastic melanoma is a rare variant of malignant melanoma composed of spindle cells in a collagenous matrix. The antibody against NGFR (low affinity nerve growth factor receptor, also known as p75) stains cells of desmoplastic melanoma with high sensitivity; however, the specificity of this marker is not well established. Although there are established histologic criteria for recognition of desmoplastic melanoma, the evaluation of residual disease in cutaneous reexcision scars can be challenging. If residual spindle cells in scar are sufficiently atypical and NGFR positive, their presence could be interpreted as residual desmoplastic melanoma. In this study, we reevaluated the use of antibody against NGFR to detect residual disease in reexcision specimens of melanocytic neoplasms as the previously published works are contradictory. Our data indicate that anti-NGFR antibody stains many cells in the scar, some of which seem to be myofibroblasts, nerve twigs, and Schwann cells. Our findings further suggest that NGFR is not a suitable marker to evaluate reexcision scars for desmoplastic melanoma, especially as a sole marker, as its specificity is low.     

Expression of nerve growth factor receptors in cutaneous inflammation

Evidence indicates that the neurotrophin nerve growth factor (NGF) is a mediator of cutaneous inflammatory responses. Cellular responses to NGF are facilitated by two receptors called trk A and p75 neurotrophin receptor (p75^NTR). In the current study we have investigated the expression of these receptors in lesional and non-lesional skin from patients with plaque psoriasis and in normal skin exposed to three times the minimal erythema dose of ultraviolet (UV) B radiation. Trk A immunostaining was confined to the basal keratinocytes in normal skin. There was a significant reduction in trk A immunostaining in both non-lesional and lesional psoriatic skin compared with control skin. In UVB-irradiated normal skin, there was a significant reduction in trk A immunostaining at 4 h after irradiation, which was still evident at 48 h. In normal skin, p75^NTR immunopositive fine nerve fibres were present throughout the dermis and occasionally seen in the epidermis. Thick nerve fibres were evident in the deep dermis and in the middle region of the dermis. p75^NTR immunopositive basal keratinocytes were occasionally seen. There was a statistically significant loss of p75^NTR immunopositive fine nerve fibres in the epidermis of lesional psoriatic skin and a statistically significant loss of p75^NTR immunopositive fine nerve fibres in the dermis in both non-lesional and lesional psoriatic skin. p75^NTR immunopositive thick nerve fibres were reduced in lesional psoriatic skin compared with normal skin. UVB irradiation of normal skin led to a statistically significant decrease in the p75^NTR immunopositive fine nerve fibres in the epidermis at 48 h after irradiation. There was no significant reduction in the dermal p75^NTR immunoreactivity. These results demonstrated that expression of both NGF receptors is decreased following an acute inflammatory stimulus and also in association with a chronic inflammatory dermatosis.     

Density of mast cells and intensity of pruritus in psoriasis vulgaris: a cross sectional study

Background:Psoriasis is a chronic and prevalent disease, and the associated pruritus is a common, difficult-to-control symptom. The mediators involved in psoriatic pruritus have not been fully established.Objective:To evaluate associations between the number of mast cells in psoriatic lesions and the intensity of pruritus.Methods:29 patients with plaque psoriasis were recruited. In all participants, Psoriasis Area and Severity Index and Body Surface Area were assessed. A questionnaire was administered to obtain clinical information and the Dermatology Life Quality Index. Pruritus was assessed using a visual analog scale and skin biopsies were performed for staining with Giemsa and Immunohistochemistry with C-Kit.Results:Pruritus was observed in 91.3% of our patients. Median VAS was 6 (p25-75: 2-8). The immunohistochemical method revealed a mean of 11.32 mast cells/field and Giemsa staining revealed a mean of 6.72 mast cells/field. There was no correlation between the intensity of pruritus and mast cell count, neither in Immunohistochemistry (p = 0.15; rho = -0.27) nor in Giemsa (p = 0.16; rho = -0.27). Pruritus did not impact on the Dermatology Life Quality Index (p = 0.51; rho = -0.13).Study limitations:The small sample size may be considered the main limitation of our study.Conclusions:Although mast cells are mediators of pruritus in many cutaneous diseases, our findings support that psoriatic pruritus is a complex disorder with multifactorial, complex pathophysiology, involving pruritogenic mediators others than mast cells.