荨麻疹患者血清中SOD、MDA的检测及其意义

为探讨荨麻疹患者血清中超氧化物歧化酶（SOD）、丙二醛（MDA）的变化及其与荨麻疹的相关性,用分光光度计方法检测20例急性荨麻疹、25例慢性荨麻疹及20名正常健康人SOD活性和MDA含量。结果：急性荨麻疹患者SOD活性均低于正常对照组和慢性患者（P〈0.01）,且慢性患者又低于正常对照组（P〈0.05）;急性患者MDA含量高于正常对照组（P〈0.001）和慢性患者（P〈0.01）,慢性患者其含量又高于对照组（P〈0.01）。氧化失衡存在于荨麻疹发病中,SOD、MDA可能在荨麻疹发生发展中发挥一定的作用。     

慢性自发性荨麻疹患者血清IL-17、IL-23水平的检测及意义

目的:探讨白细胞介素-17(Interlenkin-17,IL-17)、白细胞介素-23(Interleukin-23,IL-23)在慢性自发性荨麻疹患者中的表达及意义。方法:选取慢性自发性荨麻疹患者和健康献血者各30例,用酶联免疫吸附法检测血清中IL-17、IL-23水平,并分析它们与病情、病程之间的关系。结果:慢性自发性荨麻疹患者的血清IL-17水平[(19.3±8.1)pg/mL]、IL-23水平[(28.9±11.1)pg/mL]均高于对照组[(8.6±5.7)pg/mL,(10.9±6.2)pg/mL],组间比较差异有统计学意义(t值分别为5.92、7.72,P值均<0.01)。慢性自发性荨麻疹患者IL-17、IL-23与症状评分呈正相关关系(r=0.89、r=0.75,P值均<0.01),与病程无明显相关性(r=0.23、r=0.24,P值均>0.05),IL-17与IL-23呈正相关关系(r=0.81,P<0.01)。结论:IL-17、IL-23在慢性自发性荨麻疹发病机理中可能起着重要作用。     

荨麻疹患者血清一氧化氮的检测及其意义

以硝酸还原法检测20例急性荨麻疹、25例慢性荨麻疹及20名正常健康人血清中NO含量。结果:急性荨麻疹患者NO含量高于正常对照组和慢性荨麻疹患者(P<0.01,P<0.05),慢性荨麻疹患者其含量高于正常对照组(P<0.01)。NO在荨麻疹发生、发展过程中可能起一定的作用。     

43例急性荨麻疹患者血清ECP和TIgE的水平及相关性分析

采用UniCAP-100全自动变态反应分析仪,对43例急性荨麻疹患者发疹时进行血清TIgE和ECP检测,并设20例正常人对照。结果:43例患者中血清TIgE水平为(220.6±234.3)ku/L,高于对照组(P<0.05);血清ECP为19.9±14.6,显著高于对照组(P<0.01);两者间略趋正相关(r=0.0376,t=0.241,P>0.05);发疹组血清TIgE水平与病情严重程度略趋正相关(r=0.2840,t=1.8966,P>0.05),发疹组血清ECP水平与病情严重程度呈正相关(r=0.3658,t=2.5167,0.01相似文献   

负性急性时相蛋白在慢性荨麻疹患者的研究

目的 探讨急性时相反应与慢性荨麻疹的关系。 方法 慢性荨麻疹患者50例,按症状分为轻型（1级）、中型（2级）、重型（3级）3组,同时选取健康体检者28例,用免疫比浊法测定血清前白蛋白（PA）、转铁蛋白（TRF）水平,采用酶联免疫吸附法测定胰岛素样生长因子1（IGF-1）和肿瘤坏死因子α（TNF-α）水平;比较两组之间的差异、各检测项目之间的相关性及与病情分级的关系。 结果 慢性荨麻疹患者PA（229.99 ± 54.16） mg/L、IGF-1（177.23 ± 46.48） μg/L均明显低于健康对照组,两组差异有统计学意义（均P < 0.05）。TNF-α（25.39 ± 11.01） ng/L高于健康对照组（14.13 ± 6.12） ng/L,差异有统计学意义（P < 0.05）。TRF水平（2.48 ± 0.49） g/L与健康对照组（2.48 ± 0.25） g/L比较,差异无统计学意义（P > 0.05）。血清PA与TNF-α呈显著负相关（P < 0.05）,并与病情严重程度呈显著负相关（P < 0.01）,而TNF-α则与病情严重程度呈显著正相关（P < 0.01）;其余各指标之间无明显相关性（均P > 0.05）。 结论 在慢性荨麻疹患者中,部分急性时相反应负性蛋白水平降低且与病情呈负相关,急性时相反应可能参与慢性荨麻疹的发病。     

赤芍、甘草等中药合剂治疗急性荨麻疹机理的实验研究

目的 赤芍、甘草等中药合剂(简称抗敏口服液)治疗急性荨麻疹的机理。方法 ①动物实验:肥大细胞脱颗粒实验,被动皮肤过敏实验;②实验室检测:双抗体夹心ELISA法检测急性荨麻疹患者治疗前后IL-2、IL-4水平。结果 抗敏口服液组肥大细胞脱颗粒百分数及吸光度值明显低于其它各组药物(P<0.01),抗敏口服液可使急性荨麻疹患者体内升高的IL-4及降低的IL-2恢复到正常。结论 抗敏口服液可稳定肥大细胞膜、抑制抗原抗体结合、调整IL-2和IL-4浓度,对急性荨麻疹有较好的治疗效果。     

依匹斯汀治疗慢性荨麻疹疗效观察及血清总IgE水平检测

目的观察依匹斯汀治疗慢性荨麻疹患者疗效及血清总IgE变化。方法 45例慢性荨麻疹患者采用口服依匹斯汀治疗,共服28d,同时测定治疗前后血清总IgE水平。结果患者治疗第l4天和第28天与治疗前相比差异有统计学意义（P〈0.01）。治疗前血清总IgE水平明显高于正常值,症状缓解后血清总IgE水平下降,患者治疗前后血清总IgE水平差异有显著性（P〈0.01）。结论依匹斯汀治疗慢性荨麻疹疗效好,能降低血清总IgE水平。     

急性时相反应标志物及凝血、纤溶标志物与慢性荨麻疹的相关性研究

目的 探讨急性时相反应、凝血/纤溶系统与慢性荨麻疹的关系。 方法 用酶联免疫吸附法测定53例慢性荨麻疹患者及25例健康人血清白介素6（IL-6）、淀粉样A物质（SAA）水平,同时用免疫比浊法测定血清超敏C反应蛋白（Hs-CRP）及血浆D-二聚体水平,比较两组之间的差异。慢性荨麻疹患者按症状严重程度分为3级（3组）,分析各检测项目之间的相关性以及各检测项目与慢性荨麻疹症状严重程度的关系。结果 慢性荨麻疹患者组IL-6（10.70 ± 4.94 ng/L）、SAA［M（P25,P75）为4.92（8.22,12.51） μg/L］、D-二聚体（222.32 ± 163.69 μg/L）水平均高于健康对照组［分别为7.49 ± 3.41 ng/L、2.11（1.21,2.83） μg/L、104.72 ± 43.12 μg/L］,两组差异均有统计学意义（P ＜ 0.05）;Hs-CRP水平［0.30（0.10,1.40） mg/L］与健康对照组［0.30（0.10,0.55） mg/L］比较,差异无统计学意义（P ＞ 0.05）。慢性荨麻疹患者IL-6水平与Hs-CRP、SAA、D-二聚体水平及症状严重程度均无显著相关性（均P ＞ 0.05）,Hs-CRP水平与SAA水平（r = 0.67,P ＜ 0.01）、Hs-CRP水平与D-二聚体水平（r = 0.49,P ＜ 0.01）、SAA水平与D-二聚体水平（r = 0.38,P ＜ 0.01）均呈显著正相关;Hs-CRP、SAA、D-二聚体水平与症状严重程度呈显著正相关（r值分别为0.63、0.62、0.47,均P ＜ 0.01）。 结论 慢性荨麻疹患者存在急性时相反应及凝血系统的激活,两者的发生可能存在相关性。     

急性荨麻疹患者血清Eotaxin与TNF-α的检测

为分析血清Eotaxin与TNF-α含量变化与急性荨麻疹发病的关系,采用ELISA法测定26例急性荨麻疹患者血清中Eotaxin与TNF-α的含量.结果:急性荨麻疹患者血清Eotaxin与TNF-α水平显著高于正常对照组(P<0.05),且皮损面积大者明显高于皮损面积小者(P<0.01).结论:急性荨麻疹患者血清Eotaxin与TNF-α水平升高,并与急性荨麻疹皮损的面积密切相关.     

荨麻疹

993500 不同类型荨麻疹患者血清IL-4及IgE水平测定/程少为（首都医大附属红十字朝阳医院）//白求恩医科大学学报。-1999,25（2）。-151 患者血清IgE水平升高是导致荨麻疹发生的主要原因之一,而血清IL-4又是IgE的一个主要调控因子。因而,血清IL-4及IgE水平是衡量荨麻疹发生、发展的2个重要指标。通过对35例不同类型的荨麻疹患者血清IL-4及IgE的检测,急性荨麻疹组（9例）、人工荨麻疹组（12例）、既往荨麻疹组（14例）、正常对照组（19例）,结果发现9例急性荨麻疹患者血清IL-4及IgE水平均明显高于正常人群（P相似文献   

特异性免疫治疗对慢性荨麻疹患者临床及外周血IL-4和sVCAM-1水平的影响

目的探讨特异性免疫治疗对慢性荨麻疹患者的疗效和作用机理。方法对30例吸入组皮肤试验阳性的慢性荨麻疹患者进行特异性免疫治疗并观察疗效,用ELISA法检测患者治疗前后及健康对照组IL-4和sVCAM-1的血清水平。结果病例组经特异性免疫治疗3个疗程,有效率83.33%。病例组治疗前IL-4和sVCAM-1血清浓度明显高于对照组(P<0.05和0.01),经特异性免疫治疗后浓度下降,较治疗前均有显著差异(P<0.01和0.001)。sVCAM-1与IL-4血清浓度无直线相关关系(r=0.0268,P>0.05)。结论特异性免疫治疗对慢性荨麻疹患者安全有效。IL-4和sV-CAM-1可作为监测慢性荨麻疹病情变化指标之一。特异性免疫治疗可能是通过免疫调节达到其治疗作用。     

咪唑斯汀治疗荨麻疹前后患者血浆中组胺含量的变化及其意义

目的　探讨组胺在荨麻疹发病中的意义及咪唑斯汀在治疗荨麻疹中的抗组胺作用。方法　采用酶免疫法测定 45例荨麻疹患者在应用咪唑斯汀治疗前后血浆中的组胺含量。结果　 2 4例急性荨麻疹和 2 1例慢性荨麻疹患者血浆中组胺水平较正常对照组升高 ,差异有显著性 ;症状缓解后组胺含量下降 ,与对照组间差异无显著性。急、慢性荨麻疹组胺含量在治疗前后差异均有显著性。结论　组胺是参与荨麻疹发病的主要介质之一 ,结合治疗观察有利于进一步了解荨麻疹的发病机理并指导临床用药。     

荨麻疹患者血清5-羟色胺测定及其临床意义

目的 探讨５－羟色胺（５－ＨＴ）在荨麻疹的发病机理及其意义。方法 用荧光分光光度法测定４６例患者治疗前后血清５－ＨＴ含量，并与正常对照组相比较。结果 ２３例急性荨麻疹（含４例急性胃肠型荨麻疹）和２３例慢性荨麻疹治疗前血清５－ＨＴ含量低于正常对照组，治疗后血清５－ＨＴ含量与正常对常组相接近。结论 ５－ＨＴ在荨麻疹的发病中起着重要的作用，其机理可能与５－ＨＴ和血管内皮细胞膜５－ＨＴ受体结合，引起内波细     

荨麻疹患者血中组胺的测定及其意义

目的探讨组胺(HA)在荨麻疹发病中的意义。方法 用荧光分光光度法测定56例患者治疗前后血中HA含量,并与正常对照组相比较。结果31例急性荨麻疹和25例慢性荨麻疹治疗前血浆中HA含量高于正常对照组,治疗后血中HA含量与正常对照组相接近。结论HA是参与荨麻疹病理生理过程的主要介质之一,测定患者血中HA水平可反映机体对HA的释放情况,有利于临床观察病情、判断疗效,解释其发病机理。     

特异性免疫治疗对慢性荨麻疹患者血清白介素-18和白介素-10水平的影响

目的:检测慢性荨麻疹患者特异性免疫治疗(specific immunotherapy SIT)前后Th1型细胞因子白介素-18(IL-18)和Th2型细胞因子白介素-10(IL-10)血清水平。方法:ELISA法检测30例变应原皮肤试验阳性荨麻疹患者特异性免疫治疗前后及20例正常人血清IL-18和IL-10水平。结果:慢性荨麻疹患者SIT前IL-18水平低于正常人(P<0.05),SIT后升高(P<0.05);SIT前IL-10水平高于正常人(P<0.05),SIT后下降(P<0.05)。结论:变应原皮试阳性荨麻疹患者IL-18降低,IL-10升高,Th1/Th2失衡在慢性荨麻疹的发病中具有重要作用。特异性免疫治疗可能通过调节Th1/Th2平衡而发挥治疗作用。     

Usefulness of the Autologous Serum Test for the Diagnosis of Chronic Idiopathic Urticaria

Background

The majority of chronic urticaria cases are chronic idiopathic urticaria (CIU) with no specific identifiable etiology. The role of autoantibodies in such cases remains controversial.

Objective

This study determined the positivity rate of autologous serum tests in CIU patients.

Methods

This study was performed on 30 patients with CIU and 30 individuals without any systemic or dermatologic disease. After the volar parts of right and left forearms were cleansed, 0.05 ml serum physiologic and 0.05 ml autologous serum were injected intradermally on the right forearm 5 cm apart from each other, resulting in the formation of small papules; meanwhile, 0.05 ml histamine alone was injected to the left forearm. The test results were evaluated after 30 minutes as positive in positive cases.

Results

The autologous serum test produced significant and non-significant results in patients with CIU and controls, respectively. The positivity rates of the autologous serum test in the CIU and control groups were 53.3% and 26.6%, respectively. There was no relationship between autologous serum test positivity and sex in either group. In male patients with CIU, positive results ranged widely with age, while in female patients, positive results were mainly observed at younger ages with a narrow age range.

Conclusion

The autologous serum test is a useful test in the diagnosis and treatment of CIU as well as the selection of immunotherapy, especially in patients refractory to classic therapy.     

CHRONIC AUTOIMMUNE URTICARIA: WHERE WE STAND?

It is well-recognized that 30-40% of chronic idiopathic urticaria is autoimmune in nature. Chronic autoimmune urticaria is caused by anti-FcεRI and less frequently, by anti-IgE autoantibodies that lead to mast cell and basophil activation, thereby giving rise to the release of histamine and other proinflammatory mediators. Activation of the classical complement pathway and formation of C5a are important in dermal mast cell activation. C5a is also a neutrophil and eosinophil chemoattractant. Chronic autoimmune urticaria has been found to be associated with autoimmune thyroid disease. The autologous serum skin test is used as a screening test for chronic autoimmune urticaria and has a sensitivity and specificity of about 70 and 80%, respectively. The current gold standard diagnostic test is the basophil histamine release assay. The treatment of chronic autoimmune urticaria, as in chronic idiopathic urticaria, is with H1 antihistamines. Oral corticosteroids may be used during acute flares. Refractory cases have been shown to respond to cyclosporine and other immunomodulators. The prevalence of chronic autoimmune urticaria in Singapore is similar to that reported in Western countries at about 42%. The presence of thyroid autoimmunity appears to be higher than reported, with 22.5% of patients with chronic idiopathic urticaria here, exhibiting presence of thyroid autoantibodies.     

慢性荨麻疹患者血清组胺释放活性检测

目的 检测慢性荨麻疹患者血清组胺释放活性,探讨慢性荨麻疹的发病机制.方法 通过体外分离人皮肤肥大细胞,进行肥大细胞组胺释放试验,测定组胺释放率.结果 62例慢性荨麻疹患者中,自体血清皮肤试验阳性者24例占38.71%.混合细胞悬液中肥大细胞的组胺自发释放率<5%.血清活化皮肤肥大细胞引起的组胺释放率从3.1%～79.5%(16.44%±14.26%),明显高于正常人对照组(P<0.01),其中27例组胺释放率>15%(43.55%);自体血清皮肤试验(+)组的组胺释放率及阳性率均明显高于自体血清皮肤试验(-)组(P<0.01).结论 部分慢性荨麻疹患者血清中存在组胺释放活性,可直接活化肥大细胞,释放组胺等血管活性介质,引起荨麻疹.     

MTX对银屑病患者血清白介素-8和组胺水平的影响

目的:探讨甲氨蝶呤(MTX)对银屑病患者血清白介素-8和组胺水平的影响。方法:用酶联免疫吸附实验(ELISA)检测银屑病患者和正常人外周血IL-8水平;用荧光分光光度计测定银屑病患者和正常人外周血组胺水平。结果:(1)治疗前银屑病患者血清IL-8和组胺水平明显高于正常对照组(P<0.01),经MTX治疗后,患者血清IL-8和组胺水平与正常对照组差异无显著性(P>0.05)。结论:抑制组胺的释放和IL-8的分泌,降低中性粒细胞和T淋巴细胞的趋化活性,减轻炎症反应及组织损伤可能是MTX治疗银屑病的作用机制之一。     

Effects of local corticosteroids on acute experimental urticaria

Corticosteroids are often used in the treatment of acute or chronic urticaria. However, their effects on mastocyte activation as well as on the histamine-induced dermal oedema remain poorly investigated. The aim of the present study was to investigate the effects of corticosteroids (CS) on the development of acute experimental urticaria induced by prick-tests with histamine and codeine. This experimental model corresponds to the common form of urticaria. CS were administered at the site of the histamine and codeine prick tests in order to test for a direct effect on the development of acute urticaria. Two types of experiments were performed: 1) after a 48-hour period of topical CS application on the forearm, 7 healthy volunteers were skin prick-tested with histamine and codeine simultaneously in duplicate, one series in the pretreated area and the other in a non-treated area. 2) six other volunteers were prick-tested with histamine and codeine on their forearm, in duplicate. Immediately after testing, intradermal methyprednisolone was injected at the site of the prick-tests in the last series. Skin wheal and flare responses were measured after 20 mns and statistically compared with and without CS treatment. Whereas short-term CS topical application did not appear to modify cutaneous reactivity to histamine and codeine, local CS injection was associated with a significant increase in the flare induced by histamine and codeine (respectively + 18 +/- 3% and + 38 +/- 3%; P = 0.05). The wheal tended to be increased after injected CS. In conclusion, these results show that CS are neither able to prevent nor to improve experimental urticaria, i.e. wheal and flare, and even increase the histamine and codeine-induced erythema. That a similar result could apply to patients with chronic urticaria and with systemic CS remains to be studied.