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1.
耿明霞  马杰  何峰容  滕志勇  杨楷 《微循环学杂志》2005,15(3):27-28,F0005,F0008
目的:探讨弥漫性毒性甲状腺肿(GravesDisease,GD)对人体血清白细胞介素-2(IL-2)、白细胞介素-8(IL-8)、肿瘤坏死因子(TNF)水平的影响。方法:采用放射免疫技术,检测135例GD患者治疗前后的IL-2、IL-8、TNF水平。结果:GD治疗前IL-2水平均低于治疗后和正常对照组,而IL-8、TNF水平在治疗后降低,且组间比较具有显著性意义(P<0.01)。对GD未治疗组血清中IL-2、IL-8、TNF与FT3、FT4、TSH进行相关性分析,结果显示IL-2与FT3、FT4呈显著负相关(P均<0.01);IL-8、TNF与FT3、FT4、TSH均无相关性(P均>0.05)。结论:IL-2、IL-8、TNF参与GD的发生与发展过程,与GD的免疫紊乱与功能状态异常间存在十分重要的内在联系。  相似文献   

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目的分析广州地区老年人恙虫病临床特点,以期降低老年人恙虫病的误诊率、漏诊率及病死率。方法将1983年5月至2008年1月收治的50例广州地区老年人恙虫病从流行病学、主要临床表现、实验室及辅助检查、预后等方面进行回顾性分析研究。结果广州地区老年人恙虫病仍具有发热、焦痂溃疡、淋巴结肿大的特点,但皮疹少见,外周血白细胞数多升高,血小板降低多见,起病隐匿,临床表现趋向多样化、复杂化,多脏器损害多见,易发生误诊、漏诊,病死率达14%。结论老年人恙虫病从流行病学、临床特征、实验室检查方面趋向不典型,极易造成误诊、漏诊,且病死率高,尤其是对病程超过两周的患者,应引起临床医师的高度重视。  相似文献   

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It is believed that the pathogenesis of dengue is generated by a deregulation of the immunological response. Dengue virus-infected monocytes/macrophages are likely to secrete monokines, which play a role in clinical features observed in patients with dengue haemorrhagic fever or dengue shock syndrome. This is a report on a study on 45 individuals presenting clinical and laboratory characteristics of dengue virus infection. During the acute phase of infection, immunophenotyping of peripheral mononuclear leukocytes was carried out in 19 patients and demonstrated a reduced frequency of CD2+ lymphocytes and their CD4+ and CD8+ subsets. Normal ratios were recovered during convalescence. Also, during the acute phase, mononuclear cells proliferated poorly in response to mitogens and dengue antigens as detected by incorporation of radiolabeled thymidine. During convalescence the lymphoproliferative response was re-established. In addition, the presence of circulating cytokines was investigated in the plasma of the same 45 patients. Concentrations of tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-10 (IL-10) and soluble tumor necrosis factor receptor (sTNF-Rp75) were found to be significantly elevated in patients when compared to normal controls. The increase in TNF-alpha was correlated with haemorrhagic manifestations and the increase in IL-10 with platelet decay. The data demonstrate that during the acute phase of dengue infection subsets of T lymphocytes are depressed in terms of both rate and function and provide evidence that circulating pro-inflammatory cytokines, such as TNF-alpha, are important in the pathogenesis and severity of dengue. IL-10 may be downregulating lymphocyte and platelet function.  相似文献   

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Gut and serum immune responses were studied in twenty-two patients with bacteriologically proved typhoid fever at different stages of the illness and six volunteers after parenteral immunizations with heat-killed typhoid vaccine. Whereas the former group had some specific antibodies in their intestinal aspirates and significant specific antibody responses in their sera, the latter could only mount a serum antibody response. Moreover, the intestinal IgA levels in the patients remained significantly decreased throughout the whole course of the illness, but a rise of IgG and IgM was observed in their jejunal secretions. In contrast, the levels of all the three major classes of serum immunoglobulins IgG, IgM and IgA were raised in the patients, as opposed to the volunteers, in whom only IgG and IgM levels were increased. It was inferred that the subjects with deficit of intestinal IgA, and thus lacking protective mucosal barrier, are more prone to develop typhoid fever.  相似文献   

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目的:比较原发性肾小球疾病和高血压肾病所致慢性肾脏疾病(CKD)患者随疾病进展血清醛固酮(Ald)水平变化的异同。方法:此两种病因导致不同程度慢性肾功能不全而未开始肾替代治疗的CKD患者共95例,依据病因分成两组,比较这两组患者的血浆肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)和血清Ald浓度以及电解质水平;PRA、AngⅡ和Ald的检测采用放射免疫分析。结果:高血压肾病所致CKD患者血清Ald水平显著高于原发性肾小球疾病所致CKD患者(P〈0.01),经肌酐清除率(Ccr)修正后高血压肾病所致CKD患者血清Ald水平仍显著高于原发性肾小球疾病所致CKD患者(P〈0.05)。结论:在肾功能可比较的情况下,高血压肾病所致CKD患者较原发性肾小球疾病所致CKD患者血清Ald水平更容易升高。  相似文献   

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目的 :探讨脑脊液 (CSF)中β -淀粉样蛋白1-42 (β -amyloidprotein1-42 ,Aβ1-42 )的水平对Alzheimer病 (AD)的诊断价值 ,寻找AD理想的生物学标志。方法 :将符合美国国立神经病、语言障碍和卒中研究所 -老年性痴呆及相关性疾病协会 (NINCDS -ADRDA)的”很可能AD”标准的 2 2例AD患者 ,同时将 2 0例血管性痴呆 (vasculardementia ,VD)和 2 1例正常对照 (normalcontrol,NC)纳入研究。用酶联免疫吸附法 (ELISA)分别检测AD组、VD组和NC组CSF中的Aβ1-42 水平。同时评定 :AD、VD组患者的简易智能量表 (MMSE)、HACHINSKI缺血量表及临床痴呆量表 (CDR)等参数。结果 :三组CSF中Aβ1-42 平均浓度 (x±s) (pg/ml)如下 :AD组 343.94± 16 5 .87;VD组 4 6 6 .6 5± 2 2 2 .4 6 ;NC组 4 80 .4 0± 2 17.16 ,AD组明显低于NC组 (P <0 .0 5 ) ;虽然AD组低于VD组、VD组低于NC组 ,但差异均无显著性(P >0 .0 5 ) ;AD组CSF中Aβ1-42 浓度与CDR、MMSE评分明显相关 (P <0 .0 5 )。结论 :Alzheimer病患者CSF中Aβ1-42浓度降低是其重要的实验室表现 ,可以作为AD的辅助的诊断指标  相似文献   

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Idiopathic pulmonary fibrosis (IPF), hypersensitivity pneumonitis (HP) and sarcoidosis belong to interstitial lung diseases (ILD) where an imbalance of regulatory, profibrotic and antifibrotic cytokines is hypothesized. The relationship of bronchoalveolar lavage (BAL) fluid (BALF) cytokines, BALF cell profile and ILD course is supposed. The aim of our study was to correlate BALF cytokine and chemokine levels with BALF cellular characteristics and lung function parameters in different ILD. Twenty-two sarcoidosis, seven IPF and 11 HP patients underwent lung function tests and BAL. The BALF differential cell counts and superficial cell markers were characterized, and MCP-1, MIP-1α, MIP-1β, RANTES, epithelial neutrophil-activating protein (ENA)-78, FGF, G-CSF, GM-CSF, IFN-γ, interleukin (IL)-1α, IL-1RA, IL-1β, -2β, -4β, -5β, -6β, -8β, -10β, -17β, tumour necrosis factor (TNF)-α, thromobopoietin (Tpo) and vascular endothelial growth factor (VEGF) values measured. The BALF VEGF values were highest in sarcoidosis ( P  = 0.0526). IL-1RA values were higher in IPF and HP compared with sarcoidosis ( P  = 0.0334). IL-8/ENA-78 ratio positively correlated with BALF neutrophil counts in IPF ( r  = 0.89, P  = 0.04). Vital capacity and TLCO values positively correlated with VEGF and negatively with IL-8 BALF levels in all ILDs but the correlations were most significant in sarcoidosis group. We suppose that VEGF plays a role in ILDs' early phases and has rather angiogenic than profibrotic effect. On the contrary, IL-8 is probably upregulated in advanced ILDs with prominent fibrosis and marked lung functions decline. We state that BALF VEGF, IL-8 and ENA-78 levels and IL-8/ENA-78 ratio could become useful markers of ILDs' phase, activity and prognosis. They might also be helpful in treatment modality choice.  相似文献   

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Incomplete Kawasaki disease (iKD) is considered to be a less complete form of Kawasaki disease (cKD), and several differences in the laboratory presentations of iKD and cKD have been noted. We investigated serum procalcitonin levels in patients with iKD, cKD, and other febrile diseases (a control group). Seventy-seven patients with cKD, 24 with iKD, and 41 controls admitted to our hospital from November 2009 to November 2011 were enrolled in the present study. We obtained four measurements of serum procalcitonin levels and those of other inflammatory markers from each patient. Samples were taken for analysis on the day of diagnosis (thus before treatment commenced; D0) and 2 (D2), 14 (D14), and 56 days (D56) after intravenous immunoglobulin infusion. We obtained control group data at D0. The mean D0 serum procalcitonin levels of cKD patients (0.71 ± 1.36 ng/mL) and controls (0.67 ± 1.06 ng/mL) were significantly higher than those of iKD patients (0.26 ± 0.26 ng/mL) (P = 0.014 and P = 0.041, resp.). No significant difference in mean procalcitonin level was evident among groups at any subsequent time. In conclusion, the serum procalcitonin level of patients with acute-stage cKD was significantly higher than that of iKD patients.  相似文献   

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In autoimmune diseases striking abnormalities of T and B cell activation and of cytokine production are present. In 14 patients with autoimmune hemolytic anemia (AIHA), idiopathic or in the course of: lymphoma, B hepatitis, carcinoma, drug therapy (α-methyldopa), systemic lupus erythematosus (SLE), and not yet submitted to immunosuppressive therapy, the PBL proliferative response to PHA and the IL1α, IL2, IL4 and IL2R serum levels have been valued. While the stimulation index of PBL was strongly reduced in 10 cases (64±56 vs 138±45 in the control group), IL1α, IL2 and IL2R were greatly increased in all the patients, and IL4 in 5 (IL1α :199±268 pg/ml in patients vs 0.30±0.2 in controls; IL2:716±311 pg/ml vs 16±4; IL4:29±13 pg/ml vs 13±7; IL2R:1233±471 U/ml vs 256±114). Cytokine serum levels were not related with the associated disease, with the CD4+ and CD8+ cells absolute number or with PBL blastogenic in vitro response. The high serum levels of cytokines and IL2R suggest that in AIHA there exist a CD4+ lymphocyte hyperactivation (the low proliferative response of PBL might imply a temporary functional exhaustion of T lymphocytes) as in the other autoimmune diseases.  相似文献   

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A large community outbreak of Q fever occurred in the Netherlands in the period 2007 to 2010. Some of the infected patients developed chronic Q fever, which typically includes pathogen dissemination to predisposed cardiovascular sites, with potentially fatal consequences. To identify the immune mechanisms responsible for ineffective clearance of Coxiella burnetii in patients who developed chronic Q fever, we compared serum concentrations of 47 inflammation-associated markers among patients with acute Q fever, vascular chronic Q fever, and past resolved Q fever. Serum levels of gamma interferon were strongly increased in acute but not in vascular chronic Q fever patients, compared to past resolved Q fever patients. Interleukin-18 levels showed a comparable increase in acute as well as vascular chronic Q fever patients. Additionally, vascular chronic Q fever patients had lower serum levels of gamma interferon-inducible protein 10 (IP-10) and transforming growth factor β (TGF-β) than did acute Q fever patients. Serum responses for these and other markers indicate that type I immune responses to C. burnetii are affected in chronic Q fever patients. This may be attributed to an affected immune system in cardiovascular patients, which enables local C. burnetii replication at affected cardiovascular sites.  相似文献   

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目的 探究慢性阻塞性肺疾病(COPD)患者不规则趋化因子(FKN)、白三烯B4(LTB4)及呼出气一氧化氮(FeNO)水平变化及其临床意义.方法 选择2019年4月至2020年4月在我院就诊的120例COPD患者,另选取同期健康体检者60例作为对照组,按病情严重程度将120例患者分为COPD急性加重期患者(n= 64)...  相似文献   

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目的 探讨骨髓微环境中细胞因子IL-Iβ、IL-2、IL-4、IL-10、INF-γ、TNF-α水平与外周血中相应细胞因子的差异。方法选取2018年1月~2019年2月云南省第一人民医院血液科诊断的缺铁性贫血(IDA)、骨髓增生异常综合征(MDS-EB-1)、慢性粒细胞白血病慢性期(CML-CP)及急性髓系白血病(AML)患者各20例。应用流式细胞仪分析IDA、MDS-EB-1、CML-CP和AML患者骨髓及外周血IL-Iβ、IL-2、IL-4、IL-10、INF-γ、TNF-α的水平。结果 IDA患者骨髓微环境和外周血中细胞因子水平比较,差异无统计学意义(P>0.05);MDS-EB-1、CML-CP及AML患者骨髓微环境中IL-Iβ、IL-2、IL-4、IL-10、INF-γ、TNF-α水平高于外周血,差异有统计学意义(P<0.05)。结论 IDA、MDS-EB-1、CML-CP及AML患者骨髓微环境中细胞因子IL-Iβ、IL-2、IL-4、IL-10、INF-γ、TNF-α的水平高于外周血中相应的细胞因子水平。在研究血液系统恶性肿瘤细胞因子时,应检测骨髓微环境中的细胞因子。  相似文献   

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Objective: To determine the level of macrophage migration inhibitory factor (MIF), its relationship with Mediterranean fever (MEFV) gene mutations and oxidative stress in familial Mediterranean fever (FMF).Methods: Fifty one unrelated attack free FMF patients (24 M and 27 F, 32.8±8.7 years) and 30 healthy controls (16 M and 14 F, 32.7±7 years) were included in the study. Serum MIF, total oxidant status (TOS) and total anti-oxidant status (TAS) were studied.Results: Age, sex distribution, anthropometrical indices, smoking status, serum lipids and TAS concentrations were similar between the patients and controls. However; erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), MIF, and TOS were significantly higher in the patients'' group compared with healthy subjects. MIF, TOS and TAS levels were not different between patients with or without M694V mutations.Conclusion: We found increased concentrations of MIF in patients with FMF. Increased MIF levels were significantly correlated with oxidative stress and in regression analysis MIF concentrations were independent from the inflammatory activity as assessed by ESR and CRP. M694V mutations seem no effect on MIF and oxidative stress.  相似文献   

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目的:探讨脑血管病患者血清同型半胱氨酸(Hcy)水平与年龄、性别、病程、病变部位及预后之问的关系。方法:采用化学发光法测定163例脑血管病患者血清Hcy水平,同时以32例其他疾病患者及健康志愿者作对照组。结果:各型脑血管病患者的血清Hcy含量均明显高于对照组(P〈0.01),且与脑血管病的病变部位、病程、性别、预后、高血压、糖尿病、高脂血症和冠心病史无明显相关性。结论:高Hcy血症是脑血管病的一种独立危险因素。  相似文献   

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BACKGROUND: Intravenous immunoglobulins (IVIG) have usually been administered for replacement therapy of humoral immunodeficiencies, but their use in treating other disorders with an immune pathogenesis is increasing. The exact mechanism of action by which IVIG are of benefit in such diseases is complex and only partly understood. One of the proposed mechanisms of action is the modulation of cytokine release. METHODS: We selected 29 patients with primary hypogammaglobulinemia (common variable immunodeficiency), receiving long-term substitutive therapy with IVIG, and 14 healthy blood donors as a control group. Blood samples were then taken before and 1 hour after finishing the IVIG infusion. Only one blood sample was obtained from the healthy controls. The cytokines studied were interleukin (IL)-1 beta, IL-1 receptor antagonist (IL-1Ra), IL-2, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. RESULTS: Patients with primary hypogammaglobulinemia showed significantly higher serum levels of IL-6, IL-8, IL-1Ra, and TNF alpha than healthy controls. IVIG infusion significantly increased serum concentration levels of IL-6, IL-8, IL-1Ra, and TNF alpha. No significant variation was observed in serum levels of IL-beta, IFN gamma, or IL-2 after IVIG infusion. Age, IVIG commercial preparation, and IVIG dose did not influence cytokine serum levels. Moreover, a significant correlation was observed between serum level variations of IL-1Ra and TNF alpha, as well as an associative trend between maximum changes in IL-6 and IL-8 concentrations. CONCLUSIONS: IVIG administration significantly alters the serum pattern of selected cytokines, which might explain, at least in part, the mechanism of action of IVIG in autoimmune or inflammatory disorders.  相似文献   

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Sputum and serum from patients with active pulmonary tuberculosis (TB), healthy purified protein derivative-positive adults, and patients with bacterial pneumonia were collected to simultaneously assess local immunity in the lungs and peripheral blood. To determine whether cytokine profiles in sputum from TB patients and control subjects were a reflection of its cellular composition, cytospin slides were prepared in parallel and assessed for the presence of relative proportions of epithelial cells, neutrophils, macrophages, and T cells. Gamma interferon (IFN-γ) in sputum from TB patients was markedly elevated over levels for both control groups. With anti-TB therapy, IFN-γ levels in sputum from TB patients decreased rapidly and by week 4 of treatment were comparable to those in sputum from controls. Further, IFN-γ levels in sputum closely followed mycobacterial clearance. Although detected at fourfold-lower levels, IFN-γ immunoreactivities in serum followed kinetics in sputum. TNF-α, interleukin 8 (IL-8) and IL-6 also were readily detected in sputum from TB patients at baseline and responded to anti-TB therapy. In contrast to IFN-γ, however, TNF-α and IL-8 levels also were elevated in sputum from pneumonia controls. These data indicate that sputum cytokines correlate with disease activity during active TB of the lung and may serve as potential early markers for sputum conversion and response to anti-TB therapy.  相似文献   

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A major hypothesis regarding the cause of chronic fatigue syndrome (CFS) is immune dysregulation, thought to be reflected in upregulated proinflammatory cytokines leading to the symptoms that are characteristic of this illness. Because the symptoms worsen with physical exertion or sleep loss, we hypothesized that we could use these stressors to magnify the underlying potential pathogenic abnormalities in the cytokine systems of people with CFS. We conducted repeat blood sampling for cytokine levels from healthy subjects and CFS patients during both postexercise and total sleep deprivation nights and assayed for protein levels in the blood samples, mRNA activity in peripheral blood lymphocytes (PBLs), and function in resting and stimulated PBLs. We found that these environmental manipulations did not produce clinically significant upregulation of proinflammatory cytokines. These data do not support an important role of immune dysregulation in the genesis of stress-induced worsening of CFS.  相似文献   

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