冠心病患者血清C反应蛋白和可溶性细胞间粘附分子1与肺炎衣原体感染的相关性

目的探讨冠心病患者血清炎症标志物C反应蛋白和可溶性细胞间粘附分子1水平的变化及其与肺炎衣原体感染的关系。方法采用酶联免疫吸附法检测60例急性心肌梗死、不稳定型心绞痛、陈旧性心肌梗死、稳定型心绞痛及40例对照者血清C反应蛋白、可溶性细胞间粘附分子1及肺炎衣原体抗体IgG、IgM。结果冠心病组肺炎衣原体IgG阳性率和浓度均高于对照组(P<0.01),冠心病各组之间肺炎衣原体IgG和IgM阳性率差异无显著性(P>0.05),急性心肌梗死组肺炎衣原体IgG浓度高于陈旧性心肌梗死组、不稳定型心绞痛组和稳定型心绞痛组(P<0.05);冠心病组C反应蛋白、可溶性细胞间粘附分子1水平高于对照组(P<0.01),急性心肌梗死组C反应蛋白、可溶性细胞间粘附分子1水平高于不稳定型心绞痛组、陈旧性心肌梗死组和稳定型心绞痛组(P<0.01),不稳定型心绞痛组C反应蛋白、可溶性细胞间粘附分子1水平高于稳定型心绞痛组(P<0.05);肺炎衣原体IgG浓度、C反应蛋白、可溶性细胞间粘附分子1之间有很好的相关性(P<0.05)。结论炎症标志物水平变化在一定程度上反映了冠心病患者病情变化,肺炎衣原体感染与冠心病有关,炎症、感染可能共同参与了冠心病的发生发展。     

血管内皮功能和同型半胱氨酸对老年冠心病患者发病的相关性探讨

目的探讨血管内皮功能和同型半胱氨酸(Hcy)在老年冠心病患者中的作用机制。方法选取老年冠心病患者150例,根据诊断分为陈旧性心肌梗死组56例,稳定性心绞痛组51例,急性冠状动脉综合征组43例。对比各组患者Hcy水平、高血压、吸烟史、TC、及LDL-C等,分析Hcy水平及内皮依赖型血管舒张率与冠心病严重程度的相关性。结果急性冠状动脉综合征组Hcy水平升高比例显著高于稳定性心绞痛组和陈旧性心肌梗死组(79.1%vs 14.3%,29.4%,P=0.000)。3组间Hcy水平正常及升高比例比较差异有统计学意义(P=0.000)。急性冠状动脉综合征组Hcy水平显著高于稳定性心绞痛组及陈旧性心肌梗死组[(19.8±7.2)μmol/L vs(11.0±4.5)μmol/L,(12.3±6.1)μmol/L,P<0.01],但内皮依赖型舒张率显著低于稳定性心绞痛组及陈旧性心肌梗死组[(4.1±2.8)%vs(7.5±5.1)%,(6.5±3.2)%,P<0.01]。相关分析显示,Hcy水平与冠心病严重程度呈正相关(r=6.332,P=0.038),而内皮依赖型血管舒张率与冠心病严重程度呈负相关(r=-7.254,P=0.038)。结论血管内皮功能及Hcy水平与老年冠心病患者的病情联系紧密,临床治疗时可对其进行监测,值得重视。     

急性冠状动脉综合征患者血浆蛋白氧化产物升高的机制及意义

目的通过检测急性冠状动脉综合征患者体内晚期蛋白氧化产物、丙二醛的水平来探讨氧化应激损伤与冠状动脉粥样硬化斑块发生发展的关系。方法入选73例急性心肌梗死(46例择期和27例急诊冠状动脉介入治疗)、49例不稳定型心绞痛及21例非冠心病患者,均经造影证实。于入院即刻2、4 h和48 h采集外周静脉血标本。紫外荧光光度法测定晚期蛋白氧化产物浓度;硫代巴比妥酸光度法测定丙二醛浓度。结果晚期蛋白氧化产物浓度在急性心肌梗死择期冠状动脉介入治疗组、不稳定型心绞痛组较非冠心病组明显升高(P<0.05);急性心肌梗死择期冠状动脉介入治疗组各时间点晚期蛋白氧化产物浓度较急性心肌梗死急诊冠状动脉介入治疗组高(P<0.01);急性心肌梗死择期冠状动脉介入治疗组与不稳定型心绞痛组差异无统计学意义(P>0.05);急性心肌梗死择期冠状动脉介入治疗组晚期蛋白氧化产物浓度与低密度脂蛋白呈正相关[r=0.370(入院即刻)、r=0.422(入院24 h)、r=0.559(入院48 h)]。与非冠心病组对应各时间点丙二醛浓度比较,急性心肌梗死择期冠状动脉介入治疗组、急诊冠状动脉介入治疗组升高(P<0.05),而与不稳定型心绞痛组比较无统计学差异。结论急性冠状动脉综合征患者血浆中晚期蛋白氧化产物、丙二醛浓度显著升高。氧化应激可能是急性冠状动脉综合征发生发展过程中的重要环节,晚期蛋白氧化产物、丙二醛是反映体内氧化应激水平较好的血清学指标。     

冠心病患者不同类型血清氧化型低密度脂蛋白和高敏C反应蛋白水平的差异

目的比较血清氧化型低密度脂蛋白、高敏C反应蛋白水平在不同类型冠心病中的差异。方法检测了82例冠心病患者(急性冠状动脉综合征42例、稳定型心绞痛20例和陈旧性心肌梗死20例)和22例正常对照者血清氧化型低密度脂蛋白、高敏C反应蛋白、高密度脂蛋白胆固醇、总胆固醇和高密度脂蛋白胆固醇水平,并比较各指标水平在不同类型冠心病中的差异。结果血清氧化型低密度脂蛋白水平在冠心病组明显高于对照组(62.5±24.8μg/L比42.3±17.9μg/L,P<0.05),在急性冠状动脉综合征组明显高于稳定型心绞痛组和陈旧性心肌梗死组(68.9±23.4μg/L比41.5±21.3μg/L和50.5±21.6μg/L,P<0.05);血清高敏C反应蛋白水平在冠心病组明显高于对照组(15.58±4.32mg/L比6.94±1.93mg/L,P<0.05),在急性冠状动脉综合征组明显高于稳定型心绞痛组和陈旧性心肌梗死组(19.31±1.43mg/L比10.29±1.01mg/L和9.56±1.72mg/L,P<0.05);血清低密度脂蛋白胆固醇水平在冠心病组明显高于对照组(3.46±1.11mmol/L比2.87± 0.82mmol/L,P<0.05),但在急性冠状动脉综合征组与稳定型心绞痛组和陈旧性心肌梗死组差异无显著性(3.64±0.85mmol/L比3.06±1.23mmol/L和3.40±1.35mmol/L);血清总胆固醇/高密度脂蛋白胆固醇比值在冠心病组明显高于对照组(3.46±1.11比2.87±0.82,P<0.05),在不同类型冠心病中亦有差异(P<0.05)。结论血清氧化型低密度脂蛋白和高敏C反应蛋白水平及总胆固醇/高密度脂蛋白胆固醇比值在冠心病不同类型中有差异,可能为诊断冠心病的指标。     

冠心病患者血浆血栓调节蛋白水平的测定及其临床意义

目的　测定冠心病患者血浆血栓调节蛋白 ( throm bom odulin,TM)水平并探讨其临床意义。方法　急性心肌梗死、不稳定型心绞痛、稳定型心绞痛三组患者及正常对照组 ,抽取血浆并用酶联免疫吸附试验测量其血浆 TM水平。结果　急性心肌梗死组、不稳定型心绞痛组、稳定型心绞痛组血浆 TM水平均高于正常对照组 ( P<0 .0 5 ) ;急性心肌梗死组与不稳定型心绞痛组间患者血浆 TM水平没有显著性差异 ( P>0 .0 5 ) ,但均高于稳定型心绞痛组和正常对照组 ( P<0 .0 5 )。结论　血浆可溶性 TM水平是反映冠心病患者内皮细胞损伤程度和范围的良好标志 ,对急性心肌梗死、不稳定型心绞痛、稳定型心绞痛的鉴别有一定的临床指导意义     

巨噬细胞炎症蛋白1α与冠状动脉粥样硬化斑块病变相关性

目的 研究血浆巨噬细胞炎症蛋白1α水平在冠状动脉粥样硬化性心脏病患者的变化及与冠状动脉粥样硬化斑块病变严重程度及宽块稳定性的关系.方法 选择正常对照组25例及冠心病组84例(稳定型心绞痛26例,不稳定型心绞痛30例,急性心肌梗死28例),均采血测血浆巨噬细胞炎症蛋白1α;冠心病组患者均行冠状动脉造影记录冠状动脉病变支数及Gensini冠状动脉病变积分,并与血浆巨噬细胞炎症蛋白1α水平进行相关分析.结果 冠心病组血浆巨噬细胞炎症蛋白1α水平明显高于正常对照组(P<0.05).血浆巨噬细胞炎症蛋白1α水平在稳定型心绞痛组、不稳定型心绞痛组和急性心肌梗死组间以及轻、中、重度冠状动脉病变组(按Gemini积分分组)间均逐级升高,差异有显著性(P<0.05),但冠心病不同冠状动脉病变支数组间血浆巨噬细胞炎症蛋白1α水平差异无显著性(P>0.05).血浆巨噬细胞炎症蛋白1α水平与Gemini冠状动脉病变积分存在正相关(r=0.28,P<0.05).结论 冠心病患者血浆巨噬细胞炎症蛋白1α升高,可能是评价冠状动脉粥样硬化斑块病变严重程度及斑块稳定性的有效指标.     

冠状动脉支架术对冠心病患者血小板活化功能的影响

目的探讨冠心病患者行冠状动脉内支架置入术前后血小板活化指标的变化,了解冠心病不同临床类型支架置入数与血小板活化指标之间的关系。方法利用流式细胞术和单克隆抗体测定48例稳定型心绞痛、45例不稳定型心绞痛患者与37例急性心肌梗死患者外周血中血小板膜糖蛋白CD62p、CD63和凝血酶敏感蛋白的阳性表达率,并与45例冠状动脉造影正常者作对照分析。结果稳定型心绞痛患者、不稳定型心绞痛患者和急性心肌梗死患者支架置入后CD62p、CD63和凝血酶敏感蛋白的阳性表达率均显著高于支架置入前(P<0.01);不稳定型心绞痛组和急性心肌梗死组治疗前亦高于对照组(P<0.01),而稳定型心绞痛组治疗前与对照组比较差异无显著性(P>0.05)。稳定型心绞痛组和不稳定型心绞痛组CD62p、CD63和凝血酶敏感蛋白的阳性表达率与支架置入个数有关,置入支架越多阳性表达率越高。结论不稳定型心绞痛患者及急性心肌梗死患者存在血小板高活化状态、动脉粥样硬化斑块破裂以及急性血栓形成。支架置入术对冠状动脉内皮的损伤加强了血小板的活化,增加了血栓形成的风险。     

高血压病并发冠心病患者血清同型半胱氨酸变化分析

目的 分析高血压病患者冠心病程度与血清血浆同型半胱氨酸(Hcy)的关系.方法 160例高血压病并发冠心病患者,依肌钙蛋白分为稳定型心绞痛组(AP)、不稳定型心绞痛组(UAP)和急性心肌梗死组(AMI),用循环酶测定3组患者血清Hcy.结果 高血压病合并冠心病患者随着病变不稳定程度的增加,稳定型心绞痛组<不稳定型心绞痛组<急性心肌梗死组,Hcy浓度依次呈增高趋势,差异有统计学意义(P<0.05).结论 高血压病患者的冠心病程度与Hcy呈正相关.     

黄芪注射液对稳定型心绞痛患者血浆血管内皮生长因子水平的影响

目的 观察黄芪注射液治疗冠心病稳定型心绞痛患者的疗效及对血浆血管内皮生长因子的影响.方法 将100例患者随机分为治疗组和对照组,对照组采用常规治疗,治疗组加用黄芪注射液静脉输注,3周后观察两组的疗效和治疗前后血浆血管内皮生长因子水平的变化.结果治疗组治疗后血浆血管内皮生长因子较前明显升高(P<0.01),治疗组的临床疗效优于对照组(P<0.05).结论 黄芪注射液可通过升高血浆血管内皮生长因子水平,而达到更好地治疗冠心病的目的 .     

冠心病患者血浆神经肽Y水平变化及其临床意义

目的 ,研究不同类型冠心病患者发病不同阶段血浆神经肽 Y（NPY）水平的变化 ,探讨其与冠心病心肌缺血的关系。方法 ,选急性心肌梗死、不稳定型心绞痛、稳定劳力型心绞痛、陈旧性心肌梗死患者各 30余例发病不同阶段血浆 NPY浓度 ,并选 32例健康者作为对照组。结果 ,急性心肌梗死急性期 （2 4h） ,不稳定型心绞痛患者疼痛发作期血浆 NPY水平均明显高于对照组 ,差异非常显著。稳定劳力型心绞痛患者 ,陈旧性心肌梗死患者血浆 NPY水平与对照组比较差异无显著性意义。不稳定型心绞痛患者疼痛发作期血浆 NPY水平高于治疗后 2周病情稳定期 ,差异非常显著 （P<0 .0 1）。急性心肌梗死患者血浆 NPY水平在心梗后 8h左右开始升高 ,2 4h达高峰 （34 6 .2± 5 9.6 pg/ ml） ,7d左右恢复至正常水平 （2 2 8.1± 38.6 pg/ m l）。结论 ,冠心病患者出现心肌急性缺血时 ,血浆 NPY水平升高 ,提示 NPY参与了冠心病患者急性心肌缺血时的病理生理过程 ,NPY可作为观察冠心病患者病情变化的一项指标。     

冠心病患者血清标志物水平与视网膜微血管病变的相关性

目的:研究冠心病(CHD)患者血清标志物水平与视网膜微血管病变(RA)的相关性。方法:选择本院2016年1月~2018年1月间收治的96例CHD患者作为CHD组,根据是否合并RA,患者被分为单纯CHD组(48例)和CHD+RA组(48例);选择同期在本院接受健康体检的48例健康受检者作为健康对照组。观察比较健康对照组和CHD组的血清血管内皮生长因子(VEGF)、细胞间黏附分子(ICAM)-1、内皮素-1 (ET-1)、血栓调节蛋白(TM)水平、及内皮细胞(ECs)、内皮祖细胞(EPCs)计数占比;并比较CHD两亚组的Syntax评分。分析上述血清指标水平与RA发生、Syntax评分的相关性。结果:与健康对照组对比,CHD组血清VEGF、ICAM-1、ET-1、TM水平,ECs、EPCs计数占比均显著升高,P均=0.001;与单纯CHD组比较,CHD+RA组上述血清指标水平和Syntax评分均显著升高,P均=0.001。Spearman相关分析显示,血清ET-1、ICAM-1、VEGF、TM水平,ECs、EPCs计数占比、Syntax评分与RA发生有显著正相关性(r=0.408~0.866,P均=0.001);Pearson相关分析显示,血清VEGF、ICAM-1、TM、ET-1水平,ECs、EPCs计数占比与Syntax评分呈显著正相关(r=0.738~0.997,P均=0.001)。结论:冠心病患者血清VEGF、ICAM-1、ET-1、TM水平,ECs、EPCs计数占比均显著高于健康者,各项血指标水平与RA的发生、病情严重程度具有显著正相关性。     

冠心病患者血清缺氧诱导因子-1α与血管内皮生长因子水平的变化

目的:研究冠心病(CHD)患者血清血管内皮生长因子(vascular endothelial growth factor,VEGF)和低氧诱导因子-1α(hypoxia inducible factor1α,HIF-1α)水平的变化意义。方法:CHD患者79例,分为急性冠脉综合征(ACS)组42例,稳定型心绞痛(SAP)组37例,另选35例作为对照组,所有患者清晨空腹抽血应用ELISA法测定VEGF和HIF-1α水平。结果:ACS组VEGF和HIF-1α水平显著高于SAP组和对照组(P0.05);SAP组VEGF和HIF-1α水平与对照组比较差异无统计学意义。结论:VEGF和HIF-1α水平升高可能是冠状动脉粥样硬化斑块的不稳定的标志。     

3种血清指标与老年急性冠状动脉综合征病情程度的相关性研究

目的探讨血清高迁移率族蛋白B1(HMGB1)、基质金属蛋白酶9(MMP-9)、骨膜蛋白与老年急性冠状动脉综合征(ACS)患者病情程度的关系。方法选取老年ACS患者220例,分为急性心肌梗死(AMI)组105例和不稳定性心绞痛(UAP)组115例,另选取健康体检者110例为对照组。对比各组血清HMGB1、MMP-9、骨膜蛋白水平,采用ROC曲线分析预测价值。结果 AMI组和UAP组血清HMGB1、MMP-9、骨膜蛋白水平明显高于对照组,且AMI组较UPA组更高(P<0.05)。血清HMGB1、MMP-9、骨膜蛋白为老年ACS发生的危险因素(P<0.01)。血清HMGB1、MMP-9、骨膜蛋白水平与冠状动脉病变支数(r=0.521,r=0.592,r=0.596,P<0.01)、Gensini评分(r=0.589,r=0.594,r=0.601,P<0.01)、病情程度(r=0.621,r=0.614,r=0.629,P<0.01)呈正相关。ROC曲线分析显示,血清HMGB1预测预后的曲线下面积为0.897,略高于血清MMP-9和骨膜蛋白,差异无统计学意义(P>0.05)。结论血清HMGB1、MMP-9、骨膜蛋白水平是老年ACS发生的重要危险因素,与冠状动脉病变支数、Gensini评分呈正相关,动态检测其水平,可为临床评估病情程度、判断预后提供指导。     

Serum levels, and bone marrow immunohistochemical expression of, vascular endothelial growth factor in patients with chronic myeloproliferative diseases

Current data suggest that angiogenesis plays a significant role in the pathogenesis and progression of chronic myeloproliferative diseases (cMPDs). In the present study, we evaluated serum levels of vascular endothelial growth factor (VEGF) in 83 patients with cMPDs [myelofibrosis with myeloid metaplasia (MMM, n = 25), essential thrombocythaemia (ET, n = 40), polycythaemia vera (PV, n = 8) and chronic myeloid leukemia (CML, n = 10)] and in 27 healthy individuals. Serum VEGF levels were significantly increased in patients with cMPDs compared to healthy individuals (all p values were < or = 0.05) and were significantly correlated with bone marrow microvessel density (MVD) (p = 0.0013). In addition, the immunohistochemical expression of VEGF protein in bone marrow biopsy specimens were analyzed in 61 patients with cMPDs, (ET, n = 36 and MMM, n = 25) and in 27 healthy individuals. The cellular distribution of VEGF expression was similar in bone marrow specimens of patients and healthy individuals. VEGF protein was detected mainly in erythroid cells, whereas myeloid cells and megakaryocytes exhibited a variable expression of the protein. The percentage of bone marrow VEGF positive cells was positively correlated with serum levels of VEGF (p = 0.001). The results of the present study suggest that, VEGF is a major angiogenetic factor in patients with cMPDs and contributes to the pathogenesis of these diseases.     

Haem oxygenase-1 expression and coronary heart disease--association between levels of haem oxygenase-1 expression and angiographic morphology as well as the quantity of coronary lesions

OBJECTIVE: The aim of this paper was to investigate the association between levels of HO-1 expression and angiographic morphology as well as the quantity of coronary lesions in patients with coronary heart disease (CHD). METHODS: 110 patients with CHD were diagnosed by coronary angiography which contained coronary lesions in some way. Firstly, the patients were divided into 3 groups according to the angiographic morphology of their coronary lesions: type I (smooth borders) group (n1= 36), type II (irregular borders) group (n2= 48) and type III (long and irregular lesions) group (n3= 26). Secondly, the patients were split into a further 3 groups, named: single-vessel group (SV, 38 cases), double-vessel group (DV, 44 cases) and multi-vessel group (MV, 28 cases) according to the number of coronary lesions. Another 30 patients with normal coronary arteries (diagnosed by coronary angiography) were selected as the control group.The levels of HO-1 protein expression in monocytes and lymphocytes from the subjects were tested by immunohistochemistry and Western blot. A computer picture analysing system was also used to measure the levels of HO-1 protein expression. RESULTS: HO-1 protein was located in cell plasma and the levels of HO-1 protein expression in patients with CHD were significantly higher than in those without CHD (p < 0.01).There were significant differences of HO-1 expression among patients with CHD. Patients with type III lesions had the highest levels, followed by those with type II lesions and the lowest levels were found in patients with type I lesions (p < 0.01). Also, levels of HO-1 protein expression in patients with multi-vessel disease and double-vessel disease were significantly higher than in those with single-vessel disease (p < 0.01). CONCLUSIONS: There is a higher expression of HO-1 in patients with CHD and the levels of HO-1 protein are associated with severity of CHD angiographically.     

冠心病患者缺氧诱导因子-1α与血管内皮细胞生长因子的关系

目的探讨冠心病患者体内缺氧诱导因子-1α(HIF-1α)与血管内皮细胞生长因子(VEGF)表达的关系。方法选取经皮冠状动脉造影确定的冠心病患者105例分为3组,其中急性心肌梗死(AMI)组37例,不稳定性心绞痛(UAP)组39例,稳定性心绞痛(SAP)组29例。另设经冠脉造影未发现异常者30例为对照组。采用酶联免疫吸附法测定所有入选对象血清VEGF与HIF-1α水平,采用相关分析法分析两者的相关性。结果 AMI和UAP组HIF-1α、VEGF表达水平明显高于SAP组和对照组(P均<0.05);AMI组HIF-1α和VEGF水平明显高于UAP组(P<0.05);SAP组与对照组比较差异无统计学意义。相关性分析发现,总体水平上HIF-1α、VEGF表达水平呈正相关(r=0.49,P<0.05),AMI、UAP、SAP各组中HIF-1α、VEGF表达水平也呈正相关(rAMI=0.47,rUAP=0.53,rSAP=0.41,P均<0.05)。结论不同类型冠心病患者HIF-1α、VEGF水平有所不同,心肌缺血程度越重则患者体内表达的HIF-1α、VEGF水平越高。冠心病患者VEGF水平的升高可能是心肌缺血诱导的HIF-1α所调控的。     

冠心病患者血尿酸、高敏C反应蛋白检测的临床意义

目的：观察冠心病患者血清尿酸（UA）、高敏C反应蛋白（hs-CRP）含量的变化及临床意义。方法：96例冠心病患者根据冠脉造影结果分为单支病变组（30例）、双支病变组（50例）和三支病变组（16例）,测定其UA、hs-CRP水平,并且与42例冠脉造影正常的胸痛患者（正常对照组）比较。结果：与正常对照组的UA含量（329.81±42.25）mmol/L,hs-CRP含量（2.69±0.81）mg/L相比,冠心病组的UA、hs-CRP含量均明显增加（P均〈0.001）,且随着病变支数的增加（单支,双支,三支病变）,UA、hs-CRP含量明显增加[UA（359.97±32.09）mmol/L：（383.32±39.31）mmol/L∶（420.81±36.47）mmol/L,hs-CRP（4.06±1.02）mg/L∶（6.36±0.78）mg/L∶（8.10±0.64）mg/L,P〈0.05~〈0.01],UA、hs-CRP水平与病变积分呈正相关（r=0.857,P〈0.001;r=0.915,P〈0.05）。结论：尿酸、高敏C反应蛋白含量与冠心病病变程度成正相关,是冠心病的危险因素。     

Serum periostin levels serve as a biomarker for both eosinophilic airway inflammation and fixed airflow limitation in well-controlled asthmatics

Objective: Periostin, a matricellular protein, is produced from airway epithelial cells and lung fibroblasts by IL-13. It has been suggested that periostin is involved in allergic inflammation and fibrosis. However, the usefulness of serum periostin measurement in the assessment of airway inflammation and remodeling and management of asthmatic patients is still debated. We aimed to determine whether serum periostin levels reflect eosinophilic airway inflammation and airway remodeling in asthma. Methods: We examined the relationship of serum periostin levels with clinical features, biomarkers for eosinophilic airway inflammation, fraction of exhaled nitric oxide (FeNO) levels and blood eosinophil counts, and pulmonary functions in 235 well-controlled asthmatic patients on inhaled corticosteroids (ICS) treatment. Results: Serum periostin levels were positively correlated with blood eosinophil counts (%) and age (r = 0.36 and 0.23, respectively), and were negatively correlated with body weight and FEV₁/FVC (%) (r = ?0.24 and ? 0.23, respectively) in well-controlled asthmatic patients on ICS treatment (daily dose of 453 µg equivalent to fluticasone propionate). Blood eosinophil counts and serum periostin levels were similarly associated with increased FeNO levels (≥40 ppb) in the asthmatics. Serum periostin levels were better associated with fixed airflow limitation (FEV₁/FVC ratio <70%) than FeNO levels, blood eosinophil counts or total IgE levels in the asthmatics. Multivariate analysis showed that fixed airflow limitation was significantly associated with high serum periostin levels (≥97 ng/ml) (Odds ratio 3.2). Conclusions: Serum periostin levels serve as a biomarker for both eosinophilic airway inflammation and fixed airflow limitation in well-controlled asthmatics on ICS treatment.     

Positive Chlamydia pneumoniae serology is associated with elevated levels of tumor necrosis factor alpha in patients with coronary heart disease

Infectious agents are possible stimulators of inflammation in atherogenesis. The aim of this study was to investigate if Chlamydia pneumoniae and Helicobacter pylori were associated with elevated levels of tumor necrosis factor alpha (TNFalpha) and interleukin-6 in coronary heart disease (CHD) patients (n=193) and age- and sex-matched controls (n=193) as markers of increased inflammatory activity. C reactive protein (CRP) and fibrinogen were also included. Serologic status towards the two bacteria was measured and levels of the inflammatory markers were compared between seropositives and seronegatives, each study group being evaluated separately. In CHD patients Chlamydia lipopolysaccharide (LPS) IgA seropositivity predicted elevated TNFalpha levels (P=0.009), still statistically significant after adjustment for traditional cardiovascular risk factors (P=0.005). Chlamydia LPS IgG seropositivity independently predicted fibrinogen levels in CHD patients (P=0.028), while no association between serology and inflammatory markers were observed among controls. H. pylori seropositivity alone was not associated with any increase in the inflammatory markers in any of the two groups. However, in CHD patients seropositivity to both agents predicted higher levels of TNFalpha (P=0.041), CRP (P=0.037) and fibrinogen (P=0.001) compared to double seronegativity. We conclude that C. pneumoniae LPS seropositivity may contribute to increased vascular inflammation in CHD patients, possibly even more pronounced when present in combination with H. pylori seropositivity.