氢饱和生理盐水对重症急性胰腺炎肺损伤的作用及对NOX2/ROS/NF-κB 通路的影响

目的:探讨氢饱和生理盐水(HRS)对大鼠重症急性胰腺炎(SAP)肺损伤的影响及其与NOX2/ROS/NF-κB通路的关系。方法:72只雄性Wistar大鼠随机分为假手术组、SAP模型组(SAP组)、SAP模型+HRS治疗组(HRS组);SAP模型以胆胰管逆行注射5%牛磺胆酸钠制备;术后5min,HRS组经尾静脉注射HRS(6mL/kg),假手术组与SAP组以等体积生理盐水代替;术后3、12、24h分批剖杀大鼠,胰腺和肺组织行病理学检查,以及血清胰酶水平、肺组织丙二醛(MDA)与超氧化物歧化酶(SOD)水平、肺组织NOX2、NF-κB及TNF-α表达水平检测。结果:与假手术组比较,SAP组和HRS组大鼠各时间点均出现明显的SAP与肺损伤表现,表现为胰腺、肺组织病理学评分增加,血清胰酶水平升高,肺组织MDA含量升高、SOD活性降低(均P0.05),但除胰酶水平外(均P0.05),HRS组各损伤指标均明显低于SAP组(均P0.05);术后12h免疫组化结果显示,SAP组和HRS组大鼠肺组织中NOX2、NF-κB和TNF-α的表达均较假手术组升高(P0.05),HRS组上述指标均较SAP组明显低于SAP组降低(均P0.05)。结论:HRS有减轻SAP大鼠肺损伤的作用,机制可能与抑制NOX2/ROS/NF-κB通路活性有关。     

阿米洛利预先给药对大鼠内毒素性急性肺损伤的影响

目的 探讨阿米洛利预先给药对大鼠内毒素性急性肺损伤的影响.方法 清洁级雄性SD大鼠32只,体重200～250 g,随机分为4组(n=8):对照组(C组)、急性肺损伤组(ALI组)、阿米洛利组(A组)和阿米洛利预先给药组(AL组).C组股静脉输注生理盐水3 ml,ALI组股静脉输注生理盐水1 ml、内毒素6 mg/kg,A组股静脉输注阿米洛利10 mg/kg、生理盐水2 ml,AL组股静脉输注阿米洛利10 mg/kg、内毒素6 mg/kg,输注速率均为0.05 ml/rain,给药间隔均为30 min.于输注内毒素结束后6 h时处死大鼠取肺,观察肺组织病理学,并行病理学评分,称重后计算肺湿干重比,检测髓过氧化物酶(MPO)活性,测定支气管肺泡灌洗液总蛋白、TNF-α和巨噬细胞炎性蛋白-2(MIP-2)的浓度,采用Western blot法检测肺组织钠氢交换体1(NHE1)、p38丝裂原活化蛋白激酶(p38MAPK)和细胞外信号调节激酶(ERK)的表达水平.结果 与C组比较,ALI组和AL组肺组织病理学评分、肺湿干重比、MPO活性、支气管肺泡灌洗液总蛋白、TNF-α和MIP-2浓度、肺组织NHE1、p38MAPK和ERK的表达水平明显升高(P＜0.01),A组上述指标差异无统计学意义(P＞0.05);与ALI组比较,AL组肺组织病理学评分、肺湿干重比、MPO活性、支气管肺泡灌洗液总蛋白、TNF-α和MIP-2浓度、肺组织NHE1和ERK的表达水平明显降低(P＜0.01),p38MAPK表达差异无统计学意义(P＞0.05).结论 阿米洛利预先给药可减轻大鼠内毒素性急性肺损伤,其机制可能与抑制ERK信号转导通路激活有关.     

紫草素对大鼠重症急性胰腺炎并发急性肺损伤的抑制作用

目的:探讨紫草素对大鼠急性胰腺炎(SAP)并发急性肺损伤(ALI)的抑制作用。方法:将24只雄性SD大鼠随机均分为对照组、模型组和治疗组。模型组与治疗组大鼠采用逆行胰胆管注入4%牛磺胆酸钠溶液的方法诱导SAP,对照组行假手术。治疗组大鼠在模型制备前2 h给予紫草素(50 mg/kg)灌胃,其余两组大鼠则以相同方式给与同体积的溶剂。术后6 h处死各组动物收集血、胰腺与肺组织标本,观察胰腺与肺组织病理学变化,检测血清中TNF-α、IL-6水平,肺组织湿干比以及肺组织中PI3K、磷酸化PI3K(p-PI3K)、NF-κB的表达。结果:对照组大鼠胰腺与肺组织均未见异常,模型组与治疗组胰腺与肺组织出现明显的病理改变,但治疗组胰腺与肺组织的病变程度均明显小于模型组,各组间胰腺与肺组织病理评分均有统计学差异(均P 0.05)。与对照组比较,模型组与治疗组血清TNF-α与IL-6水平、肺组织湿干比、肺组织p-PI3K/PI3K与NF-κB表达量均明显升高(均P0.05),但治疗组以上指标的变化程度均明显小于模型组(均P 0.05)。结论:紫草素对大鼠的SAP及其并发的ALI均有抑制作用,其机制可能与减少炎症因子的释放以及降低肺组织PI3K-Akt-NF-κB通路活化有关。     

大鼠重症急性胰腺炎肺泡巨噬细胞的活化和调控作用

目的 观察巨噬细胞中p38蛋白活化激酶对大鼠重症急性胰腺炎肺损伤的影响.方法 假手术组仅胆胰管注射生理盐水0.1 ml/100 g;5%的牛黄胆酸(0.1 ml/100 g)逆行注射到SD大鼠的胆胰管内,造成重症急性胰腺炎(SAP)分为SAP组和SB03580组(SB203580,0.5 mg/kg,静注).在6 h剖杀大鼠,查腹水,抽血检测血清淀粉酶(AMS)和肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6[酶联免疫吸附试验(ELISA)法];同时分别离心收集全肺肺泡巨噬细胞,免疫组织化学检测肺组织及其巨噬细胞中p38 MAPK的表达,同时检测肺组织中的TNF-α和IL-6;光镜下检测胰腺组织损害.结果 SAP组及SB组中AMS在6 h分别为(4865.12±890.35)IU/L和(2918.24±614.58)IU/L,差异有统计学意义.血清TNF-α分别为(106.59±43.71)ng/L和(76.43±38.43)ng/L;IL-6是(2203.76±640.85)ng/L和(1254.76±459.35)ng/L,差异有统计学意义(P<0.01).肺组织中的TNF-α和IL-6的升高与血中的一致.光镜下,胰腺组织内可见炎细胞浸润、充血、水肿和坏死;在SAP组中肺组织及其巨噬细胞中p38 MAPK强烈表达,TNF-α和IL-6的表达一致,SB治疗组表达下降.结论 TNF-α和IL-6在重症急性胰腺炎肺损伤起着重要作用;肺泡巨噬细胞中p38 MAPK表达对TNF-α和IL-6的转录和合成起重要作用.     

烟雾吸入性损伤大鼠肺组织丝裂原活化蛋白激酶通路的变化

目的 了解烟雾吸入性损伤大鼠肺组织丝裂原活化蛋白激酶(MAPK)通路及炎性细胞因子含量的变化,探讨其损伤机制. 方法建立密闭舱内烟雾吸入性损伤模型,将30只SD大鼠分为烟雾吸入性损伤后1、6、24、72 h及7 d组,另设正常对照组(6只).取各组大鼠肺组织行病理学观察,检测肺组织匀浆液中肿瘤坏死因子α(TNF-α)、巨噬细胞炎性蛋白2(MIP-2)和白细胞介素1β(IL-1β)含量,用蛋白质印迹法检测肺组织p38MAPK、c-Jun氨基末端激酶(JNK)、细胞外信号调节激酶1/2(ERK1/2)及各酶磷酸化水平.收集大鼠支气管肺泡灌洗液(BALF),检测TNF-α、MIP-2、IL-1β含量并行粒细胞分类、计数. 结果烟雾吸入使大鼠产生急性肺损伤样病理改变.伤后1 h组大鼠肺组织及BALF中TNF-α和IL-1β含量均高于正常对照组(P<0.01).各组肺组织MIP-2水平与正常对照组接近(P>0.05),伤后1 h组BALF中MIP-2水平高于正常对照组(P<0.01).各致伤组p38MAPK、ERK1/2、JNK水平接近正常对照组,但此3种酶的磷酸化水平在伤后不同时相组有高表达.伤后1 h组大鼠BALF粒细胞总数为(0.36±0.08)×106个/L,较正常对照组(0.61±0.09)×106个/L明显减少(P<0.05),伤后7 d组粒细胞总数[(1.71±0.67)×106个/L]却高于正常对照组(P<0.05).伤后6 h～7 d组中性粒细胞数多于正常对照组(P<0.05).伤后1 h组巨噬细胞数少于正常对照组(P<0.05),但6 h～7 d组逐渐增多.各组大鼠淋巴细胞数量接近(P>0.05).结论 密闭舱室内非金属材料燃烧释放的毒性气体能诱导肺组织产生明显的炎性反应,激活细胞MAPK通路中重要激酶的表达,这可能是毒性混合气体导致肺损伤的重要机制之一.     

阿司匹林诱生型脂氧素A4对脂多糖诱导小鼠急性肺损伤的影响

目的 评价阿司匹林诱生型脂氧素A4 (ATL)对脂多糖(LPS)诱导小鼠急性肺损伤的影响.方法 雄性SPF级BALB/C小鼠30只,体重25～30 g,10～ 12周龄,采用随机数字表法,将其分为3组(n=10):对照组(NS组)气管内滴定生理盐水(LPS溶媒)1.5 ml/kg,1h后尾静脉注射50％无水乙醇(ATL溶媒)0.1 ml; LPS组气管内滴定LPS 3 mg/kg,1h后尾静脉注射50％无水乙醇0.1 ml; ATL组气管内滴定LPS 3 mg/kg,1h后尾静脉注射ATL 0.2 mg/kg.气管内滴定药物后24h处死,采集支气管肺泡灌洗液(BALF),计数总细胞数、多形核粒细胞比例、单个核细胞比例及其总蛋白、TNF-α、IL-6、单核细胞趋化蛋白-1(MCP-1)、IL-10的浓度;取肺组织,测定髓过氧化物酶(MPO)活性、p38丝裂原活化蛋白激酶(p38 MAPK)、c-Jun氨基末端激酶(JNK)、细胞外调节蛋白激酶(ERK1/2)的磷酸化水平,并观察肺组织病理学结果,行肺损伤评分.结果 与NS组比较,LPS组和ATL组肺损伤评分、BALF中总细胞数、多形核粒细胞比例、TNF-α、IL-6、MCP-1浓度升高,单个核粒细胞比例降低,LPS组BALF中IL-10浓度降低,总蛋白浓度、肺组织MPO活性、p38 MAPK、JNK、ERK1/2的磷酸化水平升高(P＜0.05),ATL组BALF中总蛋白、IL-10浓度、肺组织MPO活性、p38 MAPK、JNK、ERK1/2的磷酸化水平差异无统计学意义(P＞0.05);与LPS组比较,ATL组肺损伤评分、BALF中总细胞数、多形核粒细胞比例和总蛋白、TNF-α、IL-6、MCP-1浓度降低,单个核粒细胞比例和IL-10浓度升高,肺组织MPO活性、p38MAPK和JNK的磷酸化水平降低(P＜0.05),ERK1/2的磷酸化水平差异无统计学意义(P＞0.05).结论 ATL可减轻LPS诱导的小鼠急性肺损伤,其机制与抑制p38 MAPK和JNK信号通路激活有关.     

盐酸戊乙奎醚对重症急性胰腺炎时肺损伤防治作用的研究

目的研究盐酸戊乙奎醚对重症急性胰腺炎(severacutepancreatitis,SAP)时急性肺损伤(acutelunginjury,ALI)的防治作用。方法本实验采用胰管逆行注射1·5%去氧胆酸钠制成SAP时ALI大鼠模型,随机分为三组:模型加盐酸戊乙奎醚治疗组(PHCD组);模型组(SAP组);假手术组(SHAM组)。分别于造模后24h活杀,测定动脉血气,血清和肺组织匀浆中的肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)的含量,肺湿/干系数。结果SAP组血清及组织匀浆中TNF-α、IL-6均较SHAM组明显升高(P<0·05),动脉血气显示肺损伤严重,肺湿/干比值较SHAM组明显升高,肺通透性明显升高,肺病理学形态改变加重。PHCD组血清及组织匀浆中TNF-α、IL-6均较SAP组明显降低(P<0·05),动脉血气显示肺功能较SAP组明显改善,肺湿/干比值较SAP组明显降低(P<0·05),肺病理形态学基本上接近正常。结论盐酸戊乙奎醚通过抑制TNF-α、IL-6的产生对SAP时ALI起到一定防治作用。     

戊乙奎醚预处理对脓毒症小鼠肺损伤时MAPK信号转导通路的影响

目的 探讨戊乙奎醚(PHC)预处理对脓毒症小鼠肺损伤时丝裂原活化蛋白激酶(MAPK)信号转导通路的影响.方法 健康雌性昆明小鼠105只,体重20～25 g,随机分为3组(n=35):假手术组(S组)、脓毒症(CLP)组和戊乙奎醚(PHC)组.采用盲肠结扎并穿孔法制备脓毒症模型.PHC组于造模前1 h腹腔注射戊乙奎醚0.45 mg/kg,s组和CLP组于造模前1 h注射等容量生理盐水.于造模后即刻测定肺微血管通透性;造模后12 h时进行动脉血气分析,观察肺组织病理结果,测定肺组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和磷酸化的p38丝裂原活化蛋白激酶(p38MAPK)、细胞外信号调节激酶(ERK1/ERK2)和c-jun氨基末端蛋白激酶(JNK)表达.结果 与S组比较,CLP组PaO2、PaO2/FiO2和pH值降低,肺微血管通透性和肺组织MDA含量升高,SOD活性降低,磷酸化的p38MAPK、ERK1/ERK2和JNK表达上调(P<0.05或0.01);与CLP组比较,PHC组PaO2、PaO2/FiO2和pH值升高,肺微血管通透性和肺组织MDA含量降低,SOD活性升高,磷酸化的p38MAPK和ERK1/ERK2表达下调(P<0.05或0.01).结论 戊乙奎醚预处理可通过抑制MAPK信号转导通路(p38MAPK和ERK1/ERK2)的激活,从而减轻脓毒症小鼠肺损伤.     

甘草甜素治疗重症急性胰腺炎的实验研究

目的:探讨甘草甜素对大鼠重症急性胰腺炎(SAP)疗效。方法:将大鼠随机均分为假手术组,SAP组,SAP+甘草甜素治疗组(治疗组),以5%牛磺胆酸钠胰胆管逆行注射制作大鼠SAP模型。比较各组术后的生存时间,术后不同时间点血淀粉酶及血清TNF-α,IL-1β,IL-6的水平及胰腺组织病理学评分。结果:假手术组大鼠在观察时间内无死亡,SAP组和治疗组大鼠术后的平均生存时间分别为(28.50±17.82)h和(41.50±17.59)h,两者差异有统计学意义(P<0.05);与假手术组比较,SAP组和治疗组各时间点血清TNF-α,IL-1β,IL-6水平均明显升高(均P<0.05),但治疗组上述指标升高程度均明显低于SAP组(均P<0.05);除假手术组外,SAP组和治疗组胰腺组织均呈现出不同程度的SAP病理改变,但治疗组病理改变明显较轻,各时间点组织学评分也明显低于SAP组(均P<0.05)。结论:甘草甜素治疗大鼠重症急性胰腺炎有一定的疗效。     

Hand and foot abnormalities associated with genetic diseases

Introduction  

The small bones and soft tissues of the hands and feet can be affected by systemic disorders, and frequently, the findings are quite unique and virtually diagnostic for some genetic or metabolic disorders.     

Efficacy and safety of premedication with oral ketamine for day-case adenoidectomy compared with rectal diazepam/diclofenac and EMLA

BACKGROUND: Because of its pain-attenuating and sedative properties oral ketamine has been used as premedication in children and adults. We wanted to compare in children scheduled for adenoidectomy safety and efficacy of oral ketamine with a premedication that causes similar preoperative sedation and relief of pain at the venepuncture site. We also evaluated the effect of i.v. glycopyrrolate added to these combinations. METHODS: One hundred children between 10 and 15 kg of body weight scheduled for day-case adenoidectomy were randomly assigned to one of four groups: groups DG and DS received diclofenac 12.5 mg and diazepam 0.5 mg/kg rectally, EMLA cream at the venepuncture site, and placebo orally; groups KG and KS received ketamine 6.0 mg/kg orally, placebo cream at the puncture site, and placebo rectally; additionally, groups DG and KG received glycopyrrolate 5 microg/kg, and groups DS and KS received placebo intravenously. We recorded perioperatively scores (open scale 1-9) for stridor, sedation, bleeding, nausea, pain, heart rate, the need for analgesics and registered psychotomimesis and well-being at home. RESULTS: The children of the K-groups became more tearful during separation from their parents (P=0.0072). No other differences were found between the ketamine and diazepam/diclofenac groups before and after premedication until induction of anaesthesia. Oral ketamine produced unpleasant psychotomimesis in four out of 59 children. During the first 10 min postoperatively, the score for stridor was significantly higher in group KS than in the D-groups; stridor scores > or = 6 were seen in one child of the D-groups (DS) and in six children of the K-groups (n.s.), of whom three developed laryngospasm (one reintubation). Glycopyrrolate diminished salivation in all groups, but had no effect on stridor scores. Additionally, glycopyrrolate delayed the onset of eating at home. CONCLUSION: Premedication with racemic oral ketamine 6 mg/kg does not seem to be suitable for upper airway procedures. Addition of i.v. glycopyrrolate before the induction of anaesthesia significantly reduced the scores for salivation.     

血浆凝血因子VIII水平与IgA肾病患者临床病理改变及预后的关系

目的探讨血浆凝血因子VIII(factor VIII,FVIII)水平与IgA肾病(IgAN)患者临床参数及预后的关系。方法收集2016年1月至2016年12月中南大学湘雅二医院确诊的IgAN患者的临床资料。按照时间依赖的受试者工作特征曲线(ROC)得出的血浆FVIII预测IgAN预后的临界值,将患者分为高FVIII组(FVIII>140.50%)和低FVIII组(FVIII≤140.50%),比较两组患者肾活检时基线临床参数的差异。以估算肾小球滤过率(eGFR)下降≥30%或进入终末期肾脏病(ESRD)为终点事件,采用Kaplan-Meier生存曲线及Cox回归方程法分析血浆FVIII水平对IgAN患者预后的影响。结果共93例IgAN患者纳入本研究,中位随访时间为35.15(33.77,36.76)个月,12例(12.90%)患者发生终点事件。高FVIII组患者年龄、血肌酐、尿素氮、血三酰甘油、血总胆固醇、血浆纤维蛋白原、D-二聚体、24 h尿蛋白量、蛋白C、蛋白S和eGFR下降速率高于低FVIII组(均P<0.05);eGFR、血白蛋白、中位随访时间低于低FVIII组(均P<0.05)。Kaplan-Meier生存分析结果显示,与低FVIII组比较,高FVIII组患者肾脏累积生存率降低(χ2=5.635,P=0.018)。在校正收缩压、eGFR、尿蛋白、肾小管萎缩/间质纤维化程度等因素后,多因素Cox回归分析结果显示,高血浆FVIII水平是IgAN患者肾脏预后不良的独立危险因素(HR=4.147,95%CI 1.055~16.308,P=0.042)。结论血浆FVIII水平与IgAN患者临床指标及预后相关,高血浆FVIII水平是IgAN患者肾脏预后不良的独立危险因素。     

Problems with Activated Charcoal and Alumina as Sorbents for Medical Use

Although activated charcoal and alumina have been used extensively as sorbents in uremic patients, the following problems remain to be solved: 1) elution of SO4--from activated charcoal which does not adsorb it; 2) production of methylguanidine from creatinine on the surface of activated charcoal; 3) production of lipoperoxide from fatty acids by chemical reaction of activated charcoal; 4) adsorption of Ca++ and Mg++ when alumina adsorbs inorganic phosphate. These problems are studied in vitro and clinically.     

存在肾小动脉微血管病变且非高血压IgA肾病患者的临床病理特点和预后分析

目的总结和分析非高血压的IgA肾病(IgA nephropathy,IgAN)合并肾小动脉微血管病变(microangiopathy,MA)患者的临床病理特点和预后。方法抽取北京大学第一医院IgAN前瞻性队列人群中非高血压成人患者,重新进行病理阅片,根据肾小动脉病变,分为MA组、动脉硬化病变(AS)组和无血管病变组,分析其临床病理及预后特点。复合肾脏终点事件包括终末期肾病或估算肾小球滤过率(eGFR)下降≥30%。采用Cox回归模型分析预后的危险因素。结果共420例IgAN患者被纳入本研究,其中37(8.8%)例患者合并MA,134(31.9%)例合并AS,其余249例无血管病变。相对于AS组或无血管病变组,合并MA的患者尿蛋白量更严重[1.47(1.08,2.84)g/d比1.31(0.68,2.56)g/d、1.04(0.55,2.00)g/d,P=0.002],肾功能更差[eGFR:(75.3±26.5)ml·min-1·(1.73 m2)-1比(85.7±27.0)ml·min-1·(1.73 m2)-1、(98.6±24.8)ml·min-1·(1.73 m2)-1,P<0.001],并有更高的节段性肾小球硬化和(或)球囊粘连(S1)、肾小管萎缩/间质纤维化(T1/2)、细胞/细胞纤维新月体病变(C1/2)比例(均P<0.05)。随访期间,合并MA的患者发生终点事件比例更高[54.1%比33.6%、32.9%,χ2=6.491,P=0.039]。Cox多因素分析模型显示,MA是IgAN发生进展的独立危险因素(HR=1.872,95%CI 1.044~3.357,P=0.035),而其他类型血管病变不影响预后。结论非高血压IgAN患者合并MA不少见,这提示高血压并非导致IgAN血管病变的唯一危险因素。     

类风湿关节炎行关节置换术围手术期管理的研究进展

类风湿关节炎是最常见的炎性关节病,尽管目前类风湿关节炎缓解药物不断改进,药效却只能延缓关节功能障碍的进展。人工膝或髋关节置换术现已成为晚期类风湿关节炎患者的惟一选择,经手术治疗后患者的关节功能及畸形问题可得到不同程度改善。但类风湿关节炎的病程持续进展直接影响术后的远期效果,如何完善围手术期管理,将关节置换术与药物治疗有效结合逐渐成为临床工作者关注的重点。本文拟通过对行关节置换术类风湿关节炎患者的术前药物使用、术中手术技巧、假体选择、术后治疗、康复锻炼及并发症等国内外管理现状加以概括总结,为提高此类患者远期疗效及生活质量提供有益帮助。     

Prolonged anaesthesia with isoflurane and halothane

Hepatic function was assessed pre-operatively and on the first and sixth postoperative days in 40 healthy patients who underwent prolonged maxillofacial surgery with isoflurane or halothane anaesthesia. No major changes were observed in hepatic enzymes or bilirubin. One-stage prothrombin time and Factor VII concentrations decreased on the first postoperative day and this change was more pronounced in the halothane group. The results support the use of isoflurane rather than halothane for prolonged anaesthesia in respect of the synthesising function of the liver.     

C-reactive protein in patients with COPD, control smokers and non-smokers

BACKGROUND: Patients with chronic obstructive pulmonary disease (COPD) have raised serum levels of C reactive protein (CRP). This may be related directly to COPD and its associated systemic inflammation or secondary to other factors such as concomitant ischaemic heart disease (IHD) or smoking status. The aim of this study was to evaluate IHD and smoking as potential causes of raised CRP levels in COPD and to test the association between inhaled corticosteroid (ICS) use and serum CRP levels. METHODS: Cross sectional analyses comparing cohorts of 88 patients with COPD, 33 smokers (S), and 38 non-smoker (NS) controls were performed. Clinical assessments included a complete medical history, pulmonary function, 6 minute walk test (6MWT), cardiopulmonary exercise test, and high sensitivity serum CRP measurements. RESULTS: Serum CRP levels were significantly higher in patients with COPD (5.03 (1.51) mg/l) than in controls (adjusted odds ratio 9.51; 95% confidence interval 2.97 to 30.45) but were similar in the two control groups (S: 2.02 (1.04) mg/l; NS: 2.24 (1.04) mg/l). There was no clinical or exercise evidence of unstable IHD in any of the subjects. CRP levels were lower in COPD patients treated with ICS than in those not treated (3.7 (3.0) mg/l v 6.3 (3.6) mg/l); this association was confirmed in an adjusted regression model (p<0.05). CONCLUSION: CRP levels are raised in COPD patients without clinically relevant IHD and independent of cigarette smoking, and reduced in patients with COPD using ICS. CRP may be a systemic marker of the inflammatory process that occurs in patients with COPD.