小剂量糖皮质激素抑制类风湿关节炎放射学进展的系统评价

目的 系统评价小剂量糖皮质激素抑制类风湿关节炎(RA)放射学进展的疗效.方法 计算机检索Medline(1966年1月至2010年4月)、Embase(1966年至2010年4月)、Cochrane图书馆(2010年第2期)、中国生物医学数据库、中国期刊全文数据库(CNKI)、万方及维普数据库(1979年1月至2010年4月),并检索所纳入文献的参考文献.收集所有相关随机对照试验,采用Cochrane协作网提供的软件Revman5进行Meta分析,以获得小剂量糖皮质激素抑制RA放射学进展的相关证据.结果 经全面检索及筛查后,共纳入11个随机对照试验进行评价.Meta分析表明,在用药1年后,骨与关节侵蚀的标准化均数差(SMD)是-0.39[95％CI(0.50～-0.27)].2年时,侵蚀的SMD是-0.73[95％CI(- 1.29～-0.16)].结论 小剂量糖皮质激素能减缓RA放射学病损的进展.     

孟鲁司特在哮喘合并过敏性鼻炎患者中的疗效:荟萃分析

目的荟萃哮喘合并过敏性鼻炎患者的临床随机对照研究(RCT)评估孟鲁司特疗效。方法用关键词途径,对MEDLINE和Cochrane Library数据库从建库至2017年1月发表的孟鲁司特相关临床试验进行荟萃分析。入选标准为:研究哮喘合并鼻炎患者;持续≥14天;对照组为安慰剂、吸入型糖皮质激素(ICS)或ICS联合支气管扩张剂,治疗组加用孟鲁司特;临床终点为鼻部症状评分和最大呼吸流量(PEF)。结果最终纳入5篇可合并研究(2701例),鼻部症状评分的均数差(MD)及其95%置信区间(95%CI)为-0.09[-0.12,-0.06](P=0.0001),异质性P值为0.83。PEF的MD及95%CI为4.50[-2.24,11.24](P=0.19),异质性P值为0.004。鼻塞、喷嚏和流涕症状有明显下降。结论在安慰剂组或其他药物基础上加用孟鲁司特能够显著改善哮喘合并鼻炎患者的鼻炎症状。鼻塞、喷嚏和流涕症状均明显缓解。     

抗反流药物治疗对支气管哮喘伴胃食管反流患者哮喘症状影响的荟萃分析

目的 荟萃分析抗反流药物治疗对支气管哮喘(简称哮喘)伴胃食管反流患者哮喘症状的影响.方法纳入对合并胃食管反流的哮喘患者行抗反流治疗的前瞻性随机对照试验,抗反流治疗干预要求使用双肓法,样本量大小、匹配方式不限,研究对象为年龄＞13岁的伴胃食管反流病的哮喘患者.检索PubMed数据库、Embase数据库、Cochrane图书馆临床对照试验数据库、OVID数据库、中国生物医学文献数据库、中国知网全文数据库、万方科技期刊全文数据库.手工检索<中华结核和呼吸杂志>、<中华消化杂志>、<中华内科杂志>、CHEST及纳入文献的参考文献.所有检索均截至2009年11月.排除研究对象在进入研究前3 d内服用过抗反流药物、重复或多重发表、方法学质量评价为B级以下的文献.运用Cochrane荟萃分析的方法,由2名评价员独立对试验进行筛选、质量评价、数据提取和交叉核对.使用Revman 4.3.2软件对数据合并进行统计分析,评价抗反流药物治疗对哮喘伴胃食管反流患者哮喘的疗效.结果共纳入14项临床随机对照试验,包括1555例患者.抗反流治疗组与安慰剂组相比,FEV1增加[加权均数差(WMD)为0.11 L;95%可信区间(95%CI)为0.02～0.20;Z=2.49,P=0.010];日间最大呼气流速(PEF)增加(WMD为42.33 L/min;95%CI为3.39～81.28;Z=2.13,P=0.030);早晨PEF增加(WMD为16.16 L/min;95%CI为5.91～26.41;Z=3.09,P=0.002);夜间PEF增加(WMD为18.35 L/min;95%CI为6.77～29.92;Z=3.11,P=0.002).抗反流治疗与安慰剂治疗后比较,FEV1较基础对照值降低达20%时的吸入乙酰胆碱浓度(PC20-FEV1)减低(WMD为-0.07 mg/L;95%CI为-0.33～0.19),但差异无统计学意义(Z=0.55,P=0.590).14项研究中有8项研究在抗反流治疗后观察到哮喘症状改善,但荟萃分析显示哮喘日间症状和夜间症状的改善均无统计学意义.结论抗反流治疗可改善合并胃食管反流病哮喘患者的肺通气功能,但对气道高反应性和哮喘症状无显著影响.     

补钾对原发性高血压患者血压影响的荟萃分析

目的探讨口服补钾对原发性高血压患者血压的影响,对其降压效应进行荟萃分析。方法按照Cochrane系统评价方法,通过电子数据库检索Pubmed、Embase、Cochrane Liberary、中国生物医学文献数据库、中国期刊全文数据库,收集口服补钾用于原发性高血压患者效果分析的所有相关随机对照试验(RCT)和半随机对照试验(qRCT),提取有效数据后用Cochrane协作网提供的RevMan软件包(version 5.3)进行统计分析,比较口服补钾组患者与对照组血压变化的差异。结果共纳入14项RCT,10项qRCT,1646例,其中口服补钾组患者827例,对照组患者819例。荟萃分析结果显示,口服补钾组患者收缩压、舒张压均显著低于对照组[收缩压:加权均数差(WMD)=-4.46mm Hg,95%CI-5.47~-3.46;舒张压:均数差(MD)=WMD=-3.64mm Hg,95%CI-4.28~-3.00],差异有统计学意义(均P0.001)。对两组患者试验后与基线情况对比发现,口服补钾组患者收缩压降幅(WMD=-8.25mm Hg,95%CI-11.81~-4.69;I~2=75%)与舒张压降幅(WMD=-6.11mm Hg,95%CI-10.02~-2.21;I~2=93%)均显著大于对照组,差异有统计学意义(均P0.001)。口服补钾不良反应发生率较低,最常见的为排便改变、腹痛、胃肠不适如胀气。此外,亚组分析结果显示口服补钾在美洲、欧洲及亚洲地区高血压患者中均有降压效果,且存在一定的剂量-效应关系。结论口服补钾对原发性高血压患者有明确的降压效果,可显著降低收缩压和舒张压,口服补钾可作为原发性高血压患者的一种辅助治疗手段。     

不同剂型曲前列环素治疗肺动脉高压的临床疗效及安全性

目的:系统评价不同剂型曲前列环素治疗肺动脉高压的临床疗效及安全性。方法:由两名研究者独自在英文数据库(PubMed、Cochrane Library、EMBASE)及中文数据库(万方、中国生物医学文献数据库、维普及中国知网)检索,检索时间至2018年6月。根据纳入及排除标准由两名研究者独立选择文献、提取数据及评价文献质量,采用Stata 14.1软件对效应值分别进行Meta分析。结果:最终共纳入11项研究,共纳入曲前列环素治疗肺动脉高压患者933例,其中42.0%为皮下注射型,5.0%为静脉注射型,33.4%为口服型及19.6%为吸入型。研究结果显示曲前列环素治疗肺动脉高压的病死率仅为2.5%,以静脉注射型治疗较常见。Meta分析结果显示曲前列环素可明显提高6MWD,SMD皮下=4.34(95%CI[1.46,7.30],P=0.003)、SMD静脉=3.27(95%CI[0.01,6.53],P=0.049)、SMD吸入=0.33(95%CI[0.12,0.53],P=0.002)及SMD口服=0.30(95%CI[0.05,0.54],P=0.017);其中皮下注射型可降低Borg呼吸困难评分(SMD=-2.87,95%CI[-4.44,1.30],P0.001);而静脉注射型不仅可有效降低患者的Borg评分(SMD=-3.27(95%CI[-4.48,-2.48],P0.001),同时提高心脏指数(SMD=5.24,95%CI[4.08,6.41],P0.001),降低患者平均肺动脉压力(SMD=-1.65,95%CI[-2.58,-0.72],P0.001)及肺循环阻力(SMD=-4.66,95%CI[-7.53,-1.79],P=0.001)。口服型及吸入型曲前列环素相关研究显示其并不能有效改善患者心功能、呼吸功能及临床恶化率。结论:曲前列环素为肺动脉高压的安全性药物,而不同剂型的临床疗效存在一定差异,其中皮下注射型及静脉注射型可明显改善患者的运动耐量及呼吸功能,且后者对肺血管有明显改善作用;但口服型及吸入型曲前列环素的有效性有待进一步研究。     

基础胰岛素联合阿卡波糖对比预混胰岛素治疗2型糖尿病疗效和安全性的Meta分析

目的系统评价基础胰岛素联合阿卡波糖对比预混胰岛素治疗T2DM的有效性和安全性,为临床治疗提供循证参考。方法计算机检索Medline、PubMed、Science Direct、Springer Link、中国期刊全文数据库、万方和维普数据库从2000~2016年的文献,收集基础胰岛素联合阿卡波糖(试验组)对比预混胰岛素(对照组)治疗T2DM的随机对照试验(RCT),提取资料并进行质量评价后,采用RevMan 5.3和Stata 12.0统计软件进行Meta分析。结果共纳入21项RCTs,试验组818例,对照组809例。Meta分析结果显示,试验组FPG[SMD(95%CI)=-0.26(-0.42~-0.10),总体效应检验:Z=3.14,P=0.002]、2hPG[SMD(95%CI)=-0.27(-0.47~-0.07),总体效应检验:Z=2.66,P=0.008]、BMI[SMD(95%CI)=-0.83(-1.45~-0.20),总体效应检验:Z=2.6,P=0.009]及低血糖发生率[OR(95%CI)=0.33(0.22~0.48),总体效应模型:Z=5.66,P0.00001]低于对照组,而两组HbA_1c水平比较,差异无统计学意义[SMD(95%CI)=-0.20(-0.44~0.04),总体效应检验:Z=1.61,P=0.11]。结论基础胰岛素联合阿卡波糖治疗T2DM在降低患者FPG、餐后血糖、BMI及低血糖发生率方面均优于预混胰岛素。     

绿茶提取物影响代谢综合征患者体质量控制的荟萃分析

目的 系统评价绿茶提取物对代谢综合征患者体质量控制的有效性. 方法 计算机检索美国国立生物医学信息中心PubMed医学数据库、爱思唯尔文摘索引数据库(Scopus)、美国心理协会心理学文摘数据库(PsycINFO)、荷兰医学文摘Embase数据库以及维普数据库、中文科技期刊全文数据库(CNKI)和万方数据库,全面收集绿茶提取物与代谢综合征患者体质量控制相关的随机对照试验,严格按照纳入和排除标准提取有效数据,采用RevMan 5.2.2软件进行荟萃分析. 结果 经过筛选最终纳入10篇随机对照研究,共626例代谢综合征患者,荟萃分析结果显示,与对照组比较,绿茶提取物组患者体质量(SMD=-0.19,95％ CI:-0.34～-0.03,Z=2.34,P=0.02)、腰围(SMD=-0.19,95％CI:-0.36～-0.02,Z=2.15,P=0.03)明显降低,绿茶提取物对两组患者BMI(SMD=0.14,95％CI:-0.31～0.03,Z=1.63,P=0.10)、臀围(SMD=0.15,95％ CI:-0.11～0.42,Z=1.12,P=0.26)和腰臀比(WMD=-0.02,95％ CI:-0.05～0.01,Z-1.32,P=0.19)差异均无统计学意义. 结论 绿茶提取物可有效降低代谢综合征患者体质量和腰围水平.     

微生态制剂治疗肝硬化的Meta分析

目的系统评价微生态制剂治疗肝硬化的有效性。方法计算机检索PubMed、Embase、Cochrane Library以及中国期刊全文数据库、维普、万方数据库,全面收集关于微生态制剂治疗肝硬化的随机对照试验,筛选后的文献应用Rev Man5.3软件进行Meta分析,其中二分类变量采用率差(RD)及其95%可信区间(95%CI)作为效应量;连续性变量若测量单位一致则采用加权均数差(WMD),测量单位不一致采用标准化均数差(SMD)及其95%CI进行评估。发表偏倚采用漏斗图进行分析。结果纳入符合标准的文献18篇,共1411例肝硬化患者,其中治疗组726例,对照组685例。与对照组相比,微生态制剂治疗可显著提高临床总体有效率(RD=0.28,95%CI:0.22~0.34,P0.001);亦可以明显改善肝功能生化指标:ALT(SMD=-0.90,95%CI:-1.14~-0.66,P0.001)、TBil(WMD=-15.99,95%CI:-26.42~-5.57,P0.001)、Alb(SMD=0.66,95%CI:0.40~0.93,P0.001),降低内毒素(SMD=-1.13,95%CI:-2.11~-0.15,P0.001)及血氨水平(WMD=-15.86,95%CI:-21.54~-10.18,P0.001)。结论微生态制剂可明显改善肝硬化患者的肝功能,有效抑制肝硬化进展,降低肝性脑病等并发症的发生风险,提高临床总有效率,且耐受性较好。     

布地奈德干粉吸入剂治疗中国新诊断的轻度持续性支气管哮喘患者的随机、双盲、多中心临床疗效研究

目的：评估早期使用布地奈德干粉吸入剂对治疗中国新诊断的轻度持续性支气管哮喘(简称哮喘)患者的临床疗效。方法采用随机、对照、双盲、多中心的研究方法,选取年龄5~66岁,被早期诊断为轻度持续性哮喘,诊断时间距第1次访视不超过2年,尚未采用糖皮质激素治疗的患者869例。随机分为布地奈德组[435例,给予布地奈德400μg/次,1次/d (如患者年龄<11岁：200μg/次,1次/d)加常规哮喘治疗]和安慰剂组[434例,给予安慰剂(用法同布地奈德组)加常规哮喘治疗],随访时间为期3年。结果相对于安慰剂组,布地奈德降低63%的严重哮喘相关事件(severe asthma-related events,SAREs)的发生风险,并显著延迟首次发生 SAREs 的时间[风险比(hazard ratio,HR)：0.37;95%置信区间(95% CI )：0.20~0.68;χ2=10.11,P =0.0015]。在访视的第1和第3年,两组患者吸入支气管舒张剂后 FEV1%pred 相对于基线均有降低。其中布地奈德组在访视的第1年,该指标的改善显著优于安慰剂组(95% CI ：1.24~3.76;t =3.89,P =0.0001),在访视的第3年,两组间差异无统计学意义(95% CI ：-0.25~2.62;t =1.62,P =0.1057)。两组相比,布地奈德组患者对药物耐受性良好,布地奈德能改善患者的哮喘控制,并减少额外糖皮质激素的使用,吸入支气管舒张剂前 FEV1%pred 在访视第1年(95% CI ：1.64~5.24;t =3.75,P =0.0002)和第3年 (95% CI ：0.05~3.68;t =2.02,P =0.0435)均有明显改善。结论长期使用布地奈德(1次/d)治疗中国新诊断的轻度持续性哮喘患者,该治疗方案能改善患者的哮喘控制,并明显延缓首次发生 SAREs 的时间。     

硒治疗自身免疫性甲状腺疾病的荟萃分析

目的 评价元素硒治疗自身免疫性甲状腺疾病(AITD)的有效性和安全性.方法 通过5个数据库(MEDLINE,Cochrane Central Register of Controlled Trials,中国期刊全文数据库,中国生物医学文献数据库和维普数据库)检索所有研究元素硒治疗AITD的随机对照试验(RCT).由两名研究者独立筛选文献、提取数据和进行结果的统计分析.将结果数据形式一致的同类临床试验的结果进行荟萃分析,对不能荟萃分析的数据进行描述性分析.共纳入30项RCT,涉及2 963例AITD患者.结果 (1)与对照组相比,硒治疗组桥本甲状腺炎患者甲状腺过氧化物酶抗体(TPOAb)和甲状腺球蛋白抗体(TgAb)水平明显下降[标准化均数差(SMD)=-1.35,95％ CI:-1.93～-0.67,P ＜0.000 01和SMD=-0.92,95％ CI:-1.53～-0.31,P＜0.01].(2)硒治疗组与对照组相比,Graves病患者促甲状腺激素受体抗体(TRAb)水平降低(均数差=-2.5,95％ CI:-2.99～-2.01,P＜0.000 01).(3)元素硒可以降低Graves病患者血清游离T3(FT3)和游离T4(FT4)水平(均数差=-1.57,95％ CI:-2.56～-0.58,P＜0.001和均数差=-3.74,95％ CI:-5.65～-1.82,P=0.000 01),但对桥本甲状腺炎患者FT3、FT4和促甲状腺激素的作用不明显(P均＞0.05).结论 对AITD患者使用200 μg∥d的元素硒治疗3～12个月,能够有效降低抗甲状腺自身抗体(TPOAb,TgAb和TRAb)的水平,并具有较好的安全性.     

Recent cigarette smoking and HIV disease progression: no evidence of an association

The association between smoking and HIV disease progression has been examined in several studies; however, findings have been inconsistent. We examined the effect of recent cigarette smoking on CD4(+) T cell count/μl (CD4 count) and HIV RNA concentration (HIV viral load (VL)) among two HIV-infected cohorts with alcohol problems in Massachusetts in the periods 1997-2001 and 2001-2006 using a prospective cohort design and linear mixed models. Smoking groups were defined as: minimal or non-smokers, light smokers, moderate smokers, and heavy smokers. Age, alcohol use, injection drug use, depressive symptoms, gender, annual income, and antiretroviral therapy adherence were considered as potential confounders. Among 462 subjects, no significant differences in CD4 count or VL were found between smoking groups. Using minimal or non-smokers as the reference group, the adjusted mean differences in CD4 count were: 8.2 (95% confidence interval (CI): -17.4, 33.8) for heavy smokers; -0.1 (95% CI: -25.4, 5.1) for moderate smokers; and -2.6 (95% CI: -28.3, 3.0) for light smokers. For log10 VL, the adjusted differences were: 0.03 (95% CI: -0.12, 0.17) for heavy smokers; -0.06 (95% CI: -0.20, 0.08) for moderate smokers; and 0.14 (95% CI -0.01, 0.28) for light smokers. This study did not find an association between smoking cigarettes and HIV disease progression as measured by CD4 cell count and VL.     

Smoking decreases the duration of life lived with and without cardiovascular disease: a life course analysis of the Framingham Heart Study.

AIMS: To compare the burden of cardiovascular disease in terms of lifetime risk and life years lived with disease between smokers and non-smokers. METHODS AND RESULTS: We constructed multi-state life tables describing transitions through various cardiovascular diseases for 4723 smokers and non-smokers observed during 20 biannual observations in the Original Framingham Heart Study. Non-smokers live 8.66 (95% CI 7.61-9.63) (men) and 7.59 (95% CI 6.33-8.92) (women) years longer than smokers and more years free of cardiovascular disease: 6.22 (95% CI 5.09-7.30) years for males and 4.93 (95% CI 3.54-6.29) for females. But non-smokers spend more years with cardiovascular disease over the life course: 2.43 (95% CI 1.72-3.16) years for males and 2.66 (95% CI 1.87-3.38) years for females. The risk of cardiovascular disease before age 70 is higher among smokers, but over the entire lifecourse male non-smokers have higher risks of coronary heart disease, myocardial infarction, stroke and congestive heart failure, and female non-smokers have higher risks of coronary heart disease and congestive heart failure. CONCLUSION: Smoking, by shortening life, decreases both the probability and duration of cardiovascular disease throughout the life course. Non-smokers live many years longer and longer free of cardiovascular disease than smokers, but at the end of their life non-smokers will have lived longer with cardiovascular disease.     

生长抑素联合乌司他丁治疗消化道出血的Meta分析

目的 系统评价生长抑素联合乌司他丁治疗消化道出血的有效性和安全性。方法 计算机检索中国知网、维普、万方、CBM、PubMed、Cochorane library、Embase数据库,搜集有关生长抑素联合乌司他丁治疗消化道出血的随机对照试验。使用Revman 5.3软件进行Mete分析。结果 共纳入16项研究,1466例患者。结果显示,在总有效率[RR=1.24,95%CI(1.19～1.31),P <0.000 01]、白细胞介素-2[SMD=1.10,95%CI(0.38～1.81),P=0.003]、白细胞介素-6[SMD=-3.40,95%CI(-4.69～-2.12),P <0.000 01]、白细胞介素-10[SMD=2.77,95%CI(1.66～3.87),P <0.000 01]、肿瘤坏死因子-α[SMD=-2.56,95%CI(-3.26～-1.87),P<0.000 01]、住院时间[SMD=-1.75,95%CI(-2.24～-1.26),P<0.000 01]、消化道出血时间[SMD=-3.55,95%CI(-4.11～-2.99)...     

P—选择素在速激肽类致气道高反应性中的作用

目的 探讨黏附分子Ｐ－选择素和速激肽类Ｐ－物质、血管活性肠肽（ＶＩＰ）与气道高反应性的关系。方法 测定５７例支气管哮喘病人（激素治疗组２７例,非激素治疗组３０例）和２２例正常人的气道反应性,观察血浆Ｐ－选择素、Ｐ－物质和ＶＩＰ的变化。结果５３例哮喘病人气道激发试验阳性（９２．９８％）,４例阴性（７．０２％）,２２例正常人全部阴性。非激素治疗组患者血浆Ｐ－选择素和Ｐ－物质较正常人及激素治疗组显著升     

Airway reactivity to inhaled mannitol in cigarette smokers: a longitudinal study

Smoking induces airway hyperresponsiveness (AHR). Bronchial provocation with mannitol is used to identify AHR in subjects with asthma. This study aimed to determine the prevalence of airway hyperresponsiveness to mannitol in asymptomatic smokers compared to non-smokers and to assess if airway responsiveness to mannitol changes after smoking cessation. Airway responsiveness to inhaled mannitol was measured in smokers (n=42), and non-smokers (n=45). In smokers, the mannitol test was repeated 3 months after smoking cessation. Demographics including age, lung function and atopy status were similar for smokers and non-smokers (p=ns). Compared with non-smokers (2.2%), AHR to mannitol expressed by 15%> or = fall in FEV(1) was significantly more common in smokers (26.2%) (p=0.001). The provoking dose to induce a 15%> or = fall in FEV(1) (PD(15)), a measure of sensitivity, was median [IQR] 291 mg [207-377] in the 11 positive smokers. The response-dose ratio (RDR) (% fall in FEV(1)/cumulative dose), a measure of reactivity, was significantly higher in smokers (0.013 [0.006-0.029]) compared with non-smokers (0.004 [0.002-0.007]), (p<0.0001). After successful smoking cessation, the RDR decreased in most cases (p=0.01) and only one patient still recorded a 15% fall in FEV(1). None of the patients with a negative mannitol test turned positive, irrespective of the outcome of smoking cessation. AHR to mannitol is quite common in smokers compared to non-smokers and decreases significantly after smoking cessation. Thus, the mannitol test may be sensitive to non-asthmatic inflammation of the airways.     

Respiratory consequences of light and moderate smoking in young adults in Chile.

OBJECTIVE: To assess the association between smoking and respiratory symptoms, lung function and bronchial hyperresponsiveness (BHR) in young adults in Chile. SETTING: Selected sample of 1232 subjects aged 22-28 years. DESIGN: In this cross-sectional study, the outcome measures were: respiratory symptoms, forced expiratory volume in one second (FEV1), forced vital capacity (FVC), forced expiratory flow between 25% and 75% (FEF25-75), FEV1/FVC and BHR. RESULTS: Among the 1232 subjects, 67.7% of the men and 49.4% of the women were smokers; the median cigarettes smoked per day was four for men and three for women. Smoking was associated with wheezing, waking up with a cough, breathlessness following exercise and persistent cough, with odds ratios (OR) between 1.94 (95% CI 1.41-2.66) and 3.12 (95% CI 2.21-4.40) among those smoking > or = 5 cigarettes per day, compared to non-smokers. Smoking < 5 cigarettes was significantly associated with wheezing and waking up with a cough. Smokers had a lower FEV1/FVC than non-smokers by approximately 0.8%. Smoking was not associated with FEV1, FEF25-75 or BHR status. CONCLUSIONS: This study highlights the early effects of smoking on respiratory symptoms. It could help governments in Latin America take vigorous action to deter young people from starting smoking.     

Total nitrite/nitrate in expired breath condensate of patients with asthma.

Production of nitric oxide (NO) is generally increased during inflammatory diseases including asthma. The eventual fate of NO is oxidation to nitrite (NO2) and nitrate (NO3), both of which are end-products of NO metabolism. Hydrogen Peroxide (H2O2) is increased in exhaled breath condensate of asthmatic subjects and may be used as a non-invasive marker of oxidative stress. NO has in some cases been shown to attenuate oxidant-induced lung injury. Total NO2/NO3 concentration and H2O2 levels were measured in expired breath condensate in 50 clinically stable asthmatics [all males, all atopics, mean age 22 (3) SD yrs, forced expiratory volume in 1 sec (FEV1) 91 (10)% predicted, PD20 to histamine 0.262 (0.16) mg 20 on inhaled steroids, 20 smokers, all steroid-naive] and in 10 normal, non-atopic subjects [all males, age 23 (4) yrs, FEV1 101 (14)% predicted, PD20 to histamine 1.3 (0.55) mg]. NO2/NO3 levels were significantly higher in patients with asthma than in normal subjects (1.08, 95% CI 0.86-1.3 microM vs. 0.6; 95% CI 0.46-0.8, P < 0.001). Patients who were on inhaled steroids had significantly ower values compared to steroid-naive (0.71, 95% CI 0.55-0.87 microM vs. 133, 95% CI 1-1.65 microM, P < 0.001). Similar results were observed between smokers and non-smokers (1.11, 95% CI 0.74-1.47 microM vs. 1.77, 95% CI 1.1-24 microM, P < 0.0001).There was a significant positive correlation between NO2/NO3 levels and H2O2 concentration in expired breath condensate (r = 0.48, P < 0.0001). No correlation was observed between NO2/NO3 levels, airway obstruction and bronchial hyper-reactivity as assessed by PD20 to histamine. Total NO2/NO3 levels in expired breath condensate are raised in patients with stable asthma and are significantly related to oxidative stress as assessed by H2O2 concentration. Measurement of expired breath NO2/NO3 and H2O2 levels may be clinically useful in the management of oxidation and inflammation mediated lung injury.     

Acute and chronic effects of cigarette smoking on arterial stiffness

OBJECTIVES: Pulse wave velocity (PWV) is an indicator of arterial stiffness, especially in the aorta, and a marker for vascular damage. Smoking is reported to increase arterial stiffness. We examined the acute and chronic effects of smoking on arterial stiffness by measuring brachial--ankle PWV (baPWV) using an oscillometric method (VP 1000, Colin Co., Komaki, Japan). METHODS: All healthy male subjects (chronic smokers, n=40, 30.3 years old vs non-smokers, n=40, 28.3 years old) smoked two cigarettes (nicotine 1.5 mg) within 10 min and measured blood pressure (BP), heart rate and baPWV at baseline, 5, 15, 30, 45 and 60 min and compared with controls (n=20, 29.3 years old). RESULTS: Systolic BP was higher in chronic smokers than non-smokers or controls. Smoking increased the systolic and diastolic BP and heart rate significantly at 5 min in both chronic smokers and non-smokers as compared with baseline levels or controls (respectively, p<0.001) and returned to baseline level at 15 min. Pulse pressure did not increase significantly. baPWV increased significantly in both chronic smokers and non-smokers at 5 min (12.1--17.3 m/s vs 11.1--12.7 m/sec, respectively) and remained higher for 30 min compared with controls (p<0.001). Smoking increased baPWV to a greater extent in chronic smokers than in non-smokers (p<0.01). CONCLUSION: Acutely, cigarette smoking increased BP, heart rate and baPWV in chronic smokers and non-smokers. These effects were more prominent in chronic smokers than in non-smokers. These findings suggest that cigarette smoking have deleterious effects on cardiovascular system by stiffening arteries.     

Association of smoking status with obesity and diabetes among elderly people

The present study was aimed to examine associations of current and ex-smoking status with obesity and diabetes among elderly people. Nationwide study of Finnish elderly people based on biennial surveys from 1985 to 1995, were used to study 7482 people aged 65-79 years. Smoking status included non-, ex-light, ex-heavy, current light, and current heavy smokers. Obesity was set as body mass index (BMI) > or = 30. Information of smoking, BMI, and diabetes was based on self-reports. Logistic regression was used as the main method of analyses. Compared to non-smokers (reference category), ex-heavy smokers had higher (odds ratio, 1.42; 95% confidence interval: 1.09, 1.85) and current light smokers (OR, 0.46; 95% CI: 0.31, 0.69) lower relative risk of obesity. Current light smokers had also lower and ex-heavy smokers higher rate of diabetes than non-smokers. Ex-heavy smokers had a higher risk of obesity (OR, 1.75; 95% CI: 1.30, 2.36) and diabetes (OR, 1.48; 95% CI: 1.10, 2.01) than ex-light smokers. Same pattern for current smokers was found. Heavy ex- and current elderly smokers are at risk of obesity and diabetes. Thus, heavy smokers should be emphasized in programs promoting smoking cessation.     

Mortality from all causes and from coronary heart disease related to smoking and changes in smoking during a 35-year follow-up of middle-aged Finnish men.

AIMS: The risk of early and late death in relation to smoking and ex-smoking were studied. METHODS AND RESULTS: A cohort of 1711 Finnish men born between 1900 and 1919 were recruited in 1959 and followed up for 35 years. Information on smoking status was collected at each of six examinations made from 1959 to 1989 using a standardized questionnaire. Vital status at the end of 1994 was collected for every man. The effect of smoking on mortality was assessed using Cox proportional hazards model. Adjusted ratios for 35-year all-cause mortality were 1.62 (95% CI 1.40-1.88) in current smokers and 1.13 (CI 0.93-1.36) in former smokers compared with non-smokers. The hazards ratios for 35-year coronary heart disease mortality were 1. 63 (CI 1.24-2.13) and 1.39 (CI 1.00-1.94), respectively. The risk for 10 year mortality was stronger than for 35 year mortality among both former and current smokers, given the same amount of cigarettes consumed. Men smoking persistently were most at risk, while those who persisted in quitting had no increased risk of death compared with non-smokers. CONCLUSION: Smoking increases the risk of premature death in middle-aged men and giving up smoking earlier in life can prevent smoking attributable premature death.