吸烟对支气管哮喘患者糖皮质激素治疗的影响

目的通过本实验进一步探讨吸烟对支气管哮喘(简称哮喘)患者气道炎症的影响,了解吸烟哮喘患者对激素治疗的敏感性。方法选取35例慢性持续期哮喘患者,根据是否吸烟,分为吸烟组14例和非吸烟组21例。所有患者给予吸入糖皮质激素(ICS)治疗,必要时可吸入β2受体激动剂,发放哮喘日记卡及峰流速仪。分别记录治疗前及治疗28d后哮喘症状评分、哮喘控制测试(ACTTM)评分;第一秒用力呼气容积占预计值百分比(FEV1占预计值%)、第一秒用力呼气容积占用力肺活量百分比(FEV1/FVC%)、最大呼气流速占预计值百分比(PEF占预计值%)、每日晨间及夜间PEF;诱导痰中嗜酸粒细胞及中性粒细胞百分比并测定痰液中白介素8(IL-8)及嗜酸粒细胞趋化因子(eotaxin)水平。结果两组患者ICS治疗后ACTTM评分有明显改善,组间ACTTM评分比较差异具有统计学意义(t=5.542,P<0.05)。治疗后两组哮喘患者肺功能均有改善,组间比较FEV1占预计值%(t=4.740,P<0.05)、PEF占预计值%(t=5.190,P<0.05)差异有统计学意义。两组患者ICS治疗后组内比较嗜酸粒细胞百分比、eotaxin水平差异均有统计学意义。中性粒细胞百分比治疗前、后差异无统计学意义。治疗后组间比较中性粒细胞(t=7.707,P<0.05)、IL-8水平(t=4.557,P<0.05)、嗜酸粒细胞百分比(t=4.740,P<0.05)及eotaxin水平(t=2.064,P<0.05)差异均有统计学意义。结论两组患者ICS治疗28d后,其临床症状、肺功能及痰中炎性介质均有改善,但吸烟组改善程度较非吸烟组差。吸烟组哮喘患者诱导痰中中性粒细胞及IL-8水平高于非吸烟组哮喘患者,而嗜酸粒细胞及eotaxin水平低于后者。     

吸烟对北京,广州地区人群肺通气功能的影响

目的探讨吸烟对肺功能的影响。方法通过整群抽样和队列研究方法，对北京，广州城乡３５～５９岁男女资料完整者７９８３人，分吸烟组与不吸烟组进行肺功能调查。结果吸烟组人群的一秒种用力呼气容积（ＦＥＶ１）／身高平方（Ｈ＾２），用力呼气流量（ＦＥＦ）／Ｈ＾２及ＦＥＶ１／用力肺活量（ＦＶＣ）均值均低于不吸烟组；男性吸烟各年龄组的ＦＥＶ１／Ｈ＾２实测值低于相应的预测值，且２～４年后随访复查时，ＦＥＶ１／Ｈ＾２随年     

吸烟与慢性阻塞性肺疾病的关系及对老年患者肺功能的影响

目的分析吸烟与慢性阻塞性肺疾病发病(COPD)的关系及对老年患者肺功能的影响。方法选取180例老年男性实验志愿者,其中处于病情缓解期的COPD组患者60例,健康者120例。健康者包括健康吸烟组60例与健康非吸烟组60例。COPD组又分为已戒烟(1年以上)组30例,未戒烟组30例。检查患者肺功能指标,COPD戒烟、COPD未戒烟组行支气管舒张试验。分析吸烟与COPD发病的关系及对老年患者肺功能的影响。结果 COPD组与吸烟、非吸烟组相比,第1秒用力呼气容积占用力肺活量百分比(FEV1/FVC)及FEV1%预计值明显低于吸烟、非吸烟组(P<0.05);COPD患者中戒烟组FEV1/FEC及FEV1%预计值高于未戒烟组(P<0.05);COPD戒烟、COPD未戒烟组支气管舒张试验结果显示COPD组FEV1改变率高于COPD未戒烟组,COPD戒烟组FEV1阳性率(31.2%)较COPD未戒烟组(21.8%)高,差异均有统计学意义(P<0.05)。结论吸烟是COPD的重要发病因素,对老年患者的肺功能有明显影响,及早戒烟对延缓疾病发展、改善患者生活质量有重要意义。     

吸烟对轻度支气管哮喘患者吸入激素疗效的影响

目的　观察吸烟对轻度支气管哮喘患者吸入激素疗效的影响。方法　对不吸烟 (1 8例 )及吸烟 (1 7例 )的支气管哮喘患者每日吸入二丙酸倍氯米松 5 0 0μg治疗 4周 ,治疗前后进行肺功能测定及气道反应性试验 ,用药过程中监测呼气峰流速 (peak expiratory flow,PEF)。结果　不吸烟组患者治疗后的清晨 PEF、睡前 PEF、FEV1 %及气道反应性均较治疗前改善 (P<0 .0 5 )。而吸烟组患者在治疗前后上述指标却变化不大 (P>0 .0 5 )。结论　吸烟能明显减弱支气管哮喘患者吸入激素的疗效 ,支气管哮喘患者应积极戒烟以取得较好的疗效     

吸烟与支气管哮喘研究进展

吸烟是支气管哮喘(简称哮喘)发病的危险因素之一.吸烟的哮喘患者在临床表型、影像学表现和气道炎症方面与普通哮喘患者不同.吸烟可加速肺功能下降,加重哮喘病情.吸烟哮喘患者气道重塑更严重.吸烟降低哮喘患者激素治疗敏感性.     

吸烟与支气管哮喘研究进展

吸烟是支气管哮喘(简称哮喘)发病的危险因素之一。吸烟的哮喘患者在临床表型、影像学表现和气道炎症方面与普通哮喘患者不同。吸烟可加速肺功能下降,加重哮喘病情。吸烟哮喘患者气道重塑更严重。吸烟降低哮喘患者激素治疗敏感性。     

吸烟对40岁以上人群的肺功能的影响

目的 观察吸烟对40岁以上人群的肺功能的影响.方法 本研究前瞻性调查了2 682例居民的吸烟状况、规律合并用药情况、性别、年龄、身高、体质量等资料,并进行了肺通气功能检测.结果 随访时间2年.2 290例(85.4%)得到了有效随访,其中1 197例(52.3%)从不吸烟,467例(20.4%)曾经吸烟,626例(27.3%)现吸烟.三组人群的年龄、性别、BMI、肺功能、COPD患者例数及合并用药差异均有统计学意义.随访结果显示,肺功能FEV1、FEV1%pred、FVC、FEV1/FVC均逐年下降.经调整上述差异性变量(年龄、性别、BMI、COPD患者例数、合并用药及基线肺功能),曾吸烟组肺功能FEV1(P=0.030)、FEV1%pred(P=0.011)和FEV1/FVC(P<0.001)较从不吸烟组显著下降.现吸烟组FEV1/FVC较从不吸烟组下降快.结论 从不吸烟居民肺功能下降最慢,提倡不吸烟或尽可能早期戒烟.     

吸烟对支气管哮喘患者吸入糖皮质激素治疗的影响

目的 探讨吸烟对支气管哮喘(简称哮喘)患者临床症状、肺功能及气道炎症的影响,以及对激素治疗的敏感性.方法 选取2009年12月至2011年1月门诊就诊的40例慢性持续期哮喘患者,根据是否吸烟分为吸烟组(15例)和非吸烟组(23例).所有患者给予糖皮质激素(布地奈德)吸入治疗,必要时可吸入β2受体激动剂.发放哮喘日记卡及峰流速仪.记录治疗前及治疗28 d后哮喘症状评分、哮喘控制测试(ACT)评分、肺功能、晨间及夜间最高呼气流速(PEF),诱导痰中嗜酸粒细胞及中性粒细胞百分比,并测定痰液中白介素8(IL 8)及嗜酸粒细胞趋化因子(eotaxin)水平.结果 两组患者治疗前除性别构成外,年龄、病程、ACT评分、肺功能指标差异均无统计学意义.两组患者治疗后ACT评分(F=39.991,P＜0.05)、FEV1％ pred(F=56.075,P＜0.05)、PEF％ pred(F=53.535,P＜0.05),嗜酸粒细胞百分比(F=15.271,P＜0.05)及eotaxm(F=24.172,P＜0.05)水平均较治疗前有明显改善,哮喘症状评分显著降低(P ＜0.05).其中非吸烟组以上指标的改善程度均优于吸烟组(P＜0.05).结论 吸烟降低了哮喘患者对ICS治疗的反应性.对吸烟的哮喘患者,治疗可能需要特殊调整.     

吸烟对支气管哮喘的影响

吸烟与支气管哮喘（简称哮喘）关系密切,吸烟可导致哮喘的发生、发展。吸烟哮喘患者在气道炎症,临床症状和治疗等方面均与非吸烟哮喘患者有差异。本文旨在讨论吸烟对哮喘的影响。     

Effects of early onset asthma and in utero exposure to maternal smoking on childhood lung function

Both in utero exposures to maternal smoking and asthma are associated with chronic deficits in lung function. We hypothesized that in utero exposure affects lung function in children without asthma and synergistically affects children with early onset asthma. To investigate effects of in utero exposure and age at asthma diagnosis on lung function, we examined longitudinal medical history, tobacco smoke exposure, and lung function data from 5,933 participants in the Children's Health Study. We found that children exposed in utero, but without asthma, showed decreased FEV1/FVC, FEF25-75, and FEF25-75/FVC ratio. Among children without in utero exposure, early asthma diagnosis was associated with larger decreases in FEV1, FEF25-75, and FEV1/FVC ratio compared with later diagnosed asthma. Children with in utero exposure alone and early onset asthma showed deficits in FEV1 (-13.6%; 95% confidence interval [CI], -18.9 to -8.2) and FEF25-75 (-29.7%; 95% CI, -37.8 to -20.5) among boys; and FEF25-75 (-26.6%; 95% CI, -36.4 to -15.1) and FEV1/FVC (-9.3%; 95% CI, -12.9 to -5.4) among girls. The absolute differences in FEF25-75 associated with in utero exposure increased with age in children with early onset asthma. We found little evidence for effects from environmental tobacco smoke exposure alone. In summary, deficits in lung function were largest among children with in utero exposure and early onset asthma.     

The effect of maternal smoking during pregnancy on early infant lung function.

We studied the effect of prenatal maternal cigarette smoking on the pulmonary function (PF) of 80 healthy infants tested shortly after birth (mean, 4.2 +/- 1.9 wk). Mothers' prenatal smoking was measured by: (1) questionnaire reports at each prenatal visit of the number of cigarettes smoked per day, and (2) urine cotinine concentrations (corrected for creatinine) obtained at each visit. Infant PF was assessed by partial expiratory flow-volume curves and helium-dilution measurement of FRC. Forced expiratory flow rates were significantly lower in infants born to smoking mothers, both when unadjusted and after controlling for infant size, age, sex, and passive exposure to environmental tobacco smoke (ETS) between birth and the time of PF testing. Flow at functional residual capacity (VFRC) in infants born to smoking mothers was lower than that found in infants whose mothers did not smoke during pregnancy (74.3 +/- 15.9 versus 150.4 +/- 8.9 ml/s; p = 0.0007). Differences remained significant when flow was corrected for lung size (VFRC/FRC: 0.87 +/- 0.26 versus 1.77 +/- 0.12 s-1; p = 0.013). No differences in pulmonary function were evident among infants exposed and unexposed to ETS in the home after stratifying by prenatal exposure status. We conclude that maternal smoking during pregnancy is associated with significant reductions in forced expiratory flow rates in young infants. The results suggest that maternal smoking during pregnancy may impair in utero airway development and/or alter lung elastic properties. We speculate that these effects of maternal prenatal smoking on early levels of forced expiratory flow may be an important factor predisposing infants to the occurrence of wheezing illness later in childhood.     

The effect of parental smoking on lung function and development during infancy

While the adverse effects of parental smoking on respiratory health during childhood are well recognized, its potential impact on early lung development is less clear. This review summarizes current evidence on the effect of parental smoking on lung function during infancy. It is difficult to separate the effects of pre- and postnatal exposure, since the majority of mothers who smoke in pregnancy (currently around 30% worldwide) continue to do so thereafter. Nevertheless, measurements undertaken prior to any postnatal exposure have consistently demonstrated significant changes in tidal flow patterns in infants whose mothers smoked in pregnancy. While there is, as yet, no convincing evidence from studies in human infants that smoking during pregnancy is associated with increased airway responsiveness at birth, many studies have demonstrated a reduction in forced expiratory flows (on average by 20%) in infants exposed to parental smoking. While maternal smoking during pregnancy remains the most significant source of such exposure and is likely to be responsible for diminished airway function in early life, continuing postnatal tobacco smoke exposure will increase the risk of respiratory infections, the combination of both being responsible for the two- to fourfold increased risk of wheezing illnesses observed during the first year of life in infants whose parents smoke. These findings emphasize the need to keep infants in a smoke-free environment both before and after birth, not least because of growing awareness that airway function in later life is largely determined by that during foetal development and early infancy.     

Effects of maternal food restriction on offspring lung extracellular matrix deposition and long term pulmonary function in an experimental rat model

Intrauterine growth restriction (IUGR) increases the risk of respiratory compromise throughout postnatal life. However, the molecular mechanism(s) underlying the respiratory compromise in offspring following IUGR is not known. We hypothesized that IUGR following maternal food restriction (MFR) would affect extracellular matrix deposition in the lung, explaining the long‐term impairment in pulmonary function in the IUGR offspring. Using a well‐established rat model of MFR during gestation to produce IUGR pups, we found that at postnatal day 21, and at 9 months (9M) of age the expression and abundance of elastin and alpha smooth muscle actin (αSMA), two key extracellular matrix proteins, were increased in IUGR lungs when compared to controls (P < 0.05, n = 6), as determined by both Western and immunohistochemistry analyses. Compared to controls, the MFR group showed no significant change in pulmonary resistance at baseline, but did have significantly decreased pulmonary compliance at 9M (P < 0.05 vs. control, n = 5). In addition, MFR lungs exhibited increased responsiveness to methacholine challenge. Furthermore, exposing cultured fetal rat lung fibroblasts to serum deprivation increased the expression of elastin and elastin‐related genes, which was blocked by serum albumin supplementation, suggesting protein deficiency as the predominant mechanism for increased pulmonary elastin deposition in IUGR lungs. We conclude that accompanying the changes in lung function, consistent with bronchial hyperresponsiveness, expression of the key alveolar extracellular matrix proteins elastin and αSMA increased in the IUGR lung, thus providing a potential explanation for the compromised lung function in IUGR offspring. Pediatr Pulmonol. 2012; 47:162–171. © 2011 Wiley Periodicals, Inc.     

母体维生素D缺乏对妊娠及后代的影响

维生素D不仅与钙、磷代谢以及骨骼运动系统有关,还与免疫调节、细胞分化和凋亡以及神经系统发育有关.妊娠期母体的维生素D水平对孕妇及后代都有重要的影响.目前有研究表明:先兆子痫、妊娠期糖尿病、细菌性阴道炎和早产等与母体维生素D缺乏关系密切,后代的骨营养不良、呼吸道感染、哮喘和其他自身免疫疾病也与母体妊娠期维生素D缺乏相关.妊娠女性维生素D缺乏很常见,因而适当补充维生素D十分必要.     

Influence of maternal nutritional status on vascular function in the offspring

Suboptimal maternal nutritional status has been implicated in the development of cardiovascular risk in the child. Initially inferred from studies of low-birthweight children, investigations in cohorts of women subjected to famine provide direct evidence for an independent influence of the mother's diet on the cardiovascular health of her child. Animal studies from rodents and sheep have shown associations between maternal undernutrition and raised blood pressure, as well as abnormalities in resistance artery function, particularly in endothelium-dependent responses. Early life exposure to the influences of maternal over nutritional states, e.g. obesity and excessive gestational weight gain, has also been associated with markers of cardiovascular risk in man, and animal models have shown raised blood pressure and endothelial dysfunction in offspring of diet-induced obese dams. Increased sympathetic tone is commonly associated with hypertension in animal models of both under nutritional and over nutritional states. This and several other similarities may indicate commonality of mechanism and could reflect supranormal nutritional status in postnatal life in both conditions.