UMLS:C0432222 - FACTA Search

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Ethane is a product of lipid peroxidation and can be measured in the exhaled air as an index of oxidative stress. Oxidant/antioxidant imbalance is important in the pathogenesis of chronic obstructive pulmonary disease (COPD). Therefore, we measured exhaled ethane in 22 patients with COPD (mean age +/- SEM, 59 +/- 8 yr; 19 male) and compared it with other noninvasive markers of oxidative stress and inflammation such as carbon monoxide (CO), measured electrochemically, and nitric oxide (NO), measured by chemiluminescence. Exhaled ethane was collected during a flow and pressure-controlled exhalation into a reservoir, discarding dead space air contaminated with ambient air. A sample of the collected expired air was analyzed by chromatography. Compared with normal subjects (n = 14; eight men; age, 33 +/- 2.8 yr), patients with COPD not on steroid treatment (n = 12; FEV(1), 58 +/- 6%) had elevated levels of exhaled ethane (2.77 +/- 0.25 and 0.88 +/- 0.09 ppb, respectively, p < 0.05), CO (5.96 +/- 0.50 and 2.8 +/- 0.25 ppm, p < 0.05) and NO (11.86 +/- 0.53 and 6.77 +/- 0.50 ppb, p < 0.05) levels. Ethane was correlated to FEV(1) (r = -0.67, p < 0.05). Patients receiving steroid treatment (n = 10; FEV(1), 56 +/- 2%) had lower levels of ethane (0.48 +/- 0.05 ppb) than did steroid-treated patients, whereas CO (5.99 +/- 0.63 ppm) and NO (9.11 +/- 0.53 ppb) levels were similar in the two treatment groups. Exhaled ethane is elevated, correlates with FEV(1), and is significantly lower in patients treated with steroids, so it may be complementary to the use of NO and CO in assessing and monitoring oxidative stress in COPD.
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PMID:Exhaled ethane, a marker of lipid peroxidation, is elevated in chronic obstructive pulmonary disease. 1093 55

We have previously shown that in healthy subjects, deep inspiration (DI) has not only a bronchodilatory but also a bronchoprotective effect that is absent in asthmatic subjects. We conducted the study reported here to test the hypothesis that the bronchoprotective effect is stronger than the bronchodilatory effect, and to determine the extent to which these two effects are related. Ten healthy subjects underwent provocations in which single doses of methacholine, previously shown to reduce FEV(1) by 10% to 20% (Dose 1) and by 20% to 40% (Dose 2) were administered after a 20-min period devoid of DI. To measure the bronchodilator effect, DIs were performed immediately after the first spirometry after methacholine, and were followed by another lung function test. To measure their bronchoprotective effect, DIs were performed before administration of a single dose of methacholine, and the FEV(1) after methacholine was compared with that of another single-dose challenge in which DIs were not included. From these outcomes, bronchodilation and bronchoprotection indices were constructed and compared with each other. At Dose 1 (mild obstruction), the ability of DIs to reverse methacholine-induced obstruction was equal to their ability to prevent it (bronchodilation index [BDI] versus bronchoprotection index [BPI]: 1.62 +/- 0.21 versus 2.02 +/- 0.40 [mean +/- SEM], p = 0.26). At Dose 2, the relative potency of both the bronchodilating and bronchoprotective effects of DIs increased, but bronchoprotection was significantly stronger (BDI versus BPI: 3.40 +/- 0.43 versus 6.98 +/- 1.42, p = 0.02). Correlation analysis of the two indices indicated that as the BPI increased, the BDI reached a plateau. We conclude that in healthy humans, the bronchoprotective effect of lung inflation is stronger than the bronchodilatory effect.
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PMID:Deep inspiration-induced bronchoprotection is stronger than bronchodilation. 1098 4

This study aimed at documenting airway inflammation and subepithelial collagen deposition in patients using only inhaled beta(2)-agonists with either recently diagnosed asthma (RDA: </= 2 yr, n = 16) or long-standing asthma (LSA: >/= 13 yr, n = 16) and at the influence of an intense inhaled corticosteroid (ICS) treatment on these parameters, in relation to changes in airway responsiveness. Patients had a methacholine inhalation test and a bronchoscopy with bronchial biopsies before and after an 8-wk treatment with inhaled fluticasone propionate (FP), 1,000 microgram/day. Baseline FEV(1) (mean +/- SEM) was normal and similar in both groups (RDA: 98.1 +/- 2.7, LSA: 94.5 +/- 4.6%). Geometric mean methacholine PC(20) was lower in LSA than in RDA (0.44 versus 3.37 mg/ml) at baseline and improved similarly by 1.85 and 1.86 double concentrations with FP treatment. PC(20) normalized (>/= 16 mg/ml) in five patients with RDA and two patients with LSA. Baseline mean bronchial cell counts (per mm(2) connective tissue surface) for CD3(+), CD4(+), CD8(+), CD25(+), EG1(+), CD45ro(+), and AA1(+) cells were similar in both groups. With FP, EG1(+) (p < 0.001), EG2(+) (p = 0.018), and AA1(+) counts (p = 0.009) decreased significantly in both groups while CD45ro(+) (p = 0.02) counts decreased only in LSA. Baseline type 1 and type 3 collagen deposition underneath the basement membrane was similar in RDA and LSA and did not change significantly after FP. This study shows that recent compared to long-standing mild asthma is associated with a similar degree of airway inflammation and subepithelial fibrosis, and a similar improvement in airway hyperresponsiveness after 8 wk on high-dose ICS. It also indicates that once asthma becomes symptomatic, airway responsiveness cannot normalize in most subjects over such a time period, even with a high dose of ICS.
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PMID:Airway hyperresponsiveness, inflammation, and subepithelial collagen deposition in recently diagnosed versus long-standing mild asthma. Influence of inhaled corticosteroids. 1102 36

Airway and alveolar inflammation have been described in asthma. Prolonged inflammation may lead to airway remodeling, which can result in physiologic abnormalities. Elderly lifetime nonsmokers are an ideal population in which to examine the consequences of longstanding asthma. To test the hypothesis that airflow limitation and hyperinflation are associated with the duration of asthma, we evaluated airflow and lung volumes in a cohort of elderly asthmatic individuals. All subjects were > 60 yr of age and were lifetime nonsmokers (n = 75). Patients with asthma of long duration (LDA; n = 38) had asthma for >/= 26 yr (median = 40.0 yr); patients with asthma of short duration (SDA; n = 37) had asthma for < 26 yr (median = 9 yr). Patients with LDA had a significantly lower FEV(1)% predicted than did those with SDA (59.5 +/- 2.6% versus 73.8 +/- 3.1% [mean +/- SEM], respectively; p < 0.007). Regression analysis demonstrated that duration of asthma was inversely associated with FEV(1)% predicted (r = 0.264, p < 0.03). After bronchodilator administration, the patients with LDA continued to show airflow obstruction (FEV(1)% predicted = 65.4 +/- 2.9). Only 18% of patients with LDA attained a normal postbronchodilator FEV(1), whereas 50% of those with SDA were able to do so (p < 0.003). The FRC% predicted was significantly higher in subjects with LDA than in those with SDA (142.9 +/- 5.6 versus 124.1 +/- 4.4, respectively, p < 0.01). Multiple regression analysis revealed an association between FRC and duration of asthma that was independent of the degree of airflow limitation. These data suggest that the duration of asthma is associated with the degree of airflow limitation and hyperinflation. Moreover, these abnormalities can become irreversible over time, and may reflect distal airway and/or parenchymal changes as well as proximal airway remodeling.
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PMID:Duration of asthma and physiologic outcomes in elderly nonsmokers. 1102 56

Ethane is a product of lipid peroxidation as a result of oxidative stress and can be detected in the exhaled air. Oxidative stress plays a role in the pathogenesis of asthma. We measured exhaled ethane in 26 asthmatic subjects (mean age +/- SEM, 38 +/- 8 yr; 15 male, FEV(1) 60 +/- 4%) and compared it with exhaled nitric oxide (NO) measured by chemiluminescence, a noninvasive marker of oxidative stress and inflammation. Exhaled ethane was collected during a flow- and pressure-controlled exhalation into a reservoir discarding dead space air contaminated with ambient air. A sample of the expired air was analyzed by chromatography. Exhaled ethane levels were elevated in asthma patients not receiving steroid (n = 12, 2.06 +/- 0.30 ppb) compared with steroid-treated patients (n = 14, 0.79 +/- 0.10 ppb, p < 0.01) and to 14 nonsmoking control subjects (0.88 +/- 0.09 ppb, p < 0.05). In patients not receiving steroid treatment there was a positive correlation between exhaled ethane and NO (r = 0.55, p < 0.05) and air trapping assessed by the ratio of residual volume to total lung capacity (RV/ TLC) (r = 0.60, p < 0.05). In addition, untreated patients with FEV(1) < 60% predicted value had higher concentrations of ethane (2.86 +/- 0.37 ppb) compared with less obstructed patients (FEV(1) > 60%, 1.26 +/- 0.12 ppb, p < 0.05). NO concentrations were higher in patients not on steroid treatment (14.7 +/- 1.7 ppb) than in steroid-treated patients (8.6 +/- 0.5 ppb, p < 0.05). Exhaled ethane is elevated in asthma, reduced in steroid-treated patients, and correlates with NO and airway obstruction. It may be a useful noninvasive marker of oxidative stress.
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PMID:Elevation of exhaled ethane concentration in asthma. 1102 60

The mechanism responsible for diminished exercise performance in cystic fibrosis (CF) is not clear. We hypothesized that reduced muscle size, rather than an intrinsic muscle defect, was the primary factor in such diminished exercise performance. Twenty-two subjects with CF (14 females and eight males, aged 6.5 to 17.7 yr, with FEV(1) of 46% to 111% predicted) participated in a study of this hypothesis, and were compared with healthy children tested in the same laboratory. Muscle size was estimated from midthigh muscle cross-sectional area (CSA) obtained by magnetic resonance imaging, and fitness was determined by progressive cycle ergometer exercise testing with breath-by-breath measurements of gas exchange. Peak oxygen consumption (V O(2)) was reduced in CF subjects (956 +/- 81 [mean +/- SEM] ml/min, as compared with 1,473 +/- 54 ml/min in controls; p < 0.00001). Surprisingly, CF subjects had a lower peak V O(2) per CSA (mean for CF subjects 70 +/- 3% predicted, p < 0.0001) than did controls, whereas muscle CSA in CF subjects was not significantly smaller than in controls. The scaling parameters of peak V O(2) and muscle CSA did not differ significantly between healthy controls (0.80 +/- 0.16) and CF subjects (1.03 +/- 0.12). Indexes of aerobic function that are less effort-dependent than peak V O(2) were also lower in the CF subjects (e.g., the slope of V O(2) versus work rate [WR] (DeltaV O(2)/DeltaWR) was 68 +/- 2% predicted; p < 0.005). The study data did not support the initial hypothesis, and suggest a muscle-related abnormality in oxygen metabolism in patients with CF.
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PMID:Muscle size and cardiorespiratory response to exercise in cystic fibrosis. 1106 20

We studied interrelationships between exercise endurance, ventilatory demand, operational lung volumes, and dyspnea during acute hyperoxia in ventilatory-limited patients with advanced chronic obstructive pulmonary disease (COPD). Eleven patients with COPD (FEV(1.0) = 31 +/- 3% predicted, mean +/- SEM) and chronic respiratory failure (Pa(O(2)) 52 +/- 2 mm Hg, Pa(CO(2 ))48 +/- 2 mm Hg) breathed room air (RA) or 60% O(2) during two cycle exercise tests at 50% of their maximal exercise capacity, in randomized order. Endurance time (T(lim)), dyspnea intensity (Borg Scale), ventilation (V E), breathing pattern, dynamic inspiratory capacity (IC(dyn)), and gas exchange were compared. Pa(O(2)) at end-exercise was 46 +/- 3 and 245 +/- 10 mm Hg during RA and O(2), respectively. During O(2), T(lim) increased 4.7 +/- 1.4 min (p < 0.001); slopes of Borg, V E, V CO(2), and lactate over time fell (p < 0.05); slopes of Borg-V E, V E-V CO(2), V E-lactate were unchanged. At a standardized time near end-exercise, O(2) reduced dyspnea 2.0 +/- 0.5 Borg units, V CO(2) 0.06 +/- 0.03 L/min, V E 2.8 +/- 1.0 L/min, and breathing frequency 4.4 +/- 1.1 breaths/min (p < 0.05 each). IC(dyn) and inspiratory reserve volume (IRV) increased throughout exercise with O(2) (p < 0.05). Increased IC(dyn) was explained by the combination of increased resting IRV and decreased exercise breathing frequency (r(2) = 0.83, p < 0.0005). In conclusion, improved exercise endurance during hyperoxia was explained, in part, by a combination of reduced ventilatory demand, improved operational lung volumes, and dyspnea alleviation.
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PMID:Effects of hyperoxia on ventilatory limitation during exercise in advanced chronic obstructive pulmonary disease. 1128 62

The impact of denture wear in edentulous subjects while performing routine spirometric measurements has never been systematically investigated. We compared the values of FVC, FEV(1), PEFR, FEF(50%), FIV(1), and FIF(50%) recorded with and without dentures in three groups of edentulous subjects: 36 asymptomatic subjects with normal spirometry (N), 22 patients with chronic obstructive pulmonary disease (COPD), and 18 with interstitial lung disease (ILD). In 14 subjects retropharyngeal space with and without dentures was assessed by cephalometry. Subjects with N and ILD had significantly lower airflow rates without dentures, whereas subjects with COPD had no significant difference in spirometric values recorded with or without dentures. The retropharyngeal space was significantly decreased by removing dentures (from 1.52 +/- 0.07 to 1.16 +/- 0.09 cm, SEM, p < 0.0001). These findings indicate that in edentulous subjects with a normal or restrictive pattern, the recording of flow-volume curves with or without dentures produces small but significant differences. Although such differences do not appear to have clinical significance, the fact that when dentures are used some respiratory flows are higher would favor the use of dentures in edentulous subjects during spirometric evaluation.
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PMID:Effect of edentulism on spirometric tests. 1128 82

To determine whether macrolide antibiotics improve pulmonary function and decrease airway inflammation in cystic fibrosis (CF), we treated 10 patients (females; aged 19-26 years, all colonized with P. aeruginosa, none with atypical Mycobacteria) with 3 weeks of placebo, followed by 6 weeks of clarithromycin (500 mg BID) in a single-blind prospective study. We also determined the safety of sputum induction and the reproducibility of assessing inflammatory markers in induced sputum. Subjects performed spirometry and underwent sputum induction (12-min inhalation of 3% saline) at 3-week intervals. We found that sputum induction was well-tolerated. We also found that the reproducibility was high for neutrophil (PMN) number (R = 0.87, P = 0.009), interleukin (IL)-8 (R = 0.73, P < 0.05, free neutrophil elastase (NE) (R = 0.82, P < 0.05), and myeloperoxidase (MPO) levels (R = 0.86, P < 0.05), but was less so for tumor necrosis factor (TNF)-alpha (R = -0.15, P = 0.7). We found no significant difference in pulmonary function after 6 weeks of treatment with clarithromycin (FEV(1) (% predicted) (mean +/- SEM), 2.2 +/- 0.9 (60 +/- 24%) vs. 2.3 +/- 1 (61 +/- 29%)), and no significant differences in any of the inflammatory indices measured. The median (and range) values before and after treatment for indices of airway inflammation in the induced sputum samples were: for PMNs, 8 (1-326) and 21 (0.2 -175) x 10(6) cells/mL sputum; for IL-8, 156 (24-656) and 202 (16-680) ng/mL; for free NE, 260 (31-1,264) and 237 (49-1,048) microg/mL; for TNF-alpha, 20 (7-128) and 35 (17-87) pg/mL; and for MPO, 169 (13-960) and 195 (14-816) microg/mL. We conclude that clarithromycin is not uniformly effective in improving airway obstruction or in decreasing airway inflammation in patients with CF.
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PMID:Effect of clarithromycin on airway obstruction and inflammatory markers in induced sputum in cystic fibrosis: a pilot study. 1141 73

The aim of this study was to evaluate the feasibility and reproducibility of forced expiratory maneuvers during standard spirometric evaluation in preschool children. Among 570 young children attending our laboratory, we retrospectively selected 355 patients (14% 3-4-year-olds, 48% 4-5-year-olds, and 38% 5-6-year-olds) who carried out spirometric tests for the first time. The indications for such tests were history of asthma (70%), followed by chronic cough (20%) and other miscellaneous conditions (10%). Eighty-eight, 175, and 92 children performed one, two, and three acceptable tests respectively. Forced expired volume in 1 sec (FEV(1)) and forced vital capacity (FVC) did not differ significantly between attempts in children performing either two or three attempts. Forced expiratory time (FET), i.e., the total time required for the forced expiratory maneuver, was 1.7 +/- 0.1 sec (mean +/- SEM), and was no greater than 1 sec in 21.3% of all tested children. Consequently, FEV(1) does not appear to be well-suited to this age group. Forced expiratory volume in 0.50 and 0.75 sec (FEV(0.5), FEV(0.75)) were thus measured in the group of children performing three attempts (n = 92), and there was no statistical difference between attempts. In 267 children performing two or three tests, the ATS criteria of reproducing FEV(1) and FVC within <or= 0.1 L seemed to be preferable in this young population. Indeed, more than 70% of the tested children presented their two best efforts (FVC and FEV(1)) not varying by more than 0.1 L. Individual coefficients of variation (CV = SD/mean x 100%) over three tests for FEV(1) and FVC were 6.71 +/- 0.53% and 6.35 +/- 0.41% (mean +/- SEM), respectively. These results show that forced expiratory tests are not always feasible in young children, but that 55% (196/355) of our selected population performed reliable maneuvers (at least two FVC and FEV(1) reproducible within 0.1 L), provided that they were supervised by a carefully trained pediatric medical staff.
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PMID:Spirometry in children aged 3 to 5 years: reliability of forced expiratory maneuvers. 1141 77

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