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Biomedical subjects

Arthur F Gelb

Publications and source records attributed to Arthur F Gelb.

8 recordsLinked to original sources
PubMed2006

Role of spirometry and exhaled nitric oxide to predict exacerbations in treated asthmatics.

OBJECTIVE: To evaluate the complementary roles of exhaled nitric oxide (NO) and spirometry to predict asthma exacerbations requiring one or more tapering courses of systemic corticosteroids. METHODS: We prospectively studied 44 nonsmoking asthmatics (24 women) aged 51 +/- 21 years (mean +/- SD) who were clinically stable for 6 weeks and receiving 250 mug of fluticasone/50 mug of salmeterol or equivalent for 3 years. Total exhaled NO (FENO), small airway/alveolar NO (CANO), large airway NO flux (J'awNO), and spirometry were measured. RESULTS: Baseline FEV(1) was 2.1 +/- 0.7 L, 70 +/- 20% of predicted after 180 mug of albuterol. Twenty-two of 44 asthmatics had one or more exacerbations over 18 months, 16 of 22 asthmatics had two exacerbations, and 6 of 22 asthmatics were hospitalized, including 1 asthmatic with near-fatal asthma. When baseline FEV(1) was </= 76% predicted, exacerbations occurred in 20 of 31 asthmatics (65%). If baseline FEV(1) was > 76% of predicted, exacerbations occurred only in 2 of 13 asthmatics (15%) [p = 0.003, chi(2)]. Using a receiver operating characteristic (ROC) curve for first exacerbation, the area under the curve was 0.67 with cutoff FEV(1) of 76% of predicted (sensitivity, 0.91; specificity, 0.50; positive predictive value, 0.65; negative predictive value, 0.85; positive likelihood ratio [LR(+)], 1.8; negative likelihood ratio [LR(-)], 0.18). When baseline FENO was >/= 28 parts per billion (ppb), exacerbations occurred in 13 of 17 asthmatics (76%); if baseline FENO was < 28 ppb, exacerbations occurred in only 9 of 27 asthmatics (33%) [p = 0.005, chi(2)]. Using the ROC curve for first exacerbation, the area under the curve was 0.71 with FENO cutoff point of 28 ppb (sensitivity, 0.59; specificity, 0.82; positive predictive value, 0.77; negative predictive value, 0.87; LR(+), 3.3; LR(-), 0.5). Independent of baseline FEV(1), FENO >/= 28 ppb increased the relative risk (RR) for exacerbation by 3.4 (95% confidence interval [CI], 1.3 to 9.1; Mantel-Haenszel, p = 0.007). An abnormal increase in CANO increased RR by 3.0 (95% CI, 0.9 to 9.9; p = 0.04), and abnormal J'awNO increased RR by 2.4 (95% CI, 1.0 to 5.6; p = 0.04). Independent of baseline FENO, FEV(1) </= 76% predicted increased RR by 1.7 (95% CI, 1.0 to 2.7; p = 0.02). Combined baseline FENO >/= 28 ppb and FEV(1) </= 76% of predicted identified 13 stable asthmatics with 85% probability for future exacerbation, whereas 9 asthmatics with FENO < 28 ppb and FEV(1) > 76% of predicted had a 0% probability of exacerbation. CONCLUSION: Combining FENO and FEV(1) percentage of predicted can stratify risk for asthma exacerbation.

Adrenal Cortex Hormones↗
PubMed2004

Alveolar and airway sites of nitric oxide inflammation in treated asthma.

The goal of this study was to identify airway and alveolar site(s) of inflammation using exhaled nitric oxide (NO) as a marker in treated patients with asthma, including response to oral corticosteroids, and correlate these sites with expiratory airflow limitation. In 53 (24 male) patients with asthma, age 43 +/- 23 years (mean +/- SD) and all on inhaled corticosteroids, post 180 microg aerosolized albuterol, FEV(1) was 74 +/- 23% predicted and FEV(1)/FVC was 68 +/- 11%. Exhaled NO at 100 ml/second was 27 +/- 23 ppb (p < 0.001 compared with normal, 12 +/- 15 ppb). Bronchial NO maximal flux was 2.4 +/- 3.1 nl/second (p < 0.001 compared with normal, 0.85 +/- 0.55). Alveolar NO concentration was 7.0 +/- 7.4 ppb (p = 0.01 compared with the normal value, 3.2 +/- 2.0 ppb). There was no significant correlation between FEV(1) % predicted or lung elastic recoil and NO bronchial flux or alveolar concentration. However, there was a weak but significant correlation between NO bronchial flux and alveolar concentration (Spearman r = 0.50, p < 0.001). In 10 subjects with asthma on inhaled corticosteroids, 5 days of 30 mg prednisone resulted in isolated significant decreases in NO alveolar concentration, from 13 +/- 10 to 4 +/- 4 ppb (p = 0.002). Despite treatment, including inhaled corticosteroids, patients with asthma may have ongoing separate airway and alveolar sites of NO inflammation, the latter responsive to oral corticosteroids.

Administration, Inhalation↗
PubMed2004

Innovative approaches to lung volume reduction for emphysema.

The 10 years of resurgent interest in lung volume reduction surgery (LVRS) and recent National Emphysema Treatment Trial findings for emphysema have stimulated a range of innovative alternative ideas aimed at improving outcomes and reducing complications associated with current LVRS techniques. Concepts being actively investigated at this time include surgical resection with compression/banding devices, endobronchial blockers, sealants, obstructing devices and valves, and bronchial bypass methods. These novel approaches are reaching the stage of clinical trials at this time. Theory, design issues, methods, potential advantages and limitations, and available results are presented. Extensive research in the near future will help to determine the potential clinical applicability of these new approaches to the treatment of emphysema symptoms.

Animals↗
PubMed2004

Risk factors for near-fatal asthma.

BACKGROUND: There is a paucity of lung function data in patients, both before and after episodes of near-fatal asthma (NFA), requiring transient endotracheal intubation and mechanical ventilation. METHODS: Lung function was initially measured in 43 asthmatic patients (age range, 16 to 49 years), who were observed and treated in a tertiary referral asthma clinic and were clinically stable at the time of study. Subsequently, clinical and physiologic follow-up studies were obtained over > 5 years. The primary outcomes were to determine (1) the integrity of lung elastic recoil and (2) the severity of expiratory airflow limitation, and (3) to correlate these outcomes with adverse clinical complications. RESULTS: Fourteen of 26 asthmatic patients (54%) [age range, 30 to 49 years] had significantly reduced lung elastic recoil pressures at all lung volumes compared to 3 of 17 asthmatic patients (18%); p = 0.02 [chi(2) test and Fisher exact test] [age range, 16 to 26 years]. In asthmatic patients between the ages of 30 and 49 years, significant loss of lung elastic recoil was noted in 4 of 10 patients with mild reduction in FEV(1) (FEV(1), > 79% predicted), 6 of 12 patients with moderate reduction in FEV(1) (FEV(1), 61 to 79% predicted), and all 4 patients with severe reduction in FEV(1) (FEV(1), < 61% predicted). In asthmatic patients between the ages of 16 and 26 years, significant loss of lung elastic recoil was noted in 0 of 11 patients with mild reduction in FEV(1), 2 of 5 patients with moderate reduction in FEV(1), and 1 of 1 patient with severe reduction in FEV(1). A subgroup of 10 asthmatic patients (7 men) [mean (+/- SD) age, 37 +/- 11 years] were studied when clinically stable, both before and after an episode of NFA in 8 cases and only after an episode of NFA in 2 additional cases. In 1 of 10 cases, the FEV(1) was mildly reduced, in 4 cases it was moderately reduced, and in 5 cases it was severely reduced, both before and after an episode of NFA. The sensitivity was 90%, the specificity was 61%, the positive predictive value was 41%, and the negative predictive value was 95% for NFA with an FEV(1) < or = 79% predicted or FEV(1)/FVC ratio of < 75%. Prior to an episode of NFA, all 8 asthmatic patients had significant loss of lung elastic recoil pressure, and afterward all 10 had significant loss of lung elastic recoil pressure (ie, less than the predicted normal mean minus 1.64 SD at a total lung capacity [TLC] of 100 to 70% predicted). The sensitivity was 100%, the specificity was 79%, the positive predictive value was 59%, and the negative predictive value was 100% for NFA with the loss of lung elastic recoil. The mean TLC measured with a plethysmograph in 10 patients with NFA was 7.2 +/- 1.41 (124 +/- 16% predicted). The sensitivity for TLC of > 115% predicted was 70%, the specificity was 70%, the positive predictive value was 88%, and the negative predictive value was 41% for NFA. CONCLUSION: A persistent reduction in FEV(1) of < or = 79% predicted or an FEV(1)/FVC ratio of < 75%, and, especially, the loss of lung elastic recoil and hyperinflation at TLC are risk factors for NFA. The loss of lung elastic recoil in asthmatic patients was associated with increased age, duration of disease, and progressive expiratory airflow limitation.

Adolescent↗
PubMed2004

Simplified detection of dynamic hyperinflation.

STUDY OBJECTIVE: To detect dynamic hyperinflation by comparing reduction in inspiratory capacity (IC) during both paced hyperventilation and cycle ergometry in patients with moderate-to-severe COPD, studied before and after acute bronchodilation. METHODS: IC and FEV(1) were measured before and after metronome-paced hyperventilation at twice the resting respiratory rate for 20 s in 16 patients with COPD before and after 54 microg aerosolized ipratropium bromide (IB). We also studied the same 16 patients before and after administration of 54 microg aerosolized IB during symptom-limited incremental cycle ergometry when the final respiratory rate was also twice the resting rate. RESULTS: Resting IC was 2.23 +/- 0.53 L (mean +/- SD), and the mean decrease in IC from baseline was 0.36 +/- 0.25 L after exercise (p < 0.001), and not significantly different (p = 0.64) from mean decrease in IC of 0.40 +/- 0.29 L following hyperventilation. Results following hyperventilation and exercise were similar after bronchodilator. The mean difference for decrease of IC between hyperventilation and exercise was 0.138 L (95% confidence interval, - 0.347 to 0.622; r = 0.66, p = 0.006). The decrease in FEV(1) was 0.01 +/- 0.13 L after exercise and 0.06 +/- 0.18 L after hyperventilation. Separately, baseline and peak end-expiratory and end-inspiratory lung volumes were similar with hyperventilation vs exercise both before and after bronchodilator. CONCLUSION: Both metronome-paced hyperventilation and incremental cycle ergometry, when resting respiratory rate was doubled, provoked similar significant decrease in IC, even after administration of 54 microg aerosolized IB. The noninvasive simplicity of hyperventilation for 20 s provides a clinically useful screening surrogate to monitor changes in IC following exercise.

Administration, Inhalation↗
PubMed2002

Lung elastic recoil in acute and chronic asthma.

This review emphasizes the mechanisms responsible for maximum expiratory airflow limitation in acute and chronic persistent asthma. The phenomenon of acute but reversible loss of lung elastic recoil during acute asthma is reviewed, although no plausible physiologic explanations are offered. The authors have recently studied adult chronic, stable asthmatics with persistent forced expiratory volume in 1 second less than 80% predicted, despite optimal polytherapy. The asthmatics had unsuspected marked loss of lung elastic recoil in the absence of emphysema that was responsible for a 32 to 35% reduction in maximum expiratory airflow at 80% total lung capacity and a 28 to 60% reduction in maximum expiratory airflow at 70% total lung capacity. Work in progress indicates that persistent reduced maximum expiratory airflow may be present for at least 12 +/- 4 years (mean +/- SD) and suggests possible early loss of lung elastic recoil. These observations provide a challenge to the concept of intrinsic airway narrowing resulting from airway remodeling as the major cause of expiratory maximum expiratory airflow limitation in chronic, moderate asthma and severe, persistent asthma. No morphologic or physiologic abnormalities readily explain the chronic, persistent loss of lung recoil.

Acute Disease↗
PubMed2002

Unsuspected loss of lung elastic recoil in chronic persistent asthma.

STUDY OBJECTIVES: To investigate the progression and mechanism(s) for fixed maximum expiratory airflow (max) limitation in patients with chronic persistent asthma. METHODS: When optimally treated and in clinically stable condition, we studied 21 asthmatic patients and classified them into three groups based on the severity of expiratory airflow limitation: (1) group A included 5 asthmatic patients (four women; mean +/- SD age, 51 +/- 17 years) with mild persistent asthma (FEV(1) > 80% predicted) with serial FEV(1) measurements obtained prior to the present study for 16 +/- 4 years; (2) group B included 11 asthmatic patients (three women; mean age, 64 +/- 11 years) with moderate persistent asthma (FEV(1) of 60 to 80% predicted) with serial FEV(1) measurements for 12 +/- 4 years; and (3) group C included 5 asthmatic patients (three women; mean age, 55 +/- 16 years) with severe persistent asthma (FEV(1) < 60% predicted) with serial FEV(1) measurements for 11 plus minus 5 years. RESULTS: Lung CT indicated no or trivial emphysema, and diffusion was normal in all asthmatics. There was a marked loss of lung elastic recoil at total lung capacity (TLC) in all asthmatic patients in group B (16 +/- 4 cm H(2)O) and group C (15 +/- 5 cm H(2)O), but none or minimal in group A (22 +/- 1 cm H(2)O) [p < 0.01], and loss of elastic recoil accounted for 34% and 50% of decreased maximal expiratory airflow (max) at 80% and 70% TLC, respectively. Comparison with previous longitudinal data indicated individual asthmatics when in clinically stable condition remained predominantly in the same FEV(1) percent predicted classification group as in the current study. CONCLUSION: Patients with chronic moderate and severe persistent asthma, despite optimal therapy, have reduced max for many years in part due to (early?) loss of lung elastic recoil from unknown mechanism(s). This challenges current concept of airway remodeling.

Aged↗