Relationships among pulmonary function, anxiety and depression in mild asthma: An exploratory study

2021 ◽  
pp. 108244
Author(s):  
Paul Lehrer ◽  
Charles G. Irvin ◽  
Shou-En Lu ◽  
Frederick S. Wamboldt
Author(s):  
Y. Denisenko ◽  
E. Mineeva ◽  
M. Antonyuk ◽  
A. Yurenko ◽  
T. Gvozdenko ◽  
...  

1991 ◽  
Vol 71 (2) ◽  
pp. 438-444 ◽  
Author(s):  
H. M. Hollingsworth ◽  
M. R. Pratter ◽  
J. M. Dubois ◽  
L. E. Braverman ◽  
R. S. Irwin

To determine whether thyrotoxicosis has an effect on the asthmatic state in subjects with mild asthma, airway responsiveness, lung function, and exercise capacity were measured in a randomized double-blind placebo-controlled trial before and after liothyronine (triiodothyronine, T3)-induced thyrotoxicosis. Baseline evaluation of 15 subjects with mild asthma included clinical evaluation, thyroid and routine pulmonary function tests, airway responsiveness assessment by methacholine inhalation challenge, and a symptom-limited maximal exercise test. For all subjects, the initial testing revealed that the dose of methacholine which provoked a 20% fall in forced expiratory volume in 1s (PD20) was in a range consistent with symptomatic asthma. There was no significant change in pulmonary function tests, airway reactivity (PD20), or exercise capacity in either the placebo or the T3-treated groups. Thyroid function tests confirmed mild sustained thyrotoxicosis in the T3-treated groups. We conclude that mild T3-induced thyrotoxicosis of 4-wk duration had no effect on lung function, airway responsiveness, or exercise capacity in subjects with mild asthma.


Thorax ◽  
2008 ◽  
Vol 63 (7) ◽  
pp. 658-658 ◽  
Author(s):  
F Cousson-Gelie ◽  
J-M Vernejoux ◽  
H Bazex-Chanteloube ◽  
C Raherison ◽  
A Ozier ◽  
...  

2018 ◽  
Vol 17 ◽  
pp. S53
Author(s):  
I. Lalic ◽  
A. Vukić Dugac ◽  
T. Zovko ◽  
V. John ◽  
D. Tješić-Drinković ◽  
...  

1990 ◽  
Vol 6 (1) ◽  
pp. 155-171 ◽  
Author(s):  
L. Jack Roger ◽  
Donald H. Horstman ◽  
William Mcdonnell ◽  
Howard Kehrl ◽  
Philip J. Ives ◽  
...  

Two experiments were conducted to determine respiratory responses of persons with asthma performing intermittent moderate exercise while exposed to low concentrations of NO2. In the first, preliminary experiment, 13 male subjects, aged 19–35, with mild asthma were exposed on separate days in a chamber (natural breathing, 20°C, 40% RH) to 0.30 ppm NO2 and to a control or “clean air” exposure (0.0 ppm NO2). Exposure included three 10–min periods of moderate treadmill exercise (VE = 44.5 liter/min), each followed by symptom measurement and pulmonary function testing. The average decrease in FEV1 following the initial 10 min exercise in 0.30 ppm was 11% which was significantly greater (p < 0.05) than that observed in clean air (7%). Differences in FVC and SRaw were not significantly different at this time. Slight cough and dry mouth and throat were apparent only after the first exercise in NO2. After the second and third exercises, decreases in FEV1 and FVC and increases in SRaw were significantly greater in 0.30 than in 0.0 ppm NO2. Individual subject responses were variable. These results suggested that some asthmatics who perform moderate exercise while exposed to 0.30 ppm NO2 may experience bronchoconstriction and reduction in spirometric performance. Because of these preliminary findings, a more comprehensive, concentration-response experiment was conducted. Twenty-one male volunteers with mild asthma were exposed for 75 min with natural breathing to 0.0, 0.15, 0.30, and 0.60 ppm NO2. Exposure included three 10–min periods of moderate treadmill exercise (VE = 43 liter/min), each exercise followed by symptoms measurement and pulmonary function testing. In addition, airway responsiveness was measured two hr after each exposure by methacholine bronchial challenge testing. In the control exposures (0.0 ppm NO2), the exercise alone caused substantial decrements in pulmonary function. These decrements (as measured by decreases in FEV1 and FVC, and increases in SRaw) were not increased relative to the control exposure after any exercise session in any concentration of NO2. Furthermore, there was no overall group-averaged indication of a concentration-related effect of the NO2 on pulmonary function. Likewise, symptoms reported after NO2 exposure were not significantly different from those reported in clean air. Group-averaged airway responsiveness after exercise in NO2 was also not different from responsiveness after exercise in clean air. For only two subjects was there any indication of a concentration-related increase in airway responsiveness due to exposure to NO2. The findings of no effects in this larger concentration-response study do not support the findings of single-concentration studies by us and others. Possible explanations are differences in subject sampling, variability in subjects' responses, or other factors such as seasonal variation in response.


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