Objectives. The present study was performed to examine the occurrence of dynamic hyperinflation following hyperventilation in COPD and ex-smokers without COPD and the efficacy of short-acting anti-cholinergic agents (SAAC) and β 2 -agonists (SABA) for lung hyperinflation following metronome-paced hyperventilation in COPD.
Methodology.Fifty-nine patients with COPD, 20 ex-smokers without COPD, and 20 healthy subjects who had never smoked were examined for dynamic hyperinflation by metronome-paced hyperventilation increasing respiratory rate from 20 to 30 and 40 tidal breaths/min. Dynamic hyperinflation was evaluated as the decrease in inspiratory capacity (IC) following hyperventilation, and the effects of SAAC and SABA on dynamic hyperinflation.Results. COPD patients showed a significant increase in end-expiratory lung volume (EELV) and decrease in IC following hyperventilation, and ex-smokers without COPD also showed mild and significant dynamic hyperinflation. Multiple stepwise linear regression analysis revealed that DLco/V A and RV/TLC were significant and independent determinants for dynamic hyperinflation in COPD. Treatment with SAAC and SABA significantly increased IC at each rate of breaths/min, independent of the increases in FEV 1 . Furthermore, SABA significantly inhibited the decrease in IC by 2 hyperventilation.Conclusions. These findings suggest that lung hyperinflation following hyperventilation may be a useful method to detect dynamic hyperinflation observed not only in patients with COPD but also in ex-smokers without COPD, and both SAAC and SABA are effective to reduce the dynamic hyperinflation in COPD.3 Key Words: chronic obstructive pulmonary disease (COPD), hyperventilation, air trapping, lung hyperinflation, and bronchodilator.Runnig Head: Effect of bronchodilator on dynamic hyperinflation. 4
The predominantly young woman-orientated systemic lupus erythematosus (SLE) is a disease that involves an extremely complicated and multifactorial interaction of various genetic and environmental factors. Crystalline silica (Si) may act as an immunoadjuvant to increase secretions of inflammatory endogenous substances and antibody production. In addition, previous studies have suggested that exposure to Si may induce SLE. Although the biologic mechanism of Si in SLE is unclear, defective apoptosis leading to the prolonged survival of pathogenic lymphocytes was thought to be one of mechanisms of Si-associated SLE (sSLE). In the present study, a rare case of an elderly man suffering from sSLE responded well to glucocorticoid therapy. The present findings were reviewed with reference to previous literature.
Background: Iodine-123 metaiodobenzylguanidine (123I-MIBG) lung uptake in the early phase has been proposed as a potential marker of endothelial function because MIBG behaves qualitatively similarly to norepinephrine in pulmonary circulation. Objectives: The purpose of the present study was to examine the lung uptake of 123I-MIBG in patients diagnosed with myeloperoxidase antineutrophil cytoplasmic antibodies (MPO-ANCA)-associated vasculitis without clinical or radiological abnormalities of the thorax. Methods: Six patients with MPO-ANCA-associated vasculitis were enrolled. They had severe renal damage (mean creatinine: 5.1 mg/dl, mean blood urea nitrogen: 54.6 mg/dl), but no respiratory symptoms clinically or radiographic findings on chest computed tomography. The total lung to upper mediastinum ratio of 123I-MIBG uptake (L/M) 15 min after the injection was measured. The result was compared with those for 6 patients with renal damage due to other diseases (mean creatinine: 6.2 mg/dl, blood urea nitrogen: 51.7 mg/dl) and for 8 healthy subjects. Results: The mean value of L/M in patients with MPO-ANCA-positive vasculitis was 1.21 ± 0.04, which was significantly less than that of other groups (1.41 ± 0.06 for patients with renal failure and 1.45 ± 0.03 for normal volunteers). There were no significant differences in MIBG accumulation in the heart among the groups. Conclusions: The reduction in kinetic behavior of MIBG in the lung reflects the presence of pulmonary endothelial impairment in patients with MPO-ANCA-associated vasculitis, even though there are no clinical manifestations in the lungs.
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