Showing papers on "Pulmonary diffusion published in 2005"

Dietary salt, airway inflammation, and diffusion capacity in exercise-induced asthma.

Abstract: PURPOSE Recent studies have supported a role for dietary salt as a modifier of the severity of exercise-induced asthma. The main aim of this study was to demarcate a possible mechanism by which dietary salt modification may alter exercise-induced airway narrowing in asthmatic patients. METHODS Twenty-four patients participated in a randomized, double-blind crossover study. Subjects entered the study on their normal salt diet (NSD) and were then placed on either a low-salt diet (LSD) or high-salt diet (HSD) for 2 wk with a 1-wk washout period occurring between diets. Pre- and postexercise spirometry, pulmonary diffusion capacity (DLCO) and its subdivisions, and induced sputum were obtained on the NSD and at the end of each 2-wk treatment period (LSD and HSD). RESULTS FEV1 decreased by 7.9 +/- 2.8% on LSD, 18.3 +/- 4.0% on NSD, and 27.4 +/- 3.2% on HSD at 20 min postexercise. The NSD and HSD induced significant reductions (P 0.05) being observed on LSD. Postexercise-induced sputum neutrophil and eosinophil differential cell counts and induced sputum supernatant concentration of eosinophil cationic protein, interleukin (IL)-1beta, IL-8, leukotriene (LT) C(4)-E(4), LTB(4), and prostaglandin D(2) were significantly elevated (P < 0.05) on NSD and HSD compared with LSD. CONCLUSION Our findings indicate that dietary salt loading enhances airway inflammation following exercise in asthmatic subjects, and that small salt-dependent changes in vascular volume and microvascular pressure might have substantial effects on airway function following exercise in the face of mediator-induced increased vascular permeability.

[Respiratory failure and pulmonary fibrosis as a late side-effect after chemotherapy-induced by oxygen administration].

Abstract: Pulmonary fibrosis (PF) may develop following successful chemotherapy for malignancy, even if such therapy is not combined with radiotherapy. Bleomycin, which is known to induce acute pneumonitis and lung fibrosis, is especially associated with chemotherapy-induced PF, and bleomycin-induced pulmonary fibrosis can occur more than five years after such therapy. Additionally, supplemental oxygen therapy can trigger the onset of pneumonitis and lethal PF in patients who have previously received bleomycin therapy. Careful assessment of lung function via spiroergometry and arterial blood gas analysis during exercise are required if the administration of supplemental oxygen is considered. Two case reports reveal the potential lethal risk of oxygen for patients who have been treated with bleomycin: (1) a patient with successfully resected and treated basal tongue carcinoma and (2) a patient in remission after being treated for non-Hodgkin lymphoma. Single and double lung transplantation is the only therapeutic option for patients with severe, oxygen-induced PF and should be included as an indication for lung transplantation. Early recognition of pulmonary diffusion abnormalities and establishing a risk profile, as well as consequent monitoring of pulmonary function, may help to avoid or at least reduce the risk of PF induced by oxygen therapy when administered to patients who have previously been given bleomycin.

Avaliação da função pulmonar na sarcoidose Assessment of the pulmonary function in sarcoidosis

Abstract: Introduction: pulmonary function testing often is used in the management of the sarcoidosis. These study objectives were: to determine what is the most common functional disorder and the diffusion alterations frequency; to compare them with the thorax radiographic ones. Methodology: thirty-two non-smoking patients with pulmonary sarcoidosis were studied. Spirometry, pulmonary volumes measurement by dilution with helium and pulmonary diffusion capacity measurement by carbon monoxide (DLCO) were performed. The thorax radiographs were classified as types 0, 1, 2, 3 or 4. Results: according to findings of chest radiography, nine patients had type 0, four patients had type 1, seven patients had type 2, ten patients had type 3, and two patients had type 4 sarcoidosis. Airflow limitation occurred in 16 (50%) patients in all disease stages. Restrictive syndrome occurred in 9 (28.1%) patients. A low DLCO occurred in 11 (34.4%) patients, while a increase DLCO occurred in 5 (15.6%) patients. Conclusion: the most common ventilation disorder in pulmonary sarcoidosis is the obstructive one, possibly associated with endobronchial lesions, peribronchial fibrosis and bronchial hyper-reactivity. The DLCO is reduced in more than one third of the patients, principally in cases of restrictive syndrome.