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Exercise tolerance is an important outcome measure in patients with COPD, mostly because there is evidence that exercise testing is superior to other functional measurements obtained at rest in demonstrating the positive effect of a specific intervention. We assessed the effect of a 5-day treatment with formoterol 12 microg twice daily on lung function, exercise capacity and dyspnea in 22 stable COPD patients, and compared 6-MWT with 12-MWT in evaluating formoterol efficacy. All subjects entered a crossover design. They underwent 6-MWT or 12-MWT in a randomised order and soon after started the 5-day treatment. After a 3-day washout, patients who had first performed 6-MWT, underwent 12-MWT, and the contrary. Formoterol induced a progressively significant increase in pre-drug FEV1 and IC and also significant changes in these parameters 2 h after its inhalation at each test day. Moreover, it increased the walked distance by 53.6 m at the end of 6-MWT and 59.9 m at the end of 12-MWT. Formoterol also induced a significant change in Borg score for dyspnea caused by the 6-MWT when compared with the pre-treatment values, whereas it significantly changed dyspnea induced by 12-MWT only after the first dose. Our study not only strengthens the importance of walking tests as a useful tool for evaluating the impact of a bronchodilator on some COPD patient-centred outcomes, but also indicates that 6-MWT seems to be a more appropriate instrument than 12-MWT for assessing the exercise response to a bronchodilator in COPD.

Objective. Although rhinitis is extremely frequent in children, methods for assessing the severity of nasal inflammation produce results with wide variability and hence weak clinical significance. We designed this epidemiologic investigation to define the clinical usefulness of assessing nasal cellularity in children. Methods. We studied 183 of 203 eligible unselected schoolchildren who were aged 9 to 11 years and whose parents gave informed consent and completed a questionnaire on the history of atopic and respiratory symptoms. In all children, nasal swabs were obtained from both nostrils and eluted in saline and slides were prepared from cytospin preparations for staining and white cell counts. Children also underwent determination of nasal volume, skin prick tests with 7 common local allergens, flow volume curves, and nitric oxide measurement in expired air. Blood samples were drawn for the measurement of total immunoglobulin E, eosinophil percentage, and detection of Chlamydia pneumoniae antibodies. C pneumoniae DNA was also sought in eluates from nasal swabs. The percentage, standard deviations, and percentiles of the various nasal white cell populations were determined. Results. No correlation of the percentage of these cells was found with the history of allergies or respiratory disease or with functional or laboratory finding. Repeat nasal swabs obtained 1 month after the initial examination in 31 children (20 with neutrophils higher and 11 lower than 14%) in 77.4% of the cases confirmed the previous (high or normal) result. Twelve of the 16 eligible children with persistently high nasal neutrophil counts completed a 15-day cycle of intranasal flunisolide therapy (200 μg twice a day). Therapy significantly reduced nasal neutrophil percentage and increased nasal volume. Conclusions. Increased nasal neutrophils, although related neither to the clinical history nor to laboratory variables, are a common important finding in children. A 15-day cycle of intranasal flunisolide is sufficient to restore normal nasal neutrophilia.

Hereditary myopathy with early respiratory failure (HMERF) is a rare disorder characterized by severe respiratory involvement at onset, muscle weakness starting in the early adulthood, and cytoplasmic bodies with peculiar immunohistochemical reactivity on muscle biopsy. Here we describe a patient who presented with hypercapnic coma at age 32. A detailed light and electron microscopy analysis on muscle biopsy was performed and, together with clinical data, led to the diagnosis. The R279W mutation in the TTN gene was excluded. This report expands the geographical region of incidence and encourages additional studies to clarify the genetic heterogeneity of the condition.

Most outcomes do not deeply express the degree of disability in patients with respiratory failure (RF) following inpatient pulmonary rehabilitation (IPR). The aim of our study was to evaluate the efficacy of an IPR in patients with confirmed COPD and RF using functional independence measure (FIM) that determines the degree of disability experienced by patients and the progress they make during rehabilitation. This scale includes several items: self care, mobility, locomotion, communication and social recognition. Twenty-two patients (age 70+/-2 years, PO(2) 58.18+/-7.63mmHg, PCO(2) 46.82+/-9.11mmHg) were prospectively observed and studied. IPR included respiratory and peripheral muscle training, mucus evacuation techniques, and energy conservation techniques. FIM, Medical Research Council dyspnoea scale (MRC), St. George's Respiratory Questionnaire (SGRQ), and 6-min walking distance (6-MWD) were assessed on admission (pre) and discharge (post) from IPR. After IPR there was a statistically significant improvement (p

Despite numerous studies demonstrating an association between asthma and many other chronic conditions and signs of Chlamydia pneumoniae (Cp) infection, the role of Cp in the pathogenesis of these illness remain still unclear. We investigated the prevalence of Cp antigen in the upper airways and the prevalence of detectable Cp serum antibodies in an unselected population of 207 9-yr-old schoolchildren. We also sought the presence of asthma, chronic or recurrent respiratory symptoms by means of questionnaire completed by the parents. Nasal aspirate, blood sampling and allergen skin prick tests were also performed. None of the children had obvious signs of acute infection at physical examination. Cp DNA was detected in nasal aspirates from 20 of the 207 children tested and serum IgG antibodies for Cp in 68 children. No association was found between atopy or history of atopic illness and the presence of Cp DNA or antibody production. This finding is explained by the fact that our study was conducted in an unselected childhood population, inherently including few children with asthma. A strong association between the status of antigen carrier and the presence of detectable Cp serum immunoglobulin (Ig)G or IgM suggests that subjects with detectable Cp antibodies have an impaired ability to eliminate this pathogen when infected. Because Cp eradication requires a strong Th1 lymphocyte response, the previously proven association between Cp and asthma, might reflect the known association of asthma with Th2-oriented lymphocytic activity.

Nitrogen dioxide (NO2) is a free radical and a common oxidant in polluted air. Here we present data on the time course of inflammation after NO2 exposure, as reflected in bronchial biopsy and airway lavage specimens. Healthy, nonsmoking subjects were exposed to air or 2 ppm NO2 for 4 h in random order on separate occasions. Endobronchial biopsies, bronchial washing (BW), and bronchoalveolar lavage (BAL) were done at 1.5 h (n = 15) or 6 h (n = 15) after exposure. In BW, exposure to NO2 induced a 1.5-fold increase in interleukin-8 (IL-8) (p < 0.05) at 1.5 h and a 2.5-fold increase in neutrophils (p < 0.01) at 6 h. In BAL fluid (BALF), small increases were observed in CD45RO+ lymphocytes, B-cells, and natural killer (NK) cells only. Immunohistologic examination of bronchial biopsy specimens showed no signs of upregulation of adhesion molecules, and failed to reveal any significant changes in inflammatory cells at either time point after NO2 exposure. In summary, NO2 induced a neutrophilic inflammation in the airways that was detectable in BW at 6 h after NO2 exposure. The increase in neutrophils could be related to the enhanced IL-8 secretion observed at 1.5 h after exposure. The absence of adhesion-molecule upregulation or cellular inflammation in mucosal biopsy specimens indicates that the major site of inflammation following exposure to NO2 may be in the smaller airways and not in the alveoli.

Short-term exposure to ambient levels of ozone induces neutrophilic bronchitis. To investigate the early events contributing to inflammatory cell recruitment in the airways we exposed 12 healthy nonsmoking volunteers to 0.12 ppm ozone or filtered air for 2 h on two separate occasions. Spirometry and fiberoptic bronchoscopy were performed immediately and at 1.5 h after the two exposures, respectively. Total protein, albumin, and total and differential cell counts were performed on the bronchial wash and BAL fluid. Bronchial biopsies were embedded in glycol methacrylate and immunostained for inflammatory cells, including neutrophils, mast cells, total T-cells (CD3), T-cell subset CD8, and leukocyte endothelial adhesion molecules, including VCAM-1, ICAM-1, E-selectin, and P-selectin. No significant changes were observed in FEV1, FVC, or any inflammatory indices in the bronchial wash and BAL fluid. In addition, no significant differences were seen in inflammatory cell numbers or percentages of vessels expressing VCAM-1, E-selectin, or ICAM-1 in the biopsies. The percentage of vessels expressing P-selectin increased significantly after ozone exposure: p = 0.016; median (IQR), 28.76 (26.36-36.94) versus 47.06 (38.14-56.86)%. The upregulation of P-selectin could signify an early inflammatory response to ozone such as margination and rolling of the neutrophils on the vessel wall prior to transendothelial migration.