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At least 991 records · Page 55Linked to original sources
PubMed1999

Exhaled nitric oxide is increased in active fibrosing alveolitis.

STUDY OBJECTIVES: Interstitial inflammation is a major aggravating factor in fibrosing lung disease associated with scleroderma (FASSc) and cryptogenic fibrosing alveolitis (CFA). Exhaled nitric oxide (NO) production is increased in asthma and bronchiectasis and reflects the degree of inflammation. We investigated whether measuring levels of exhaled NO is valuable in assessing disease activity in patients with CFA and patients with FASSc. MEASUREMENTS AND RESULTS: NO levels were measured in 11 patients with CFA (mean age +/- SEM, 58 +/- 12 years old; 5 were male) and 17 patients with FASSc (mean age, 48 +/- 9 years old; 5 were male), and they were compared to BAL cell counts and lung function. Patients with CFA and FASSe had elevated NO levels (11.2 +/-1.0 parts per billion [ppb] and 9.8 +/- 1.0 ppb, respectively; p > 0.05), whereas in a group of 13 nonsmoking normal subjects, the NO levels were not elevated (6.9 +/- 0.5 ppb; p < 0.05). Patients with FASSc (n = 8) who had active BAL (defined as either lymphocytes > 14%, neutrophils > 4%, or eosinophils > 3%) had significantly higher NO levels (13.2 +/- 1.8 ppb), and neutrophil (16.5 +/- 4.0%) and lymphocyte (26.8 +/- 3.4%) BAL cell counts than did patients with FASSc who had inactive BAL (6.7 +/- 1.2 ppb; 1.3 +/- 1.0% and 7.5 +/- 1.3%, respectively; p < 0.05). There was a significant correlation between exhaled NO and lymphocyte cell count in patients with FASSc (r = 0.58; p < 0.05). All patients with CFA had active BAL; however, those treated with corticosteroids (12.9 +/- 1.0% ppb, p < 0.05) had lower NO levels (9.0 +/- 1 ppb) and higher BAL lymphocyte cell couits (16.6 +/- 2.0%) than did those not treated with corticosteroids (7.2 +/- 1.7%; p < 0.05). CONCLUSIONS: We conclude that exhaled NO may be a useful addition to BAL cell counts in disease monitoring.

Breath Tests↗
PubMed2002

A randomized, placebo-controlled trial of a leukotriene synthesis inhibitor in patients with COPD.

STUDY OBJECTIVE: Patients with COPD classically have neutrophilic bronchial inflammation and raised airway concentrations of the neutrophil chemoattractant leukotriene B(4) (LTB(4)). A small phase II trial was conducted to assess the effects of a leukotriene synthesis inhibitor on bronchial inflammation in patients with stable COPD. DESIGN: A randomized, double-blind, placebo-controlled, parallel-group study. SETTING: Respiratory medicine department of a university hospital. PATIENTS AND INTERVENTION: Seventeen patients with chronic bronchitis and COPD (mean FEV(1), 35.5% predicted; SD, 14.8% predicted) were randomized to receive 14 days of the oral leukotriene synthesis inhibitor BAYx1005 (500 mg bid) or placebo. MEASUREMENTS AND RESULTS: Spontaneous sputum samples obtained at baseline and at the end of treatment were assayed for LTB(4), myeloperoxidase (an indirect marker of neutrophil numbers and/or activation), and chemotactic activity (Boyden chamber). After 14 days, there were no significant differences (p > 0.05) in absolute LTB(4) concentrations between the two treatment groups. However, BAYx1005 treatment produced a significantly greater median reduction in LTB(4) of - 3.1 nM (interquartile range [IQR], - 9.6 to - 0.2 nM) vs 3.0 nM (IQR, - 0.3 to 8.5 nM) [p = 0.001], with concentrations decreasing from 8.0 nM (IQR, 4.3 to 24.4 nM) at baseline to 4.2 nM (IQR, 1.9 to 11.9 nM) at the end of treatment (p = 0.03). There were no changes in the placebo group and no differences in sputum myeloperoxidase concentration or chemotaxis between the two treatment arms (p > 0.05). CONCLUSIONS: This small study suggests that a leukotriene synthesis inhibitor can produce modest reductions in some measures of neutrophilic bronchial inflammation in patients with COPD. This class of anti-inflammatory agent requires further study in larger numbers of patients to determine clinical benefit.

Aged↗
PubMed2003

Alveolar-capillary membrane dysfunction in heart failure: evidence of a pathophysiologic role.

Chronic heart failure (CHF) increases the resistance to gas transfer across the alveolar-capillary interface. Recent reports highlight the pathophysiologic relevance of changes in the lung leading to impaired fluid and gas exchange in the distal airway spaces. Under experimental conditions, an acute pressure or volume overload can injure the alveolar blood-gas barrier. This may disrupt its anatomic configuration, cause the loss of regulation of fluid-flux, and thereby affect alveolar gas conductance properties. These ultrastructural changes have been identified under the term of stress failure of the alveolar-capillary membrane. In the short term, these alterations are reversible due to the reparative properties of the alveolar surface. However, when the alveolar-capillary membrane is chronically challenged, for instance in patients with CHF, by noxious stimuli, such as humoral, cytotoxic, and genetic factors other than by mechanical trauma, remodeling of pathophysiologic and clinical importance may take place. These changes in some respects resemble the remodeling process in the heart. Emerging findings support the view that, in patients with CHF, alveolar-capillary membrane dysfunction may contribute to symptom exacerbation and exercise intolerance, and may be an independent prognosticator of clinical course. Angiotensin-converting enzyme inhibitors ameliorate the alveolar membrane gas conductance abnormality, reflecting improvement in the remodeling process. This article reviews the putative mechanisms involved in the impairment in gas diffusion in CHF patients and provides a link between physiologic changes and clinical findings.

Capillary Permeability↗
PubMed2006

Repeated sputum inductions induce a transient neutrophilic and eosinophilic response.

INTRODUCTION: Sputum induction is a tool to monitor airway inflammation, yet it may induce by itself a neutrophilic response when repeated within 24 to 48 h. This limits its repeated use in clinical trials. OBJECTIVE: We aimed to investigate the induction and resolution of inflammation generated by repeated sputum inductions. SUBJECTS AND DESIGN: Sixteen healthy intermittent smokers participated in a study on the short-term effects of smoking. The nonsmoking arm consisted of seven successive sputum inductions with increasing time intervals (3, 6, 12, 24, 48, and 96 h). Inflammatory cellular characteristics and different soluble mediators were investigated. MEASUREMENTS AND RESULTS: The median percentage of sputum neutrophils increased significantly from baseline to 6 h (58.9% [range, 31.8 to 94.2%] to 83.2% [range, 26.7 to 98.3%], respectively). Surprisingly, the percentage of eosinophils also increased significantly from baseline to 6, 12, 24, and 48 h, as follows: 0.3% (range, 0.0 to 1.2%) to 1.7% (range, 0.0 to 15.5%), 2.2% (range, 0.5 to 12.5%), 1.2% (range, 0.0 to 4.8%), and 0.8% (range, 0.0 to 2.8%), respectively. Interleukin-8 increased significantly from baseline to 24 h (1,553 pg/mL [range, 462 to 8,192 pg/mL] to 2,178 pg/mL [range, 666 to 128,544 pg/mL]). CONCLUSIONS: Repeated sputum inductions should preferably be avoided within 48 h. It induces not only a short-lived neutrophilic response but also a prolonged eosinophilic inflammatory response in healthy subjects, possibly by local changes in osmolarity, and subsequent epithelial and/or mast cell activation.

Administration, Inhalation↗