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The mention of a patient with chronic obstructive pulmonary disease (COPD) is likely to conjure up an image of an older man with a cigarette in one hand and an [...]

Background: Experimental studies indicate that greater skeletal muscle protein breakdown is a trigger for the cachexia that often is prevalent in chronic obstructive pulmonary disease (COPD). Objective: We compared myofibrillar protein breakdown (MPB) with whole-body (WB) protein breakdown (PB) in 9 cachectic COPD patients [[bar.x] [+ or -] SEM forced expiratory volume in 1 s ([FEV.sub.1]); 48 [+ or -] 4% of predicted], 7 noncachectic COPD patients ([FEV.sub.1] : 53 [+ or -] 5% of predicted), and 7 age-matched healthy control subjects, who were matched by body mass index with the noncachectic patients. Design: After the subjects fasted overnight (10 h) and discontinued the maintenance medication, a primed constant and continuous infusion protocol was used to infuse L-[[ring.sup.-2][H.sub.5]]-phenylalanine and L-[[ring.sup.-2][H.sub.2]]-tyrosine to measure WB protein turnover and L-[[sup.2][H.sub.3]]3-methylhistidine to measure WB MPB. Three arterialized venous blood samples were taken between 80 and 90 min of infusion to measure amino acid concentrations and tracer enrichments. Results: Body composition, WB protein turnover, and WB MPB did not differ significantly between the noncachectic COPD and control subjects. Cachectic COPD patients had lower fat mass and fat-free mass values (both: P < 0.01) than did the noncachectic COPD patients. WB MPB was significantly (P < 0.05) higher in the cachectic COPD group (18 [+ or -] 3 nmol * [kg.sup.-1] * [min.sup.-1]) than in the combined control and noncachectic COPD groups (10 [+ oe -] 1 nmol * [kg.sup.-1] * [min.sup.-1]), but WB protein turnover did not differ significantly between the groups. Correlations with fat-free mass were significant (P < 0.05) for plasma glutamate and branched-chain amino acids, and that for WB MPB trended toward significance (P = 0.07). Conclusion: Cachexia in clinically stable patients with moderate COPD is characterized by increased WB MPB, which indicates that myofibrillar protein wasting is an important target for nutritional and pharmacologic modulation. KEY WORDS Cachexia, myofibrillar protein breakdown, chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States and Europe and is expected to become the third leading cause of death by [...]

Asthma and chronic obstructive pulmonary disease (COPD) involve chronic inflammation and constriction of the bronchioles. Optimal therapy for many patients requires control of both pathologic mechanisms through the use of [...]

Study objectives: Alterations in pulmonary function and interstitial changes in the lungs of renal transplant recipients have been described, but prospective longitudinal data are lacking. Design: A prospective analysis of [...]

The lungs of some patients with Sjogren's syndrome show inflammatory lesions that obstruct the airways. Sjogren's syndrome is an autoimmune disease associated with dry eyes and other symptoms associated with damage to exocrine glands. Researchers performed physiologic measurements and examined lung biopsy samples from 61 Sjogren's patients and 53 healthy people. Patients with Sjogren's syndrome had reduced lung function, confirmed by biopsy to be inflammatory changes in the small airways. Many had only a dry cough as evidence of the changes in their lungs.

Background: Some patients with chronic obstructive pulmonary disease may share the clinical characteristics of those with asthma; their disease is sometimes called 'asthmatic bronchitis.' Whether there is a difference between asthmatics who do and do not develop chronic bronchitis is not yet clear. We investigated whether asthma and chronic bronchitis may share some 'allergic' phenotypes and whether asthmatic individuals who develop chronic bronchitis subsequently have steeper declines in lung function. Methods: Known risk factors for decline in lung function were analyzed in a representative community population of adults followed up longitudinally since 1972 in Tucson, Ariz, in groups with persistent, newly developed, and past diagnoses of asthma and chronic bronchitis. We evaluated contributions of initial level of forced expiratory volume in 1 second (FE[V.sub.1]), reversibility with isoproterenol hydrochloride nebulized aerosol bronchodilator treatment, percentage of blood eosinophils to determine eosinophilia, and IgE level. Results: The concurrence of chronic bronchitis and asthma is associated with a steeper decline in FE[V.sub.1] than is asthma as the sole diagnosis. Asthmatics (those with persistent asthma with and without chronic bronchitis) had the greatest prevalence of increased reversibility with isoproterenol therapy and with eosinophilia. The prevalence of eosinophilia was also high in those with newly diagnosed chronic bronchitis without asthma; however, this was not the case in those with persistent chronic bronchitis without asthma. Larger bronchodilator responses were related to steeper declines in FE[V.sub.1], both in persistent asthma and in chronic bronchitis. Conclusions: Bronchodilator response and eosinophilia are generally believed to be hallmarks of asthma. We show that these characteristics may be present in chronic bronchitis as well. The presence of a large (>25%) bronchodilator response is associated with a steeper decline in FE[V.sub.1].

Hyperresponsiveness of the bronchial airways is a fundamental characteristic of a number of respiratory disorders, including asthma and chronic obstructive pulmonary disease (COPD). In general, the degree of airway hyperresponsiveness correlates with the severity of the symptoms reported by patients suffering from these diseases. However, in some cases, the degree of airway hyperresponsiveness does not seem to be predictable on the basis of symptom severity. To further characterize the relationships between airway hyperresponsiveness, respiratory symptoms, and peak expiratory flow (PEF; an index of the maximum amount of gas breathed out from the lungs), a study was carried out with 221 hyperresponsive patients with moderately severe airway obstruction. The patients were categorized as having asthma (81 patients), asthmatic bronchitis (69 patients), or chronic obstructive pulmonary disease (44 patients). Twenty-seven patients could not be accurately classified into one of these groups. Airway responsiveness was quantified by measuring the degree of bronchial constriction in response to inhaled histamine (a bronchoconstrictor substance). Average airway responsiveness was significantly higher in asthmatic patients than in either COPD or asthmatic bronchitis patients, but there was a large amount of variability in all three groups. Airway responsiveness was moderately correlated with peak expiratory flow; however, for each level of airway responsiveness, there was wide variability in the PEF values obtained, indicating that the two measures are not interchangeable. Symptom severity was weakly related to airway responsiveness and PEF levels. Hence, all three variables (airway hyperresponsiveness, peak expiratory flow, and symptom severity) appear to provide related but different information on the underlying disease process. (Consumer Summary produced by Reliance Medical Information, Inc.)

Asthma and asthma-like syndromes frequently develop during sudden exposure to high doses of irritants. One situation where this frequently occurs is during and following a fire. Many of these asthmatic episodes resolve shortly after the exposure with or without medication. In many instances, however, asthmatic symptoms recur and even worsen, requiring sustained and long-term drug treatment. Three cases are presented of asthma that developed after exposure to the pyrolysis products of fires, particularly from burning plastics. These cases illustrate the development of fixed and reversible obstructive pulmonary disease, even after apparent recovery from the initial episode. Smoke residues include such toxic inhalants as ammonia, acrolein, aldehydes, SO2, NO2, hydrogen fluoride, phosgene, chlorine, HCl, and aldehydes. Various therapeutic interventions are discussed. (Consumer Summary produced by Reliance Medical Information, Inc.)

The role of cigarettes in the causation of chronic obstructive lung disease (increased resistance to the flow of air in and out of the lungs) is well established. In an attempt to reduce the health risks of cigarette smoking, manufacturers have reduced the per-cigarette yield of tar, nicotine, and carbon monoxide (CO). Studies have shown that the risk of developing certain types of cancer is reduced by switching from a brand of cigarette high in these substances to one which has lower concentrations, but the effects of tar, nicotine, and CO levels on the development of chronic obstructive lung disease is less certain. To further study this issue, 690 subjects who were regular smokers were questioned about their smoking habits and respiratory symptoms (chronic cough, phlegm, and shortness of breath); 414 of these subjects were also given tests of respiratory function. After statistical corrections had been made for the intensity and duration of smoking and for the depth of inhalation, there was no relationship between the tar and nicotine yield of a smoker's cigarette and the risk of developing chronic phlegm, cough, or shortness of breath. But among the subjects who were tested for current respiratory function, there were statistically significant relationships between the daily dose of tar, nicotine, and CO (that is, the per-cigarette yield multiplied by the number of cigarettes smoked per day) and lung function. However, the association between tar, nicotine, and CO dose and pulmonary function was weak, and was much smaller than the adverse effects caused by smoking any type of cigarette compared with not smoking at all. (Consumer Summary produced by Reliance Medical Information, Inc.)