Granulocyte inflammatory markers and airway infection during acute exacerbation of chronic obstructive pulmonary disease.

There is increasing evidence that chronic obstructive pulmonary disease (COPD) is associated with chronic inflammation in the airways and lung parenchyma; however, little is known about the inflammatory response during acute COPD exacerbation. The objectives of this study were (1) to determine if inflammatory markers associated with neutrophilic inflammation and activation increase at times of acute COPD exacerbation relative to the clinically stable state, and (2) to determine whether the presence of acute bacterial or viral infection at the time of COPD exacerbation could be correlated with increases in sputum markers of inflammation. Induced sputum was collected from patients with COPD when they were clinically stable, during the time of an acute exacerbation, and 1 mo later. Sputum was analyzed at each time point for soluble markers associated with neutrophilic inflammation; myeloperoxidase (MPO), tumor necrosis factor-alpha (TNF-alpha), and interleukin-8 (IL-8). Serologic assays on acute and convalescent sera were performed for respiratory viruses, and induced sputum was also subject to quantitative bacterial cultures, viral cultures, and polymerase chain reaction (PCR) for detection of respiratory viruses. Fourteen of the 50 patients enrolled in the study met predetermined criteria for an acute COPD exacerbation over the 15-mo study period. TNF-alpha and IL-8 were significantly elevated in the sputum of patients during acute COPD exacerbation compared with when they were clinically stable (p = 0.01 and p = 0.05, respectively). Concentrations of these cytokines declined significantly 1 mo after the exacerbation. Three of 14 patients (21%) had confirmed bacterial or viral respiratory tract infections. Patients with documented infection did not demonstrate greater increases in sputum levels of inflammatory cytokines during exacerbations compared with patients without demonstrable infection. We conclude that markers of airway neutrophilic inflammation increase at the time of acute COPD exacerbation and then decline 1 mo later, and that this acute inflammatory response appears to occur independently of a demonstrable viral or bacterial airway infection.

Preoperative prediction of pulmonary complications following thoracic surgery.

The ability of preoperative quality-of-life and physiologic variables to predict postoperative complications was tested in 117 consecutive patients undergoing thoracotomy for possible or definite lung cancer. Preoperatively, quality of life was globally assessed by the QLI and Sickness Impact Profile. Dyspnea was assessed by the Clinical Dyspnea Index and a modified Pneumoconiosis Research Unit question. Spirometry and maximal exercise testing were carried out in 115 and 46 subjects, respectively. Thirty-seven percent experienced at least one respiratory complication (eg, pneumonia, atelectasis prompting bronchoscopy, pulmonary embolism). Twofold or greater increases in respiratory complications were associated with current smoking (p < 0.05), cancer as the final pathologic condition (p < 0.10), at least moderate dyspnea (p < 0.10), FEV 1 < 60 percent of predicted (p < 0.05), ventilatory reserve < 25 L (p < 0.05), and VO2max < 1.25 L (p < 0.05). Twofold increases in the incidence of any complication (respiratory, cardiac, etc) were associated with age > or = 75 years (p < 0.05) and cancer as the final pathologic condition (p < 0.05). We conclude that simple historic information (age, smoking status, cancer status, dyspnea) indicates the risk of postoperative morbidity. General quality-of-life measures were not good predictors of morbidity. Our findings corroborate the few studies supporting the value of VO2max and suggest that the usefulness of the ventilatory reserve deserves further attention.

Chronic cough responsive to ibuprofen.

A 57-year-old woman believed that ibuprofen, prescribed for back pain, improved her idiopathic chronic cough that had been resistant to inhaled and oral corticosteroids. To confirm this observation, we performed an n-of-1 clinical trial with four treatment periods, each separated by a 4-day washout. Ibuprofen 1800 mg/day for 6 days or placebo was randomly allocated in a double-blind fashion with a block size of 4. The number of coughs during the first 30 minutes after awakening were counted daily throughout the study using a tape recorder. Sixty-two coughs/hour occurred while taking ibuprofen, compared with 164 with placebo. We conclude that ibuprofen may be effective in idiopathic chronic cough, and suggest that prostaglandins may be pathogenic factors in some patients.