Lung scintigraphy is primarily used to diagnose pulmonary embolism. Ventilation imaging is often performed using 99m Tc-DTPA or Technegas, an ultrafine dispersion of 99m Tc-labeled carbon. Despite the common use of these radioaerosols, they have not been compared in an intraindividual study, and not with ventilation-perfusion (V/P) SPECT. The aim of the present head-tohead study was to systematically investigate differences in ventilation studies performed with 99m Tc-diethylenetriaminepentaacetate (DTPA) and Technegas. Methods: Sixty-three patients, 28 without and 35 with obstructive lung disease, were examined with V/P SPECT using both 99m Tc-DTPA and Technegas. V/P SPECT images were randomized and assessed independently by 2 masked physicians according to a predefined scoring system. A paired comparison was performed using the Wilcoxon signed-rank test. Results: In both obstructive and nonobstructive disease, the overall unevenness of radiotracer deposition and the degree of central deposition were more pronounced in 99m Tc-DTPA than Technegas studies. Because of better peripheral penetration, the extent of reverse mismatch was less when Technegas was used. Additionally, in obstructive disease, the degree of focal deposition in distal airways was more pronounced with 99m Tc-DTPA. Mismatched perfusion defects were more frequently found with Technegas in obstructive disease. Conclusion: This intraindividual comparative study shows that Technegas is the preferred radioaerosol, particularly in obstructive disease.Key Words: pulmonary embolism; ventilation-perfusion singlephoton emission computed tomography (V/P SPECT); COPD; 99m Tc-DTPA; Technegas Lung scintigraphy allows imaging of ventilation and perfusion distribution and assessment of regional lung function in lung disease (1). Lung scintigraphy is used primarily to identify pulmonary embolism (PE), although other diseases such as pneumonia, heart failure, and obstructive lung disease may be identified (1-5). Ventilationperfusion (V/P) SPECT improves the diagnostic accuracy for PE (6-9). V/P SPECT performed according to the state of the art also simplifies recognition of ventilation and perfusion patterns typical of other cardiopulmonary diseases (10).Perfusion scintigraphy is most commonly achieved by microembolization with 99m Tc-labeled macroaggregates of human albumin (MAA). For ventilation studies, the inert gas 81m Kr and the aerosols 99m Tc-diethylenetriaminepentaacetate (DTPA) and an ultrafine dispersion of 99m Tc-labeled carbon (Technegas; Cyclomedica Ltd.) are currently recommended (11). 81m Kr is of limited use because of its high cost and short half-life.Previously, 133 Xe was also used for ventilation studies, but this is no longer recommended according to the guidelines of the European Association of Nuclear Medicine (11).How aerosol droplets or particles are distributed and deposited within airways and alveoli depends on their aerodynamic properties, particularly their mass median aerodynamic diameter (11). Even with the best liquid aerosol gen...
BackgroundSome patients with chronic obstructive pulmonary disease (COPD) show increased airway inflammation and bacterial colonization during stable phase. The aim of this study was to follow COPD patients and investigate chronic colonization with pathogenic bacteria during stable disease phase, and relate these findings to clinical parameters, inflammatory pattern, lung function, and exacerbations.MethodsForty-three patients with COPD were included while in a stable state and followed up monthly until exacerbation or for a maximum of 6 months. The patients completed the Clinical COPD Questionnaire and Medical Research Council dyspnea scale questionnaires, and exhaled breath condensate was collected, followed by spirometry, impulse oscillometry, and sputum induction.ResultsTen patients were chronically colonized (ie, colonized at all visits) with Haemophilus influenzae during stable phase. These patients had higher sputum levels of leukotriene B4 (P<0.001), 8-isoprostane (P=0.002), myeloperoxidase activity (P=0.028), and interleukin-8 (P=0.02) during stable phase when compared with other patients. In addition, they had lower forced vital capacity (P=0.035) and reactance at 5 Hz (P=0.034), but there was no difference in forced expiratory volume in 1 second (FEV1), FEV1 % predicted, forced vital capacity % predicted, exhaled breath condensate biomarkers, C-reactive protein, or Clinical COPD Questionnaire and Medical Research Council dyspnea scale results. Three patients had intermittent colonization (colonized at only some visits) of H. influenzae during stable phase, and had lower levels of inflammatory biomarkers in sputum when compared with the chronically colonized patients. The difference in airway inflammation seen during stable phase in patients chronically colonized with H. influenzae was not observed during exacerbations.ConclusionSome COPD patients who were chronically colonized with H. influenzae during stable phase showed increased airway inflammation and reduced lung volumes when compared with non-chronically colonized patients.
Long-term tobacco smokers with chronic obstructive pulmonary disease (COPD) or chronic bronchitis display an excessive accumulation of neutrophils in the airways; an inflammation that responds poorly to established therapy. Thus, there is a need to identify new molecular targets for the development of effective therapy. Here, we hypothesized that the neutrophil-mobilizing cytokine interleukin (IL)-26 (IL-26) is involved in airway inflammation amongst long-term tobacco smokers with or without COPD, chronic bronchitis or colonization by pathogenic bacteria. By analyzing bronchoalveolar lavage (BAL), bronchail wash (BW) and induced sputum (IS) samples, we found increased extracellular IL-26 protein in the airways of long-term smokers without further increase amongst those with clinically stable COPD. In human alveolar macrophages (AM), the exposure to water-soluble tobacco smoke components (WTC) enhanced gene and protein. In this cell model, the same exposure increased gene expression of the IL-26 receptor complex () and a proven regulator of IL-26 production. In the same cell model, recombinant human IL-26 caused a concentration-dependent increase in the gene expression of and several pro-inflammatory cytokines. In the long-term smokers, we also observed that extracellular IL-26 protein in BAL samples correlates with measures of lung function, tobacco load, and several markers of neutrophil accumulation. Extracellular IL-26 was further increased in long-term smokers with exacerbations of COPD (IS samples), with chronic bronchitis (BAL samples ) or with colonization by pathogenic bacteria (IS and BW samples). Thus, IL-26 in the airways emerges as a promising target for improving the understanding of the pathogenic mechanisms behind several pulmonary morbidities in long-term tobacco smokers.
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