No abstract

Conclusions-Serum TNF-levels were higher in patients with ARDS than in those with severe pneumonia or in control subjects. Multivariate results suggest that the levels of systemic TNF-and IL-1 reflect the severity of the lung injury rather than the diagnosis. (Thorax 2000;55:46-52)

The bronchial microbiome in severe COPD during stability and exacerbation in patients chronically colonised by Pseudomonas aeruginosa (PA), has not been defined. Our objective was to determine the characteristics of the bronchial microbiome of severe COPD patients colonised and not colonised by P. aeruginosa and its changes during exacerbation. COPD patients with severe disease and frequent exacerbations were categorised according to chronic colonisation by P. aeruginosa. Sputum samples were obtained in stability and exacerbation, cultured, and analysed by 16S rRNA gene amplification and pyrosequencing. Sixteen patients were included, 5 of them showing chronic colonisation by P. aeruginosa. Pseudomonas genus had significantly higher relative abundance in stable colonised patients (p = 0.019), but no significant differences in biodiversity parameters were found between the two groups (Shannon, 3 (2–4) vs 3 (2–3), p = 0.699; Chao1, 124 (77–159) vs 140 (115–163), p = 0.364). In PA-colonised patients bronchial microbiome changed to a microbiome similar to non-PA-colonised patients during exacerbations. An increase in the relative abundance over 20 % during exacerbation was found for Streptococcus, Pseudomonas, Moraxella, Haemophilus, Neisseria, Achromobacter and Corynebacterium genera, which include recognised potentially pathogenic microorganisms, in 13 patients colonised and not colonised by P. aeruginosa with paired samples. These increases were not identified by culture in 5 out of 13 participants (38.5 %). Stable COPD patients with severe disease and PA-colonised showed a similar biodiversity to non-PA-colonised patients, with a higher relative abundance of Pseudomonas genus in bronchial secretions. Exacerbation in severe COPD patients showed the same microbial pattern, independently of previous colonisation by P. aeruginosa.Electronic supplementary materialThe online version of this article (doi:10.1007/s10096-013-2044-0) contains supplementary material, which is available to authorized users.

The aim of the study was to assess the potential role of glucocorticoids (GC) in modulating systemic and pulmonary inflammatory responses in mechanically ventilated patients with severe pneumonia. Twenty mechanically ventilated patients with pneumonia treated at a respiratory intensive care unit (RICU) of a 1,000‐bed teaching hospital were prospectively studied. All patients had received prior antimicrobial treatment. Eleven patients received GC (mean±sd dose of i.v. methylprednisolone 677±508 mg for 9±7 days), mainly for bronchial dilatation. Serum and bronchoalveolar lavage fluid (BALF) tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐6 and C‐reactive protein levels were measured in all patients. The inflammatory response was attenuated in patients receiving GC, both systemically (IL‐6 1,089±342 versus 630±385 pg·mL‐1, p=0.03; C‐reactive protein 34±5 versus 19±5 mg·L‐1, p=0.04) and locally in BALF (TNF‐α 118±50 versus 24±5 pg·mL‐1, p=0.05; neutrophil count: 2.4±1.1×109 cells·L‐1 (93±3%) versus 1.9±1.8×109 cells·L‐1 (57±16%), p=0.03). Four of the 11 (36%) patients receiving GC died compared to six (67%) who were not receiving GC (p=0.37). The present pilot study suggests that glucocorticoids decrease systemic and lung inflammatory responses in mechanically ventilated patients with severe pneumonia receiving antimicrobial treatment. Eur Respir J 1999; 14: 218–220.

Relationships between pulmonary function testing and high-resolution computed tomography (HRCT) were studied in 39 untreated patients with idiopathic pulmonary fibrosis (IPF) at diagnosis, 23 of whom were followed during 7.5 +/- 0.3 mo (mean +/- SEM). At diagnosis, the extent of overall lung involvement in the HRCT scans showed a moderate but significant correlation only with FVC (r = -0.46, p = 0. 003) and DLCO (r = -0.40, p = 0.03). The extent of ground glass pattern also correlated with FVC (r = -0.58, p = 0.0001). Arterial PO2 at peak exercise (n = 13 patients) showed a significant association with the extent of both ground-glass pattern and overall lung involvement in HRCT (r = -0.60, p = 0.02; and r = -0.64, p = 0. 01, respectively). On multivariate analysis a significant independent correlation between the global disease extent in HRCT and both FVC and DLCO was observed. Changes over time in the total extent of the disease evaluated with HRCT scans were also related to those observed in DLCO and in FVC (r = -0.57, p = 0.01, and r = -0. 51, p = 0.01, respectively). The present study suggests that FVC and DLCO are the physiological variables that best reflect the global extent of disease in IPF and thus may provide significant information for the assessment of the disease's progression.