References of "European Respiratory Journal"
     in
Bookmark and Share    
Full Text
Peer Reviewed
See detailAdrenomedullin refines mortality prediction by the BODE index in COPD - The "BODE-A" index.
Stolz, Daiana; Kostikas, Kostantinos; Blasi, Francesco et al

in European Respiratory Journal (2014)

The BODE index is well-validated for mortality prediction in COPD. Concentrations of plasma proadrenomedullin, a surrogate for mature adrenomedullin, independently predicted 2-year mortality among ... [more ▼]

The BODE index is well-validated for mortality prediction in COPD. Concentrations of plasma proadrenomedullin, a surrogate for mature adrenomedullin, independently predicted 2-year mortality among inpatients with COPD exacerbation.We compared accuracy of initial proadrenomedullin level, BODE, and BODE components, alone or combined, in predicting 1-year or 2-year all-cause mortality in a multicenter, multinational observational cohort with stable, moderate to very severe COPD.Proadrenomedullin was significantly associated (P<0.001) with 1-year mortality (4.7%) and 2-year mortality (7.8%), and comparably predictive to BODE regarding both (C statistics: 0.691 vs. 0.745, 0.635 vs. 0.679). Relative to using BODE alone, adding proadrenomedullin significantly improved 1-year and 2-year mortality prognostication (C statistics: 0.750, 0.818; both P<0.001). Proadrenomedullin plus BOD was more predictive than was the original BODE including 6-minute-walk distance. In multivariable analysis, proadrenomedullin (LR X2 13.0, P<0.001), body mass index (8.5, P=0.004), and 6-minute-walk distance (7.5, P=0.006), but not modified MMRC dyspnoea score (2.2, P=0.14) or FEV1 % predicted (0.3, P=0.60), independently foretold 2-year survival.Proadrenomedullin plus BODE better predicts mortality in COPD patients than does BODE alone; proadrenomedullin may substitute for 6-minute-walk distance in BODE when 6-minute-walk testing is unavailable. [less ▲]

Detailed reference viewed: 6 (1 ULg)
Full Text
Peer Reviewed
See detailSurrogate markers predicting overall survival for lung cancer: ELCWP recommendations
Berghmans, Thierry; Pasleau, Françoise ULg; Paesmans, M. et al

in European Respiratory Journal (2012), 39

Detailed reference viewed: 31 (17 ULg)
Full Text
Peer Reviewed
See detailValproate–doxorubicin: promising therapy for progressing mesothelioma. A phase II study
Scherpereel, a; Berghmans, t; Lafitte, j.j et al

in European Respiratory Journal (2011), 37

No treatment is recommended for patients with malignant mesothelioma (MM) failing after first-line cisplatin-based chemotherapy. In vitro data suggested that valproic acid, a histone deacetylase inhibitor ... [more ▼]

No treatment is recommended for patients with malignant mesothelioma (MM) failing after first-line cisplatin-based chemotherapy. In vitro data suggested that valproic acid, a histone deacetylase inhibitor (HDACi), had a proapoptotic effect and synergised with doxorubicin to induce apoptosis in MM cells. Our primary end-point was to determine response rate of combined valproic acid and doxorubicin in patients with unresectable MM failing after platinum based chemotherapy. Treatment consisted of doxorubicin (60 mg?m-2) plus valproic acid. An interim analysis for response rate was planned after the first 16 registered patients. All the cases were centrally reviewed. From July 2006 to March 2009, 45 eligible patients with pleural MM were registered. The majority of the patients were male (73%), had a performance status (PS) o80 (76%) and an epithelioid subtype (80%). There were seven partial responses (response rate 16%; 95% CI 3– 25%), all in patients with PS 80–100. The best disease control rate was 36% (95% CI 22–51%). Two toxic deaths were observed (febrile neutropenia and cerebral thrombotic event), both in patients with poor PS (60–70). Valproic acid, an HDACi, plus doxorubicin appeared an effective chemotherapy regimen in good PS (80–100) patients with refractory or recurrent MM, for which no standard therapy was available. [less ▲]

Detailed reference viewed: 41 (7 ULg)
Full Text
Peer Reviewed
See detailImportance of identifying Mycobacterium bovis as a causative agent of human tuberculosis
Allix-Béguec, C.; Fauville-Dufaux, M.; Stoffels, K. et al

in European Respiratory Journal (2010), 35

Detailed reference viewed: 26 (4 ULg)
Full Text
Peer Reviewed
See detailExhaled nitric oxide as a marker of asthma control in smoking patients.
Michils, A.; Louis, Renaud ULg; Peche, R. et al

in European Respiratory Journal (2009), 33(6), 1295-301

Exhaled nitric oxide fraction (F(eNO)), which is a reliable marker of eosinophilic airway inflammation, is partially suppressed by tobacco smoking. Consequently, its potential as a biomarker in asthma ... [more ▼]

Exhaled nitric oxide fraction (F(eNO)), which is a reliable marker of eosinophilic airway inflammation, is partially suppressed by tobacco smoking. Consequently, its potential as a biomarker in asthma management has never been evaluated in smoking patients. In the present study, the authors tested the validity of F(eNO) to predict asthma control in this population. F(eNO) and the Asthma Control Questionnaire (ACQ) were recorded at least once in 411 nonsmoking (345 with at least two visits) and 59 smoking (51 with at least two visits) asthma patients. Despite similar mean ACQ scores (1.5 versus 1.7), F(eNO) was reduced in smoking asthmatics (18.1 ppb versus 33.7 ppb). A decrease in F(eNO) of <20% precludes asthma control improvement in nonsmoking (negative predictive value (NPV) 78%) and in smoking patients (NPV 72%). An increase in F(eNO) <30% is unlikely to be associated with deterioration in asthma control in both groups of patients (NPV = 86% and 84% in nonsmoking and smoking patients, respectively). It is concluded that, even in smokers, sequential changes in F(eNO) have a relationship with asthma control. The present study is the first to indicate that cigarette smoking does not obviate the clinical value of measuring F(eNO) in asthma among smokers. [less ▲]

Detailed reference viewed: 23 (1 ULg)
Full Text
Peer Reviewed
See detailEffects of ciclesonide and fluticasone on cortisol secretion in patients with persistent asthma.
Derom, E.; Louis, Renaud ULg; Tiesler, C. et al

in European Respiratory Journal (2009), 33(6), 1277-86

We compared the systemic and clinical effects of ciclesonide (CIC) and fluticasone propionate (FP) administered, in addition to CIC 160 microg x day(-1) and salmeterol 50 microg twice daily, in 32 ... [more ▼]

We compared the systemic and clinical effects of ciclesonide (CIC) and fluticasone propionate (FP) administered, in addition to CIC 160 microg x day(-1) and salmeterol 50 microg twice daily, in 32 patients with persistent asthma using a randomised double-blind, placebo-controlled, double-dummy, five-period crossover design. All patients exhibited a provocative concentration leading to a 20% decrease in forced expiratory volume in 1 s (PC(20)) methacholine <8 mg x mL(-1) and a PC(20) adenosine <60 mg x mL(-1). Primary outcome was 24-h serum cortisol suppression after 7 days. Secondary outcomes were changes in PC(20) methacholine and adenosine after 9 days. FP 500 microg x day(-1) and 1,000 microg x day(-1) significantly suppressed cortisol secretion versus placebo by -46.2 (95% confidence interval (CI) -83.8- -8.5) nmol x L(-1) and by -76.1 (95% CI -112.9- -39.3) nmol x L(-1), respectively. Neither dose of CIC (320 nor 640 microg x day(-1)) had a significant suppressive effect (-28.2 (95% CI -65.5-9.2) nmol x L(-1) and -37.3 (95% CI -74.7-0.0) nmol x L(-1), respectively). Differences between FP 1,000 microg x day(-1) and both CIC treatments were statistically significant (CIC 320 microg x day(-1): -48.0 (95% CI -84.8- -11.1) nmol x L(-1); CIC 640 microg x day(-1): -38.8 (95% CI -75.7- -1.9) nmol x L(-1)). Compared with placebo, the increase in PC(20) adenosine after the four treatments was small, but significant. Greater improvements in PC(20) adenosine were seen with FP 500 microg x day(-1) (1.8 (95% CI 1.0-2.6) doubling concentrations) compared with CIC 320 microg x day(-1) (0.9 (95% CI 0.1-1.7) doubling concentrations). No significant difference was seen between CIC 640 microg x day(-1) and FP 1,000 microg x day(-1). For a similar decrease in hyperresponsiveness, cortisol secretion was suppressed significantly with moderate-to-high doses of fluticasone propionate, but not with ciclesonide. [less ▲]

Detailed reference viewed: 27 (1 ULg)
Full Text
Peer Reviewed
See detailPulmonary veno-occlusive disease in myeloproliferative disorder.
Willems, Evelyne ULg; Canivet, Jean-Luc ULg; Ghaye, Benoît ULg et al

in European Respiratory Journal (2009), 33(1), 213-216

The present study reports a case of biopsy-proven pulmonary veno-occlusive disease as a cause of severe pulmonary hypertension in a patient suffering from a chronic myeloproliferative disorder. The ... [more ▼]

The present study reports a case of biopsy-proven pulmonary veno-occlusive disease as a cause of severe pulmonary hypertension in a patient suffering from a chronic myeloproliferative disorder. The pulmonary disease evolved favourably under treatment with defibrotide, a pro-fibrinolytic medication used in hepatic veno-occlusive disease. [less ▲]

Detailed reference viewed: 67 (22 ULg)
Full Text
Peer Reviewed
See detailTNFA-3086 > A in two international population-based cohorts and risk of asthma
Castro-Giner, F.; Kogevinas, M.; Maechler, M. et al

in European Respiratory Journal (2008), 32(2), 350-361

Genetic association studies have related the tumour necrosis factor-a gene (TNFA) guanine to adenine substitution of nucleotide -308 (-3086 > A) polymorphism to increased risk of asthma, but results are ... [more ▼]

Genetic association studies have related the tumour necrosis factor-a gene (TNFA) guanine to adenine substitution of nucleotide -308 (-3086 > A) polymorphism to increased risk of asthma, but results are inconsistent. The aim of the present study was to test whether two single-nucleotide polymorphisms, of TNFA and of the lymphotoxin-alpha gene (LTA), are associated with asthma, bronchial hyperresponsiveness and atopy in adults, by combining the results of two large population-based multicentric studies and conducting a meta-analysis of previously published studies. The European Community Respiratory Health Survey (ECRHS) and Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) used comparable protocols, including questionnaires for respiratory symptoms and measures of lung function and atopy. DNA samples from 11,136 participants were genotyped at TNFA -308 and LTA 252. Logistic regression employing fixed and random effects models and nonparametric techniques were used. The prevalence of asthma was 6%. The TNFA -3086 > A polymorphism was associated with increased asthma prevalence and with bronchial hyperresponsiveness. No consistent association was found for atopy. The LTA 252A > G polymorphism was not associated with any of the outcomes. A meta-analysis of 17 studies showed an increased asthma risk for the TNFA -308 adenine allele. The tumour necrosis factor-alpha gene nucleotide -308 polymorphism is associated with a moderately increased risk of asthma and bronchial hyperresponsiveness, but not with atopy. These results are supported by a meta-analysis of previously published studies. [less ▲]

Detailed reference viewed: 21 (4 ULg)
Full Text
Peer Reviewed
See detailGefitinib monotherapy in advanced non-small cell lung cancer (NSCLC): Experience from a large, Western community implementation study
van Puijenbroek, R.; Bosquee, Léon ULg; Meert, A. P. et al

in European Respiratory Journal (2007, June), 29(1), 128-133

Detailed reference viewed: 18 (0 ULg)
Full Text
Peer Reviewed
See detailGefitinib monotherapy in advanced nonsmall cell lung cancer: a large Western community implementation study
van Puijenbroek, R.; Bosquee, Léon ULg; Meert, A. P. et al

in European Respiratory Journal (2007), 29(1), 128-133

Epidermal growth factor receptor tyrosine kinase inhibitors represent a new treatment option for patients with advanced nonsmall cell lung cancer (NSCLC). This retrospective study examined to what extent ... [more ▼]

Epidermal growth factor receptor tyrosine kinase inhibitors represent a new treatment option for patients with advanced nonsmall cell lung cancer (NSCLC). This retrospective study examined to what extent previous clinical trial experience matches large-scale Western community implementation of this treatment. In the Belgian expanded access programme, the data from 513 patients with advanced or metastatic NSCLC, not suitable for further chemotherapy and receiving oral gefitinib 250 mg center dot day(-1) until disease progression, death or unacceptable toxicity, were analysed. The median (range) duration of gefitinib treatment was 2.3 months (0.0-32.7). Its use was predominantly in second- or third-line treatment. The overall response and disease control rates were 8.9 and 41.2%, respectively. In univariate analysis, response was more common in females and never-smokers. In multivariate analysis, female sex was the only significant predictive factor (odds ratio (OR) (95% confidence interval (Cl)) 0.329 (0.129-0.839)). Symptom improvement was reported in 108 patients of whom 32 (29.6%) had an objective response, 66 (61.1%) experienced disease stabilisation and 10 (9.3%) progressed. Gefitinib was well tolerated; only 7.8% of the patients reported grade 3 or 4 toxicity. The overall median survival was 4.7 months, with a 1-yr survival rate of 21%. Survival was strongly influenced by a better performance status (PS) (good PS: hazard ratio (HR) (95%Cl) 0.110 (0.077-0.157)) and adenocarcinoma with bronchioloalveolar carcinoma features histology (HR (95%Cl) 0.483 (0.279-0.834)). In conclusion, the activity of gefitinib was confirmed in the present large Western community implementation study. Response, present in a small subgroup, led to a rewarding survival and could be predicted by sex only. Baseline performance status and adenocarcinoma with bronchioloalveolar carcinoma features histology were significant factors for survival. [less ▲]

Detailed reference viewed: 19 (0 ULg)
Peer Reviewed
See detailEffect of substance 101333-3 on emphysema and MMP activity in a model of cadmium-induced emphysema
Fievez, Laurence ULg; Kirschvink, N.; Provins, L. et al

in European Respiratory Journal (2005), 579s

Detailed reference viewed: 12 (2 ULg)
Peer Reviewed
See detailCadmium inhalation-induced emphysema is resistant to glucocorticoids
Fievez, Laurence ULg; Kirschvink, N.; Belleflamme, M. et al

in European Respiratory Journal (2005)

Detailed reference viewed: 19 (4 ULg)
Peer Reviewed
See detailSelective decoy-mediated inhibition of activator protein-1 activity in the airways pevents experimental asthmatic inflammation
Desmet, Christophe ULg; Gosset, P.; Pajak, B. et al

in European Respiratory Journal (2005), 26

Detailed reference viewed: 14 (5 ULg)
Peer Reviewed
See detailSubstance 101333-3 reduces pulmonary oxidative stress in cadmium-exposed rats
Kirschvink, Nathalie; Fievez, Laurence ULg; Marlin, D. et al

in European Respiratory Journal (2005), 104s

Detailed reference viewed: 10 (2 ULg)
Full Text
Peer Reviewed
See detailSmooth muscle cell matrix metalloproteinases in idiopathic pulmonary arterial hypertension.
Lepetit, H.; Eddahibi, S.; Fadel, E. et al

in European Respiratory Journal (2005), 25(5), 834-42

Pulmonary arterial hypertension (PAH) results from persistent vasoconstriction, smooth muscle growth and extracellular matrix (ECM) remodelling of pulmonary arteries (PAs). Matrix metalloproteinases (MMPs ... [more ▼]

Pulmonary arterial hypertension (PAH) results from persistent vasoconstriction, smooth muscle growth and extracellular matrix (ECM) remodelling of pulmonary arteries (PAs). Matrix metalloproteinases (MMPs) are matrix-degrading enzymes involved in ECM turnover, and in smooth muscle cell (SMC) and endothelial cell migration and proliferation. MMP expression and activity are increased in experimental PAH. Therefore, this study investigated whether similar changes occur in idiopathic PAH (IPAH; formerly known as primary pulmonary hypertension). Both in situ and in vitro studies were performed on PAs from patients undergoing lung transplantation for IPAH and from patients treated by lobectomy for localised lung cancer, who served as controls. In IPAH, MMP–tissue inhibitor of metalloproteinase (TIMP) imbalance was found in cultured PASMCs, with increased TIMP-1 and decreased MMP-3. MMP-2 activity was markedly elevated as a result of increases in both total MMP-2 and proportion of active MMP-2. In situ zymography and immunolocalisation showed that MMP-2 was associated with SMCs and elastic fibres, and also confirmed the MMP-3–TIMP-1 imbalance. In conclusion, the findings of this study were consistent with a role for the matrix metalloproteinase–tissue inhibitor of metalloproteinase system in pulmonary vascular remodelling in idiopathic pulmonary arterial hypertension. The matrix metalloproteinase–tissue inhibitor of metalloproteinase imbalance may lead to matrix accumulation, and increased matrix metalloproteinase-2 activity may contribute to smooth muscle cell migration and proliferation. Whether these abnormalities are potential therapeutic targets deserves further investigation. [less ▲]

Detailed reference viewed: 19 (4 ULg)
Peer Reviewed
See detailPrednisolone reduces 8-Iso-PGF2alpha in a feline model of asthma
Kirschvink, Nathalie; Leemans, Jérôme ULg; Delvaux, F. et al

in European Respiratory Journal (2005), 137s

Detailed reference viewed: 22 (3 ULg)
Full Text
Peer Reviewed
See detailDual tachykinin NK1/NK2 antagonist DNK333 inhibits neurokinin A-induced bronchoconstriction in asthma patients
Joos, G. F.; Vincken, W.; Louis, Renaud ULg et al

in European Respiratory Journal (2004), 23(1), 76-81

Inhalation of neurokinin A (NKA) causes bronchoconstriction in patients with asthma. In vitro both tachykinin NK1 and NK2 receptors can mediate airway contraction. In this study the authors examined the ... [more ▼]

Inhalation of neurokinin A (NKA) causes bronchoconstriction in patients with asthma. In vitro both tachykinin NK1 and NK2 receptors can mediate airway contraction. In this study the authors examined the effects of a single dose of the dual tachykinin NK1/NK2 receptor antagonist, DNK333, on NKA-induced bronchoconstriction in asthma. A total of 19 male adults with mild asthma completed a randomised, double-blind, placebo-controlled crossover trial. Increasing concentrations of NKA (3.3 x 10(-9) to 1.0 x 10(-6) mol(.)mL(-1)) were inhaled at 1 and 10 h intervals after a single oral dosing with either DNK333 (100 mg) or a placebo. It was observed that DNK333 did not affect baseline lung function but did protect against NKA-induced bronchoconstriction in those patients. The mean log(10) provocative concentration causing a 20% fall in forced expiratory volume in one second for NKA was -5.6 log(10) mol(.)mL(-1) at 1 h after DNK333 treatment and -6.8 log(10) mol(.)mL(-1) after placebo. This was equivalent to a difference of 4.08 doubling doses, which decreased to a difference of 0.90 doubling doses 10 h after treatment. The results shown in this report indicate that DNK333 blocks neurokinin A-induced bronchoconstriction in patients with asthma. [less ▲]

Detailed reference viewed: 29 (2 ULg)
Full Text
Peer Reviewed
See detailClinical applications of assessment of airway inflammation using induced sputum
Pavord, I. D.; Sterk, P. J.; Hargreave, F. E. et al

in European Respiratory Journal (2002), 20(Suppl. 37), 40-43

Detailed reference viewed: 13 (2 ULg)
Full Text
Peer Reviewed
See detailMethods of sputum processing for cell counts, immunocytochemistry and in situ hybridisation
Efthimiadis, A.; Spanevello, A.; Hamid, Q. et al

in European Respiratory Journal (2002), 20(Suppl. 37), 19-23

Detailed reference viewed: 20 (4 ULg)
Full Text
Peer Reviewed
See detailEvidence of mast-cell activation in a subset of patients with eosinophilic chronic obstructive pulmonary disease
Louis, Renaud ULg; Cataldo, Didier ULg; Buckley, M. G. et al

in European Respiratory Journal (2002), 20(2), 325-331

Although asthma has been viewed mainly, as an eosinophilic disease, and chronic obstructive pulmonary disease (COPD) as a neutrophilic disease, recent studies have shown increased neutrophil counts in ... [more ▼]

Although asthma has been viewed mainly, as an eosinophilic disease, and chronic obstructive pulmonary disease (COPD) as a neutrophilic disease, recent studies have shown increased neutrophil counts in severe asthma and sputum eosinophilia in sonic COPD patients. In an attempt to further characterise these two syndromes according to pathology, the current authors have conducted a study of induced sputum in 15 subjects with COPD, 17 asthmatics, and 17 nonatopic healthy individuals. Sputum was analysed for cytology and levels of eosinophil cationic protein (ECP), albumin, tryptase and soluble intercellular adhesion molecule-1. The COPD subjects differed from the asthmatics as they had higher sputum neutrophil and lower columnar epithelial cell counts, but there were no differences in any soluble marker studied. When compared to control subjects, both the asthmatic and COPD subjects had raised eosinophil counts and ECP levels. In a subset of COPD subjects with Sputum eosinophilia (>3% of total cells), significantly increased levels of tryptase were detected. In conclusion, although chronic obstructive pulmonary disease is a more neutrophilic disease than asthma, the two diseases are difficult to distinguish on the basis of sputum levels of the soluble markers traditionally associated with asthma. However, a subset of patients with chronic obstructive pulmonary disease with airway eosinophilia and mast-cell activation might represent a distinct pathological phenotype. [less ▲]

Detailed reference viewed: 21 (5 ULg)