| Titre : |
Accuracy of line probe assays for the diagnosis of pulmonary and multidrugresistant tuberculosis : a systematic review and meta-analysis |
| Type de document : |
document électronique |
| Auteurs : |
Ruvandhi R. Nathavitharana, Auteur ; Patrick G.T. Cudahy, Auteur ; Samuel G. Schumacher, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2017 |
| Collection : |
European Respiratory Journal num. 49(1) |
| Importance : |
23 p. |
| Présentation : |
ill. ; graph. ; tab. |
| Langues : |
Anglais (eng) |
| Catégories : |
[TUBER] diagnostic [TUBER] traitement:résistance:multirésistance [TUBER] traitement:traitement curatif:médicament spécial MDR [NICO] étude:méta-analyse
|
| Index. décimale : |
TU 8.5.1. MDR (Multi Drug Resistance / XDR (X-treme Drug Resistance) |
| Résumé : |
Only 25% of multidrug-resistant tuberculosis (MDR-TB) cases are currently diagnosed. Line probe assays (LPAs) enable rapid drug-susceptibility testing for rifampicin (RIF) and isoniazid (INH) resistance and Mycobacterium tuberculosis detection. Genotype MTBDRplusV1 was WHO-endorsed in 2008 but newer LPAs have since been developed.
This systematic review evaluated three LPAs: Hain Genotype MTBDRplusV1, MTBDRplusV2 and Nipro NTM+MDRTB. Study quality was assessed with QUADAS-2. Bivariate random-effects meta-analyses were performed for direct and indirect testing. Results for RIF and INH resistance were compared to phenotypic and composite (incorporating sequencing) reference standards. M. tuberculosis detection results were compared to culture.
74 unique studies were included. For RIF resistance (21 225 samples), pooled sensitivity and specificity (with 95% confidence intervals) were 96.7% (95.6–97.5%) and 98.8% (98.2–99.2%). For INH resistance (20 954 samples), pooled sensitivity and specificity were 90.2% (88.2–91.9%) and 99.2% (98.7–99.5%). Results were similar for direct and indirect testing and across LPAs. Using a composite reference standard, specificity increased marginally. For M. tuberculosis detection (3451 samples), pooled sensitivity was 94% (89.4–99.4%) for smear-positive specimens and 44% (20.2–71.7%) for smear-negative specimens.
In patients with pulmonary TB, LPAs have high sensitivity and specificity for RIF resistance and high specificity and good sensitivity for INH resistance. This meta-analysis provides evidence for policy and practice. |
| En ligne : |
https://doi.org/10.1183/13993003.01075-2016 |
| Format de la ressource électronique : |
HTML, PDF |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=10866 |
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| Titre : |
Association of genetic variations in the CSF2 and CSF3 genes with lung function in smoking-induced COPD |
| Type de document : |
texte imprimé |
| Auteurs : |
J-Q. He, Auteur ; K. Shumansky, Auteur ; J.E. Connett, Auteur ; N.R. Anthonisen, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2008 |
| Collection : |
European Respiratory Journal num. 32 |
| Importance : |
p. 25-34 |
| Présentation : |
tab., graph. |
| Langues : |
Anglais (eng) |
| Catégories : |
[NICO] étude [NICO] tabagisme:pathologie:pathologie respiratoire:bronchopneumopathie chronique obstructive [NICO] tabagisme:risque:facteur associé:génétique
|
| Index. décimale : |
TA 3.2.2.4 Pathologies respiratoires (sauf 3.2.2.1, 3.2.2.2, 3.2.2.3) |
| Résumé : |
Granulocyte-macrophage colony-stimulating factor (CSF), also known as CSF2, and granulocyte CSF, also known as CSF3, are important survival and proliferation factors for neutrophils and macrophages. The objective of the present study was to determine whether single nucleotide polymorphisms (SNPs) of CSF2 and CSF3 are associated with lung function in smoking-induced chronic obstructive pulmonary disease. In total, five SNPs of CSF2 and CSF3 were studied in 587 non-Hispanic white subjects with the fastest (n = 281) or the slowest (n = 306) decline of lung function selected from among continuous smokers in the National Heart, Lung, and Blood Institute Lung Health Study (LHS). These SNPs were also studied in 1,074 non-Hispanic white subjects with the lowest (n = 536) or the highest (n = 538) baseline lung function at the beginning of the LHS. An increase in the number of CSF3 -1719T alleles was significantly associated with protection against low lung function (odds ratio 0.73, 95% confidence interval 0.56-0.95), and was still significant after adjustment for multiple comparisons. There was also a significant association of a CSF3 haplotype with baseline levels of forced expiratory volume in one second. No association was found for CSF2 SNPs and lung function, nor was there evidence of epistasis. In conclusion, genetic variation in colony-stimulating factor 3 is associated with cross-sectionally measured lung function in smokers. |
| En ligne : |
https://erj.ersjournals.com/content/32/1/25.long |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8069 |
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| Titre : |
Burden of non-tuberculous mycobacterial pulmonary disease in Germany : a prospective cohort study |
| Type de document : |
document électronique |
| Auteurs : |
Roland Diel, Auteur ; Josephine Jacob, Auteur ; Niklas Lampenius, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2017 |
| Collection : |
European Respiratory Journal num. 49(4) |
| Importance : |
p. 1602109 |
| Présentation : |
ill. ; graph. ; tab. |
| Langues : |
Anglais (eng) |
| Catégories : |
[DIVERS] géographie:Europe:Europe occidentale:Allemagne [TUBER] cause:bacille de Koch [TUBER] étude:épidémiologie [TUBER] type de tuberculose:tuberculose-maladie:tuberculose pulmonaire
|
| Index. décimale : |
TU 2.6. Autres types de tuberculoses |
| Résumé : |
The objective of this study was to estimate the burden of disease in incident patients with non-tuberculous mycobacterial pulmonary disease (NTM-PD).
A sample of 7 073 357 anonymised persons covered by German public statutory health insurances was used to identify patients with NTM-PD. In total, 125 patients with newly diagnosed NTM-PD in 2010 and 2011 were matched with 1250 control patients by age, sex and Charlson Comorbidity Index, and followed for 39 months.
The incidence rate for NTM-PD was 2.6 per 100000 insured persons (95% CI 2.2–3.1). The mortality rate for patients with NTM-PD and the control group in the observational period was 22.4% and 6%, respectively (p<0.001). Mean direct expenditure per NTM-PD patient was €39 559.60 (95% CI
26 916.49–52 202.71), nearly 4-fold (3.95, 95% CI 3.73–4.19) that for a matched control (€10 006.71, 95% CI 8907.24–11106.17). Hospitalisations were three times higher in the NTM-PD group and accounted for 63% of the total costs. Attributable annual direct costs and indirect work-loss costs in NTM-PD patients were €9093.20 and €1221.05 per control patient, respectively. Only 74% of NTM-PD patients received antibiotics and nearly 12% were prescribed macrolide monotherapy. Although NTM-PD is considered rare, the attributable mortality and financial burden in Germany are
high. Efforts to heighten awareness of appropriate therapy are urgently needed. |
| En ligne : |
https://doi.org/10.1183/13993003.02109-2016 |
| Format de la ressource électronique : |
Article en ligne |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=10911 |
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| Titre : |
Can we predict tuberculosis cure? What tools are available? |
| Type de document : |
document électronique |
| Auteurs : |
Delia Goletti, Auteur ; Cecilia S. Lindestam Arlehamn, Auteur ; Thomas J. Scriba, Auteur ; R. Anthony, Auteur ; Daniela Maria Cirillo, Auteur ; Tonino Alonzi, Auteur ; Claudia M. Denkinger, Auteur ; Frank Cobelens, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2018 |
| Collection : |
European Respiratory Journal num. 52(5) |
| Importance : |
1801089 |
| Présentation : |
graph. ; tab. |
| Langues : |
Anglais (eng) |
| Catégories : |
[TUBER] traitement:résistance:multirésistance [TUBER] traitement:traitement curatif [NICO] tabagisme:pathologie:pathologie respiratoire:tuberculose pulmonaire
|
| Index. décimale : |
TU 8.2. Traitement curatif |
| Résumé : |
Antibiotic treatment of tuberculosis takes ≥6 months, putting a major burden on patients and health systems in large parts of the world. Treatment beyond 2 months is needed to prevent tuberculosis relapse by clearing remaining, drug-tolerant Mycobacterium tuberculosis bacilli. However, the majority of patients treated for only 2–3 months will cure without relapse and do not need prolonged treatment. Assays that can identify these patients at an early stage of treatment may significantly help reduce the treatment burden, while a test to identify those patients who will fail treatment may help target host-directed therapies.
In this review we summarise the state of the art with regard to discovery of biomarkers that predict relapse-free cure for pulmonary tuberculosis. Positron emission tomography/computed tomography scanning to measure pulmonary inflammation enhances our understanding of “cure”. Several microbiological and immunological markers seem promising; however, they still need a formal validation. In parallel, new research strategies are needed to generate reliable tests. |
| En ligne : |
https://doi.org/10.1183/13993003.01089-2018 |
| Format de la ressource électronique : |
Article en ligne |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=10943 |
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| Titre : |
Cigarette smoke enhances {beta}-defensin 2 expression in rat airways via nuclear factor-{kappa}B activation |
| Type de document : |
texte imprimé |
| Auteurs : |
L. Chen, Auteur ; P.P. Sun, Auteur ; T. Wang, Auteur ; X. Wang, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2010 |
| Collection : |
European Respiratory Journal num. 36 |
| Importance : |
p.638-645 |
| Présentation : |
graph., ill. |
| Langues : |
Anglais (eng) |
| Catégories : |
[NICO] chimie du tabac:fumée [NICO] étude [NICO] tabagisme:pathologie:pathologie respiratoire:bronchopneumopathie chronique obstructive
|
| Index. décimale : |
TA 3.2.2.1 Expérimentation |
| Résumé : |
β-defensin 2 (BD-2), an antimicrobial peptide, participates in airway defence. Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease. This study mainly aims to investigate the effect of CS on rat BD-2 (rBD-2) expression in rat airways. Rats were exposed to CS and treated with caffeic acid phenethyl ester (CAPE), a nuclear factor (NF)-κB inhibitor, or astragaloside IV (AS-IV), an active ingredient of Astragalus mongholicus. Besides the analysis of bronchoalveolar lavage fluid (BALF) and histological changes after CS exposure, rBD-2 expression was investigated with immunohistochemistry, reverse transcription PCR and ELISA. Total glutathione and nitric oxide (NO) levels in rat lungs were also detected. CS exposure markedly increased rBD-2 immunoreactivity, as well as rBD-2 mRNA and protein levels in rat airways, which were inhibited by CAPE treatment. Moreover, associated airway inflammation induced by CS was demonstrated by histological changes, increased cell counts and pro-inflammatory cytokines in BALF, and NF-κB activation and high levels of total glutathione and NO, which were all reversed by AS-IV in a dose-dependent fashion. In conclusion, CS exposure induces rBD-2 expression in rat airways via a NF-κB-dependent pathway, and AS-IV attenuates CS-induced airway inflammation due to its anti-inflammatory and antioxidant properties, at least partly through NF-κB inactivation. |
| En ligne : |
https://erj.ersjournals.com/content/36/3/638.long |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8075 |
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| Titre : |
Cigarette smoke extract reduces VEGF in primary human airway epithelial cells |
| Type de document : |
texte imprimé |
| Auteurs : |
J.V. Thaikoottathil, Auteur ; R.J. Martin, Auteur ; J. Zdunek, Auteur ; A. Weinberger, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2009 |
| Collection : |
European Respiratory Journal num. 33:4 |
| Importance : |
p.835-843 |
| Présentation : |
tab., tab., ill. |
| Langues : |
Anglais (eng) |
| Catégories : |
[NICO] étude [NICO] tabagisme:effet du tabac:effet sur l'immunité
|
| Index. décimale : |
TA 3.2.2.2.1 Interactions avec d'autres facteurs pathogènes |
| Résumé : |
Reduced vascular endothelial growth factor (VEGF) has been reported in bronchoalveolar lavage fluid and lungs of severe emphysema patients. Airway epithelial cells (AEC) are exposed to various environmental insults like cigarette smoke and bacterial infections, but their direct effect on VEGF production in well-differentiated primary human AEC remains unclear. The current authors determined the effect of cigarette smoke extract (CSE) alone and in combination with Mycoplasma pneumoniae (Mp) on VEGF production in well-differentiated primary normal human bronchial epithelial (NHBE) and small airway epithelial cells (SAEC) in air-liquid interface cultures. Secretion and expression of VEGF were determined by ELISA and real-time RT-PCR, respectively. Cell growth, apoptosis, extracellular signal-regulated kinase (ERK)1/2 and protein kinase (PK)C signalling pathways were evaluated to further dissect VEGF regulation under CSE treatment. CSE significantly reduced VEGF secretion in NHBE and SAEC. In SAEC, Mp alone significantly increased the VEGF, while the presence of CSE attenuated Mp-induced VEGF production. While ERK inhibitor reduced VEGF secretion only in NHBE, a PKC inhibitor significantly decreased VEGF secretion in both NHBE and SAEC. In conclusion, direct cigarette smoke extract exposure significantly reduced vascular endothelial growth factor production in well-differentiated primary human airway epithelial cells, in part through modifying extracellular signal-regulated kinase 1/2 and protein kinase C signalling pathways. |
| En ligne : |
https://erj.ersjournals.com/content/33/4/835.long |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8063 |
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| Titre : |
Cigarette smoke induces CXCL8 production by human neutrophils via activation of TLR9 receptor |
| Type de document : |
texte imprimé |
| Auteurs : |
E. Mortaz, Auteur ; I.M. Adcock, Auteur ; K. Ito, Auteur ; A.D. Kraneveld, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2010 |
| Collection : |
European Respiratory Journal num. 36 |
| Importance : |
p. 1143-1154 |
| Présentation : |
graph. |
| Langues : |
Anglais (eng) |
| Catégories : |
[NICO] chimie du tabac:fumée [NICO] étude [NICO] tabagisme:effet du tabac:effet sur l'immunité [NICO] tabagisme:pathologie:pathologie respiratoire:bronchopneumopathie chronique obstructive
|
| Index. décimale : |
TA 3.2.2.4 Pathologies respiratoires (sauf 3.2.2.1, 3.2.2.2, 3.2.2.3) |
| Résumé : |
Chronic obstructive pulmonary disease (COPD) is a major health problem and cigarette smoke is the main risk factor for the development of COPD. The characteristic changes in airway morphology, inflammatory cell infiltration and mediator expression in COPD may result from direct effects of cigarette smoke on airway cells. Toll-like receptors (TLRs) are key elements in pathogen recognition by the host immune system. Although TLRs have been intensely studied in innate immunity and infection, their critical role in noninfectious challenges has only recently emerged. Here we investigate whether cigarette smoke induces TLR9 signalling in human neutrophils. Human neutrophils were isolated from buffy coat and exposed to cigarette smoke extract. The production of CXC chemokine ligand (CXCL)8 was measured as a functional readout and the role of TLR9 signalling was investigated. Cigarette smoke extract induced CXCL8 release via TLR9 activation in neutrophils, which was confirmed in TLR9 stably transfected human embryonic kidney 293 cells. Moreover, cigarette smoke extract upregulated the expression of TLR9 and the upregulated expression was suppressed by N-acetylcysteine. TLR9 mediates cigarette smoke-induced release of CXCL8 and this may contribute to the accumulation of neutrophils and inflammation within the airways of smokers. |
| En ligne : |
https://erj.ersjournals.com/content/36/5/1143 |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8071 |
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Exemplaires (1)
|
| TA 005622 | TA 3.2.2.4 MOR C | Article/Périodique | Bibliothèque FARES | Tabac | Consultation sur place Exclu du prêt |
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| Titre : |
Diagnosis and treatment of nicotine dependence with emphasis on nicotine replacement therapy : a status report |
| Type de document : |
document électronique |
| Auteurs : |
David J.K. Balfour, Auteur ; Neal L. Benowitz, Auteur ; Karl Fagerström, Auteur ; M. Kunze, Auteur ; U. Keil, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2000 |
| Collection : |
European Respiratory Journal num. 21 |
| Importance : |
p.438-445 |
| Langues : |
Anglais (eng) |
| Catégories : |
[NICO] prévention:évaluation:évaluation du tabagisme:test de dépendance à la nicotine [NICO] sevrage tabagique:méthode de sevrage:méthode individuelle:approche pharmacologique:substitution nicotinique [NICO] tabagisme:dépendance tabagique:dépendance pharmacologique
|
| Index. décimale : |
TA 4.2.2.1 Dépendance à la nicotine |
| Résumé : |
Tobacco use is a global health care problem. Repetitive exposure to nicotine produces neuroadaptation resulting in nicotine dependence. Cigarette smoking is particularly addictive due to the repeated delivery of bolus doses of nicotine to the bloodstream. Although compulsive tobacco use is sustained by nicotine addiction, it is the toxic combustion products in tobacco smoke such as carbon monoxide and oxidant gases that adversely affect the cardiovascular system. Smoking cessation produces significant health benefits and is a very cost-effective intervention. Evidence that nicotine is the addictive component of tobacco provides the rationale for using nicotine replacement therapy to aid cessation. Nicotine replacement therapy doubles successful smoking cessation rates and evidence-based guidelines for the treatment of tobacco addiction recommend routine use of nicotine replacement therapy, particularly in heavily dependent smokers. Success rates of up to 40% can be achieved in specialist clinics. Despite early concerns regarding the safety of nicotine replacement therapy in smokers with heart disease, it is now clear that the health risks of using nicotine replacement therapy to assist such patients to stop, or significantly reduce, smoking far outweigh any treatment-related risks. |
| En ligne : |
https://doi.org/10.1053/euhj.1999.1949 |
| Format de la ressource électronique : |
Article en ligne |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=10348 |
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