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Pirfenidone: significant treatment effects in idiopathic pulmonary fibrosis

Pirfenidone has been shown in three recently published trials to slow down the progression of the devastating interstitial lung disease, idiopathic pulmonary fibrosis (IPF). The precise mechanisms that initiate and perpetuate the histopathological process leading to lung fibrosis in IPF are still uncertain, but increased concentrations of reactive oxidative species and fibrogenetic factors have been observed in the pulmonary tissue of patients.

Although the exact mechanisms of its action are unknown, pirfenidone is a small molecule with antifibrotic and some hydroxyl scavenger properties that has recently been approved in Europe and elsewhere for the treatment of IPF. Along with the new ATS/ERS/JRS/ALAT 2011 statement for ‘Evidence Based Guidelines for Diagnosis and Management’...

Value of cytologic analysis of bronchial washings in lung cancer on the basis of bronchoscopic appearance

Conclusions:  The combination of forceps biopsy and washing cytologic analysis offers a better diagnostic yield than biopsy alone in diagnosing lung cancer. Both procedures should be performed during bronchoscopy even if no endobronchial lesion is present.

Significance of endothelial dysfunction in sleep‐related breathing disorder

The endothelium functions not only as a semi‐selective barrier between body tissue and circulation; it also plays an active role in the maintenance of a healthy vasculature. Endothelial dysfunction is increasingly found to play a pivotal role in the pathogenesis of atherosclerosis. Impaired endothelium‐dependent vasodilation, as a marker of endothelial dysfunction, predates and predicts cardiovascular disease.

Endothelial dysfunction is thought to result from oxidative stress, inflammatory gene activation and cytokine cascade as well as impairment of endothelial repair mechanisms.

In the context of sleep‐related breathing disorders, obstructive sleep apnea (OSA) is postulated to contribute independently to cardiovascular morbidity and mortality. Thus endothelial dysfunction i...

Les abcès et nécroses pulmonaires à germes banals : drainage ou chirurgie ?

Lung abscesses and necrotizing pneumonia are rare complications of community-acquired pneumonia since the advent of antibiotics. Their management leans first of all on the antibiotic treatment adapted on the informed germs. However, in 11 to 20% of the cases of lung abscesses, this treatment is insufficient, and drainage, either endoscopic or percutaneous, must be envisaged. In first intention, we shall go to less invasive techniques: endoscopic or percutaneous radio-controlled. In case of failure of these techniques, a percutaneous surgical drainage by minithoracotomy will be performed. In the necrotizing pneumonia, because of the joint obstruction of the bronchus and blood vessels corresponding to a lung segment, the systemic antibiotic treatment will be poor effective. In case of failure of this one we shall propose, a percutaneous surgical drainage, especially if the necrosis limits itself to a single lobe. The surgical treatment will be reserved: in the failures of the strategy of surgical drainage, in the necroses extending in several lobes.

Les abcès pulmonaires et les nécroses pulmonaires sont des complications peu fréquentes des pneumopathies aiguës à germes communautaires depuis l’avènement des antibiotiques. Leurs prises en charge s’appuient en premier lieu sur le traitement antibiotique adapté aux germes documentés. Cependant dans 11 à 20 % des cas d’abcès pulmonaires, ce traitement est insuffisant, et un drainage soit endoscopique, soit percutané doit être envisagé.

En première intention, on se dirigera vers une technique peu invasive : endoscopique ou percutanée radioguidée. En cas d’échec de ces deux techniques, le drainage chirurgical percutané par minithoracotomie sera réalisé. Dans les nécroses pulmonaires, du fait de l’obstruction conjointe de la bronche et des vaisseaux sanguins correspondant à un segment pulmonaire, le traitement antibiotique systémique sera peu efficace. On proposera donc en cas d’échec de celui-ci, un drainage chirurgical percutané, surtout si la nécrose se limite à un seul lobe. Le traitement chirurgical sera quant à lui réservé : aux échecs de la stratégie de drainage chirurgical, aux nécroses s’étendant à plusieurs lobes.

Le syndrome de Lady Windermere : données cliniques, bactériologiques et évolutives

Publication year: 2012
Source:Revue des Maladies Respiratoires, Volume 29, Issue 5

F. Bonnaud, S.-K. Adjoh, P. Wachinou, P. Abdo, F. Touraine, E. Vandeix, B. Melloni, A. Vergnenegre

Décrit par Reich et Johnson en 1992 [2], le syndrome de Lady Windermere comporte uniquement chez la femme non fumeuse, le plus souvent âgée de plus de 60ans, sans antécédents pulmonaires significatif, des dilatations de bronches intéressant typiquement le lobe moyen et la lingula surinfectées par une mycobactérie atypique (Mycobacterium avium dans les observations princeps). Parmi 17 infections respiratoires à mycobactéries atypiques, nous avons constaté au cours des 14 dernières années, sept fois l’existence de ce syndrome original. Toux, expectorations, contexte fébrile, altération de l’état général et parfois hémoptysies sont associées. Les critères diagnostics et thérapeutiques ont été définis par l’American Thoracic Society. L’hypothèse physiopathologique proposée par Reich et Johnson évoquaient une retenue volontaire de la toux, facilitant l’encombrement bronchique et la surinfection à mycobactéries atypiques. Il est actuellement plus vraisemblable d’imaginer : l’accentuation progressive de dilatations de bronches à minima de diagnostic tardif, la responsabilité de particularités morphologiques thoraciques fréquentes, une origine hormonale a été évoquée, la présence d’un déficit immunitaire commun variable, des désordres génétiques entraînant un dysfonctionnement des neutrophiles, enfin des formes hétérozygotes de mucoviscidose. Described by Reich and Johnson in 1992 [2], the Lady Windermere syndrome occurs exclusively in non-smoking women over the age of 60 years, without significant pre-existing pulmonary disease. It comprises bronchial dilatation, typically in the middle lobe and lingula, together with secondary infection by atypical mycobacteria (Mycobacterium avium in the first cases). Among the 17 cases of atypical mycobacterial infection that we have seen in the past 14 years, there were seven cases of this syndrome. It was associated with cough, sputum, sometimes haemoptysis, febrile episodes and deterioration of general health. The diagnostic criteria and treatment were defined by the American Thoracic Society. The pathophysiological hypothesis proposed by Reich and Johnson was that voluntary suppression of the cough led to congestion of the bronchi and secondary infection with atypical mycobacteria. Currently it is thought more likely that the following factors are involved: progressive increase in dilatation of small bronchi, delayed diagnosis, morphological abnormalities of the thorax, hormonal factors, immune deficiency, genetic neutrophil dysfunction, and even heterozygous forms of cystic fibrosis.




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