Recommandations pour l’oxygénothérapie chez l’enfant en situations aiguës et chroniques : évaluation du besoin, critères de mise en route, modalités de prescriptions et de surveillance
![]() |
Related Articles |
Adjuvant Surgical Treatment of Nontuberculous Mycobacterial Lung Disease.
Ann Thorac Surg. 2013 Apr 22;
Authors: Shiraishi Y, Katsuragi N, Kita H, Hyogotani A, Saito MH, Shimoda K
Abstract
BACKGROUND: According to the 2007 American Thoracic Society/Infectious Diseases Society of America statement on nontuberculous mycobacterial diseases, more evidence for the benefits of adjuvant nontuberculous mycobacterial lung disease surgical intervention is needed before its wide application can be recommended. METHODS: A retrospective review was conducted of 60 consecutive patients who met American Thoracic Society/Infectious Diseases Society of America diagnostic criteria and underwent pulmonary resection for localized nontuberculous mycobacterial lung disease between January 2007 and December 2011. All patients were receiving chemotherapy before resection. RESULTS: Included were 41 women (68%) and 19 men (32%), with a median age of 50 years (range, 20 to 72 years). Of these, 55 patients (92%) had Mycobacterium avium complex disease. Bronchiectatic disease was noted in 29 patients, cavitary disease in 25, both in 4, and nodular disease in 2. The indications for resection were a poor response to drug therapy in 52 patients, hemoptysis in 6, and a secondary infection in 2. Sixty-five pulmonary resections were performed: 1 pneumonectomy, 3 bilobectomies, 39 lobectomies, 17 segmentectomies, 3 lobectomies plus segmentectomies, and 2 wedge resections. There were no operative deaths, and all patients attained sputum-negative status postoperatively. Eleven postoperative complications occurred in 8 patients (12%); relapse was observed in only 2 (3%). CONCLUSIONS: Pulmonary resection combined with chemotherapy is safe, with favorable treatment outcomes, for patients with localized nontuberculous mycobacterial lung disease. Our results support the liberal use of operations for nontuberculous mycobacterial lung disease whenever indicated.
PMID: 23618520 [PubMed - as supplied by publisher]
![]() |
Related Articles |
Glucocorticoids are highly effective therapies for a range of inflammatory diseases. Advances in the understanding of the diverse molecular mechanisms underpinning glucocorticoid action suggest that anti-inflammatory molecules with reduced side-effect liabilities can be discovered. Here we set out to explore whether modification of the 17α position of the steroid nucleus could generate molecules with a unique pharmacological profile, and to determine whether such molecules would retain anti-inflammatory activity.
EXPERIMENTAL APPROACH: The pharmacological properties of GW870086 were compared to fluticasone propionate (FP) using a range of cellular and in vivo model systems, including extensive gene expression profiling.
KEY RESULTS: GW870086 repressed inflammatory cytokine release from lung epithelial cells in a similar manner to FP, but antagonised the effect of dexamethasone on MMTV driven reporter gene transactivation. GW870086 had a strong effect on the expression of some glucocorticoid regulated genes (such as COX-2), while having minimal impact on the expression of other known target genes (such as SGK). GW870086 retained the ability to strengthen tight junctions in epithelial cell culture, but unlike FP was unable to protect the culture from elastase mediated damage. In murine models of irritant-induced contact dermatitis and ovalbumin-induced allergic inflammation models, GW870086 showed comparable anti-inflammatory efficacy to FP.
CONCLUSIONS AND IMPLICATIONS: GW870086 is a potent anti-inflammatory compound with a unique ability to regulate only a subset of those genes that are normally affected by classical glucocorticoids. It has the potential to become a new topical steroid with a different safety profile to existing therapies.
Although the pulmonary capillaries were discovered in 1661, the ultrastructure of the wall was not elucidated until 60 years ago. Electron micrographs then showed that only 0.2 µm of tissue separated the capillary endothelium from the alveolar space over much of the area.
In retrospect this vanishingly small protective layer should have alerted physiologists to the potential fragility of the capillaries but this was not appreciated until almost 40 years later. This predicament is unique to pulmonary capillaries. No other capillaries in the body are shielded from the outside environment by such a minute amount of tissue. Reasons why the fragility of the capillaries was not recognized earlier include an inappropriate comparison with the properties of systemic capillaries, the mistaken view that the pulmonary capillary pressure is always low, and a misleading use of the Laplace equation. Evidence for the fragility comes from physiological, pathological and laboratory observations. As expected from evolutionary considerations, the fragility only becomes evident in the normal lung under exceptional conditions. These include elite human athletes at maximal exercise, and animals that have developed the capacity for extreme aerobic activity. However lung and heart diseases frequently cause capillary disruption. Remodeling of pulmonary capillaries occurs in humans in whom the capillary pressure rises over a long period. Neonatal capillaries are extremely fragile presumably because they have never been exposed to increased transmural pressures.
The capillaries conform to the general biological rule that tissue adapts its structure to carry out its required function.