Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral blood mononuclear cells (PBMCs) taken from 39 primary pulmonary MAC patients and 11 control subjects were stimulated in vitro with a protein antigen PPD-B derived from M. intracellulare. Then, the activated response of the peripheral blood lymphocytes (PBLs) and the production of interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) were measured. The 39 primary pulmonary MAC patients were divided into A and B groups the former patients satisfying all of the criteria for the diagnosis of nontuberculous mycobacterial disease proposed by the American Thoracic Society, with the exception of the bacteriologic criteria, and the latter, who satisfied all without exception. The 39 patients were also divided into 3 groups according to disease severity judged from chest CT features. Severity in grades 1, 2 and 3 groups were mild, moderate and severe, respectively. We compared the activated response of PBLs and the production of IFN-gamma and IL-10 by PBMCs of the control group and each patient group. The number of lymphocytes and activated T cells and the concentration of the IFN-gamma after stimulation with PPD-B were lower in each group of primary pulmonary MAC patients than in the control group. IL-10 was significantly higher in each group of primary pulmonary MAC patients than in the control group (36.6 +/- 11.8 pg/ml), and higher in group B (131.6 +/- 14.9) than in group A (81.1 +/- 31.5). There was no significant difference in the IL-10 concentration between the grade 1, 2 and 3 groups. These results suggested that the cell-mediated immunity of primary pulmonary MAC patients was suppressed as the disease progressed, and the increased production of IL-10 was related to this suppression.
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PMID:[Immunological studies in cases of pulmonary Mycobacterium avium complex infection without predisposing conditions]. 1506 79

Mycobacterium avium complex (MAC) is ubiquitous. It is found in various freshwater and saltwater sources around the world, including hot water pipes. Although the organism was identified in the 1890s, its potential to cause human disease was only recognized 50 years later. Only a minority of people exposed to the organism will acquire MAC lung disease, usually those with underlying lung disease or immunosuppression. MAC may, however, cause progressive parenchymal lung disease and bronchiectasis in patients without underlying lung disease, particularly in middle-aged and elderly women. Preliminary data suggest that the interferon-gamma pathways may be deficient in elderly women with MAC lung disease. Other groups of patients who are more likely to harbor MAC in their lungs include patients with a cystic fibrosis or an abnormal alpha(1)-antiproteinase gene and patients with certain chest wall abnormalities. Treatment results continue to be disappointing, and the mortality of patients with MAC lung disease remains high. A PubMed search identified 38 reports of the treatment of MAC lung disease. Apart from the British Thoracic Society study, the only published controlled investigation, the studies published since 1994 have included a macrolide, either clarithromycin or azithromycin, usually in combination with ethambutol and a rifamycin. If success is defined as eradication of the organism without relapse over a period of several years after treatment has been discontinued, the reported treatment success rate with the macrolide containing regimens is approximately 55%. The prolonged treatment period, side effects, and possibly reinfection rather than relapse are responsible for the high failure rate.
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PMID:Mycobacterium avium complex pulmonary disease in patients without HIV infection. 1588 75

The idiopathic interstitial pneumonias, especially the idiopathic pulmonary fibrosis (IPF), are life-threatening lung disorders, for which no effective treatment option exists. In view of IPF, the American Thoracic Society (ATS)/European Respiratory Society (ERS) consensus statement recommends a combined therapy with corticosteroids and azathioprine or cyclophosphamide, although data from conclusive clinical trials are yet missing and the recurrent clinical experience is that these drugs do not really help in IPF. Up to now, lung transplantation represents the last and only therapeutic option for IPF subjects. Based on new pathophysiological concepts of IPF, there are meanwhile a couple of different agents under preclinical and clinical assessment, and the increasing number of clinical trials ongoing in IPF raise the hope that an effective treatment comes into reach. The agents investigated and their targets are: acetylcysteine (reactive oxygen species [ROS] scavenging), interferon-gamma 1b (modulation of Th1/Th2 balance, direct antifibrotic effects), pirfenidone and GC 1008 (blockade of transforming growth factor-beta), FG 3019 (blockade of connective tissue growth factor), imatinib mesylate (blockade of platelet-derived growth factor), bosentan (blockade of endothelin), zileutin (blockade of leukotrienes), etanercept (blockade of tumor necrosis factor-alpha), heparin (alveolar anticoagulation). Hopefully, these new therapeutic strategies may help to improve prognosis of IPF in the future.
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PMID:[Pulmonary fibrosis--a therapeutic dilemma?]. 1660 87

We encountered five cases of pulmonary Mycobacterium kansasii (MK) disease for which the QuantiFERON-TB Gold (QFT-2G) test was useful as a supportive diagnostic method. Because none of these patients could expectorate sputum, we ultimately confirmed the clinical diagnosis of pulmonary MK disease using 6- to 8-week cultures of bronchoscopic specimens (bronchoalveolar lavage fluid) according to the guidelines for nontuberculous mycobacterial disease due to American Thoracic Society/Infectious Diseases Society of America. The tuberculin skin test showed positive responses in all cases, and the QFT-2G test showed positive response for ESAT-6 only or CFP-10 only antigens. After it was proved that the result of Mycobacterium tuberculosis (MTB)-nucleic acid amplification was negative and the result of the QFT-2G test was positive, we started treatment (isoniazid, rifampicin and ethambutol) for suspected pulmonary MK disease based on clinical findings in all cases. The clinical effect was good and the interferon-gamma response to MTB-specific antigen decreased with treatment for pulmonary MK disease. The QFT-2G test may be useful as a rapid supportive diagnostic method for pulmonary infection due to MK possessing the same MTB-specific antigen.
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PMID:Clinical usefulness of QuantiFERON TB-2G test for the early diagnosis of pulmonary Mycobacterium kansasii disease. 1946 92

We review the most interesting articles on respiratory infections published in the last trimester of 2009 and in 2010. Notable publications in bronchiectasis were the Guidelines of the British Thoracic Society, as well as several articles on the natural course of the process, the impact of exacerbations on the course of the disease, and treatment with inhaled antibiotics. Other notable publications were the SEPAR-SEIMC consensus document for the management of tuberculosis and articles on the use of interferon-gamma in the diagnosis of tuberculosis infection. The new recommendations of the Spanish Society of Pneumology and Thoracic Surgery on community-acquired pneumonia have recently been published. Equally important are studies on the viral etiology of community-acquired pneumonia, the impact of corticosteroid treatment in pneumonia, the duration of antibiotic therapy and preventive measures in both community-acquired and nosocomial pneumonia.
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PMID:[Hot topics in respiratory infections]. 2130 Feb 18