Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bronchography is essential for evaluation of morphological changes in the bronchial tree. However, conventional bronchography using Propyliodone (Dionosil) is extremely invasive, especially to those with pulmonary infections. In the present study, we developed a new less invasive method of bronchography with the aid of digital subtraction technique (DSBG), and evaluated its clinical benefits. Bronchography was performed by injecting contrast medium (Iopamidol: Iopamiron 300) via the lumen of the bronchoscope (Olympus Type 20), and image processing of the respiratory tract was performed using digital subtraction technique. From 1991 to 1992, DSBG was performed in 15 cases (8 bronchiectasis, 1 diffuse panbronchiolitis, 1 lung cancer, 1 pulmonary emphysema, and 4 others). DSBG clearly demonstrated the morphological changes of large and segmental bronchial lesions in cases of bronchiectasis and lung cancer, as well as conventional bronchography using Dionosil. In addition, it was possible to image the morphological changes of bronchiolar lesions in diffuse panbronchiolitis and pulmonary emphysema to the same detail as obtained using classical selective alveolo-bronchography (SAB). Since DSBG can provide enhanced images the bronchial tree without being affected by cardiac and respiratory movements, we could obtain detailed information on bronchial and/or bronchiolar lesions. With respect to side effects, Iopamiron was quickly drained and/or absorbed within 2 hours after injection. Pulmonary infection and bronchial bleeding, which are well known primary complications of classical bronchography using Dionosil, were not observed. We conclude that 1) DSBG is useful new technique for examining morphological changes of the respiratory tract, and 2) DSBG is less invasive than conventional bronchography.
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PMID:[A new technique for evaluating the respiratory tract--digital subtraction bronchography (DSBG)]. 846 18

Infection with Histoplasma capsulatum occurs commonly in areas in the Midwestern United States and Central America, but symptomatic disease requiring medical care is manifest in very few patients. The extent of disease depends on the number of conidia inhaled and the function of the host's cellular immune system. Pulmonary infection is the primary manifestation of histoplasmosis, varying from mild pneumonitis to severe acute respiratory distress syndrome. In those with emphysema, a chronic progressive form of histoplasmosis can ensue. Dissemination of H. capsulatum within macrophages is common and becomes symptomatic primarily in patients with defects in cellular immunity. The spectrum of disseminated infection includes acute, severe, life-threatening sepsis and chronic, slowly progressive infection. Diagnostic accuracy has improved greatly with the use of an assay for Histoplasma antigen in the urine; serology remains useful for certain forms of histoplasmosis, and culture is the ultimate confirming diagnostic test. Classically, histoplasmosis has been treated with long courses of amphotericin B. Today, amphotericin B is rarely used except for severe infection and then only for a few weeks, followed by azole therapy. Itraconazole is the azole of choice following initial amphotericin B treatment and for primary treatment of mild to moderate histoplasmosis.
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PMID:Histoplasmosis: a clinical and laboratory update. 1722 25

Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow obstruction and lung destruction with airspace enlargement. In addition to cigarette smoking, respiratory pathogens play a role in pathogenesis, but specific organisms are not always identified. Recent reports demonstrate associations between the detection of Pneumocystis jirovecii DNA in lung specimens or respiratory secretions and the presence of emphysema in COPD patients. Additionally, human immunodeficiency virus-infected individuals who smoke cigarettes develop early emphysema, but a role for P. jirovecii in pathogenesis remains speculative. We developed a new experimental model using immunocompetent mice to test the interaction of cigarette smoke exposure and environmentally acquired Pneumocystis murina infection in vivo. We hypothesized that cigarette smoke and P. murina would interact to cause increases in total lung capacity, airspace enlargement, and pulmonary inflammation. We found that exposure to cigarette smoke significantly increases the lung organism burden of P. murina. Pulmonary infection with P. murina, combined with cigarette smoke exposure, results in changes in pulmonary function and airspace enlargement characteristic of pulmonary emphysema. P. murina and cigarette smoke exposure interact to cause increased lung inflammatory cell accumulation. These findings establish a novel animal model system to explore the role of Pneumocystis species in the pathogenesis of COPD.
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PMID:Pneumocystis murina infection and cigarette smoke exposure interact to cause increased organism burden, development of airspace enlargement, and pulmonary inflammation in mice. 1849 Apr 62