Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the early molecular events of oxidant-induced pulmonary fibrosis, rats were continuously exposed to 0.4 ppm ozone and 7 ppm nitrogen dioxide. The early responses to the combined gases could be divided into three phases. Acute pulmonary inflammation indicated by an increase in pulmonary edema as well as an influx of neutrophils into the airspaces first occurred on days 1 to 3 of the exposure. The pulmonary inflammation was reversed by day 8, and no biochemical or morphologic aspects of tissue responses were detected from days 15 to 45, suggesting that rats adapted to the stimuli during that period. Pulmonary fibrosis could be detected by an increase in the biomarker of lung collagen content at day 60 and by histopathologic evaluation by day 90. Enhanced expression of macrophage inflammatory protein-2 was observed only at day 1, whereas the pulmonary expression of transforming growth factor-beta was upregulated on days 60 and 90 of the exposure. Macrophage expressions of interleukin-1beta and interleukin-6 were enhanced during acute pulmonary inflammation; however, macrophage expression of tumor necrosis factor-alpha was elevated at both day 1 and days 60-90. Activation of nuclear factor-kappa B and increased expression of thioredoxin in the lungs was also observed at day 1 and days 60-90. The expression of antioxidant enzymes, such as manganeous superoxide dismutase and glutathione peroxidase, was not altered during exposure. These results indicate that macrophage activation and the expression of macrophage-derived cytokines may play an important role in the early pulmonary responses against the combined gases.
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PMID:Early molecular and cellular events of oxidant-induced pulmonary fibrosis in rats. 1098 8

Physical examination of the pulmonary system includes inspection, auscultation, percussion, and palpation. By integrating these findings, it is often possible to diagnose and differentiate pulmonary edema, pleural effusion, pneumothorax, pulmonary fibrosis, and tracheal collapse. The veterinarian can use the physical examination optimally by initially performing examinations with those who are experienced with the methods and with an understanding of the relatively simple laws of physiology and physics governing transmission of sounds from the patient's lung.
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PMID:Physical examination of the pulmonary system. 1122 76

Noncardiogenic pulmonary edema (NCPE) is a rare and less well-recognizable pulmonotoxic syndrome of anticancer therapy than pneumonitis/fibrosis. NCPE is a clinical syndrome characterized by simultaneous presence of severe hypoxemia, bilateral alveolar infiltrates on chest radiograph, and no evidence of left atrial hypertension/congestive heart failure. The diagnosis of drug-related NCPE relies upon documented exclusion of any infectious, metabolic, or cancer-related causes. The time proximity to therapy with drugs that are known to precipitate NCPE, any preceding episodes of flu-like symptoms during previous chemotherapy courses and possible response to corticosteroids may further support such a diagnosis. Cancer therapeutic agents clearly associated with NCPE are cytarabine, gemcitabine, and interleukin-2, as well as all-trans retinoic acid in acute promyelocytic leukemia patients, while a few other compounds have rarely or occasionally been implicated. The pathophysiology of lung injury in drug-induced NCPE remains unclear. There are indications suggesting that both a direct cytotoxic insult to the lung epithelial cells and induction of a cytokine-triggered inflammatory response may be involved in its pathogenesis. By distinction to drug-induced pulmonary pneumonitis that may lead to permanent pulmonary fibrosis, NCPE if not fatal, can be reversed upon prompt recognition, following immediate discontinuation of the offensive drug and start of intensive supportive treatment and intravenous corticosteroids.
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PMID:Noncardiogenic pulmonary edema: an unusual and serious complication of anticancer therapy. 1130 27

Cobalt alone and in combination with tungsten carbide known as hard metal is capable of causing lung damage. This may vary from development of pulmonary oedema to asthma and fibrosing alveolitis. We report a case of giant cell interstitial pneumonitis caused by exposure to cobalt dust which was not identified as the etiological agent initially and hence led to progression of the disease. The patient subsequently improved following cessation of exposure and treatment with oral corticosteriods, thereby stressing the importance of occupational history in all cases of interstitial pulmonary fibrosis.
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PMID:Giant cell pneumonitis induced by cobalt. 1137 May 7

Acute respiratory distress syndrome (ARDS) is an acute form of severe alveolar-capillary injury that evolves after a direct or indirect lung insult. It begins as noncardiogenic pulmonary edema and develops into a neutrophilic alveolitis, and, later, pulmonary fibrosis. Mortality remains high among children with ARDS, particularly when serious underlying conditions co-exist, sepsis occurs, and when there is multi-organ failure. Lung function improves with time among survivors, but pulmonary fibrosis may persist. Advances in the care of children with ARDS include the use of lung-protective ventilator strategies, permissive hypercapnia, inhaled nitric oxide, high-frequency ventilation, and extra-corporeal life support. These approaches reduce ventilator-associated lung injury and may improve survival when used in combination with one another. Interventions that reduce alveolar inflammation, enhance alveolar fluid removal, and reduce pulmonary fibrosis will further improve survival and recovery from ARDS in the future.
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PMID:Current concepts in adult respiratory distress syndrome in children. 1138 62

14-membered ring macrolides have been reported to have anti-inflammatory effects and to decrease neutrophil infiltration into the airways in chronic lower respiratory tract diseases. This study investigated the potential inhibitory effects of macrolide antibiotics on bleomycin-induced acute lung injury. Four drugs were studied: two 14-membered ring macrolides, clarithromycin (CAM) and roxithromycin (RXM); a 15-membered ring macrolide, azithromycin (AZM); and a 16-membered ring macrolide, josamycin (JM). Their effects were compared with macrolide untreated, pretreated, and post-treated groups. An acute lung injury was inhibited by pretreatment with CAM or RXM, which significantly ameliorated the bleomycin-induced increases in the total cell and neutrophil counts in bronchoalveolar lavage (BAL) fluids and the wet lung weight. The pretreatment with CAM or RXM also suppressed inflammatory cell infiltration and interstitial lung edema in the histopathological study. These inhibitory effects were associated with a decreased KC concentration in the BAL fluid and a decreased number of apoptotic cells in the lungs. Posttreatment with CAM or RXM had no marked inhibitory effects. Pretreatment with AZM was much less effective, and JM showed no inhibitory effects. These findings suggest that 14-membered ring macrolides have different effects on inflammatory lung disease than 15- and 16-membered ring macrolides and may be therapeutic agents for acute lung injury and pulmonary fibrosis.
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PMID:Inhibitory effects of 14-membered ring macrolide antibiotics on bleomycin-induced acute lung injury. 1218 59

Signals from integrins are now known to play critical roles in virtually every aspect of the behavior of epithelial cells, including survival, proliferation, maintenance of polarity, secretory differentiation, and malignant transformation. The cells that line the conducting airways and alveoli of the lung, like most surface epithelia, simultaneously express multiple members of the integrin family, including several with broadly overlapping ligand binding specificities. Although multiple integrins on airway epithelial cells may support adhesion to the same ligands, the functional roles of each integrin that has been examined in detail are quite distinct. Findings from mice expressing null mutations of some of these integrins have identified roles for epithelial cells and epithelial integrins in lung development and in the regulation of lung inflammation, macrophage protease expression, pulmonary fibrosis, and the pulmonary edema that follows acute lung injury. Epithelial integrins are thus attractive targets for intervention in a number of common lung disorders.
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PMID:Functions of pulmonary epithelial integrins: from development to disease. 1284 6

It presents a 59 years old woman with atypical symptoms, which orientated the diagnostic thinking during one year to a reccurrent pneumonitis, bronchial asthma, colagenosis, interstitial pulmonary fibrosis and so on. The appearance of pulmonary edema determined a couple of cardiologic exams which came to obiectivate as the main cause, the existence of a left atrial mixoma who was invaginated in left mitral cusp. Surgical intervention permitted not only specific determination of histological type of tumor, but lead to healing of the patient. It is a discussion over epidemiology, clinical areas of manifestation and methods of diagnostic of atrial tumors.
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PMID:[Atrial myxoma: a challenge for the pneumologist]. 1470 3

All deaths occurring in patients with community-acquired pneumonia in risk classes I-III were reviewed as a quality-of-care measure. The immediate and underlying causes of death were classified according to the World Health Organization protocol. Eleven (1.8%) of the 608 low-risk patients died. Three of the patients did not have pneumonia, one of whom was admitted with atypical pulmonary oedema due to stenosis of a prosthetic heart valve. Failure to include chronic lung disease in the severity-of-illness scoring system resulted in misclassification of seven patients. The most common underlying causes of death were pulmonary fibrosis at 27%, chronic obstructive lung disease at 18% and cancer at 27%. Respiratory failure was the immediate cause of death in 64% of patients, cardiac causes in 27%, and pneumonia in 9%. To conclude, the review of deaths in patients at low risk for mortality is useful for monitoring the quality of care received by patients who require admission for the treatment of community-acquired pneumonia, and that the pneumonia-specific severity-of-illness scoring system results in misclassification of patients with chronic obstructive lung disease and pulmonary fibrosis.
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PMID:Deaths in risk classes I-III: a measure of quality of care in patients hospitalised with CAP? 1473 40

Pulmonary fibrosis is a common consequence of numerous pulmonary diseases. The current therapeutic approaches for this condition are unsatisfactory. Feitai, a composite formula consisting of several herbs, is used in China as a folk remedy for treating patients with pulmonary tuberculosis. In this study, we extensively investigate the effects and mechanisms of Feitai on bleomycin (BLM)-induced pulmonary fibrosis in rats. One hundred and twenty male Sprague-Dawley rats were randomly divided into four groups, referred to as the saline-water, saline-Feitai, BLM-water, and BLM-Feitai groups. Following a single instillation of BLM (5 mg/kg) or saline, rats were orally administered Feitai at a dose of 3 g/kg body weight or sterilized distilled water once daily. Rats were killed at 7, 14, or 28 d post-BLM. Inflammatory cell count, protein concentration, and lactate dehydrogenase activity in bronchoalveolar lavage fluid were measured, and myeloperoxidase activity and lipid peroxide content in lung homogenates were analyzed. Treatment with Feitai inhibited lung fibrotic progression induced by BLM, as indicated by the decrease in lung hydroproline content and lung fibrosis score at 28 d post-BLM. This was accompanied by significant amelioration of BLM-induced body weight loss, lung edema, and inflammatory response during the development of lung injury in the acute phase. The results strongly indicate the beneficial effects of Feitai in protecting against BLM-induced pulmonary fibrosis. Furthermore, the inflammatory response and lipid peroxidation were inhibited by Feitai, suggesting that the effect of this formula on BLM-induced lung injury and fibrosis is associated with antiinflammatory and antioxidant properties.
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PMID:Feitai attenuates bleomycin-induced pulmonary fibrosis in rats. 1513 36


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