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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We report a case of neurogenic pulmonary edema associated with epileptic seizure. A 36-year-old woman had had several episodes of fainting and postictal respiratory failure, and since July 1998 had been admitted to a nearby hospital three times. On October 12, 1999, she was again admitted to a nearby hospital with the same symptom, and was transferred from that hospital to ours for evaluation of the recurrent respiratory disorder. Low-grade fever, mild leukocytosis, hypoxemia and bilateral diffuse opacities were observed as previously on chest radiography, and improved within several days without any specific therapy. The negative C reactive protein level, normal cardiac function and faintly bloody bronchoalveolar lavage fluid were also observed. There was no evidence of aspiration pneumonia, infectious disease, or underlying heart or lung disease. Electroencephalography showed spikes in accord with the left temporal lobe, and the cause of the patient's fainting was thought to be temporal lobe epilepsy. After all other causes had been excluded, this case was diagnosed as neurogenic pulmonary edema associated with epileptic seizure. Only about 40 cases of the postictal pulmonary edema have been reported since 1908, and the pathophysiologic mechanism of this condition is still unknown. Neurogenic pulmonary edema associated with epileptic seizure is rare, but the importance of awareness of this condition needs to be emphasized because it is suspected to be the cause of unexpected sudden death in epileptics. We should consider the disease as important in the differential diagnosis of acute respiratory failure associated with epilepsy.
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PMID:[A case of neurogenic pulmonary edema associated with epileptic seizure]. 1264 14

An unilateral or predominantly lobar pulmonary edema is an unusual clinical or radiological finding, often misdiagnosed as one of the more common causes of focal lung disease. We report 2 cases of a regional pulmonary edema caused by the acute onset of a severe mitral insufficiency after the rupture of chordae tendinae resulting in a prolaps of the posterior mitral leaflet. In both cases the regional pulmonary edema was initially misdiagnosed as a pneumonic infiltration, which delayed the cardiological diagnostical procedures and the surgical intervention. The mechanism of the regional edema is an excentric recurgitation jet into the left atrium, which is usually directed to the orifice of the right upper lobe pulmonary vein which increases the hydrostatic vascular pressure in the corresponding lung segment. For the confirmation of the diagnosis, transesophageal echogradiographic is helpful in documenting the direction of the regurgitant flow and detecting differential gradients between the right and left pulmonary venous systems. The pulmonary infiltrations, which persisted for several weeks, disappeared within a few days after surgical mitral-valve-reconstruction in both cases.
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PMID:[Regional lung edema in acute mitral valve insufficiency following chordae tendineae rupture with prolapse of the posterior mitral valve leaflet]. 1265 36

Ticlopidine-induced lung disease is rare. A 52-year-old man with acute myocardial infarction developed respiratory distress 2 days after receiving ticlopidine for coronary artery stenting. The dosage of ticlopidine was 500 mg orally followed by maintenance of 250 mg twice daily. Chest radiography revealed bilateral haziness predominantly over upper lung fields. He did not respond to treatment for suspected cardiogenic lung edema and mechanical ventilation was instituted. Open lung biopsy documented diffuse alveolar damage. After discontinuing ticlopidine and treatment with systemic corticosteroid, his pulmonary condition improved gradually. Within 2 weeks, the patient was successfully weaned from the ventilator. Although rare, diffuse alveolar damage is a potential side effect of ticlopidine treatment and should be included in the differential diagnoses of heart failure patients taking ticlopidine who respond poorly to optimal therapy.
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PMID:Diffuse alveolar damage associated with ticlopidine use: a case report. 1283 91

Cardiac abnormalities has been receiving increased attention in patients with systemic lupus erythematosus (SLE). Cardiovascular system involvement has been found to have a substantial effect on mortality and morbidity in patients with SLE [1]. Recent diagnostic methods using echocardiography examination have allowed the delineation of cardiac manifestations such as myocarditis and myocardial dysfunction, valvular disease, pericardial disease or pulmonary hypertension. A report of two cases is presented: 23-year-old man with acute myocarditis with left ventricular failure and pulmonary oedema as a initial presentation of active SLE, and 51-year-old woman with SLE, antiphospholipid antibodies, with history of cerebral embolic infarction, TIA and venous thrombosis and with mitral valvular dysfunction in course of nonbacterial thrombotic endocarditis. Pulmonary hypertension has been recognised in both patients probably as a result of vasculaopathy and intimal proliferation, vasculitis, thromboembolic disease or parenchymal lung disease in SLE. Recent advances in diagnosis and treatment have substantially improved the prognosis of patients with systemic lupus erythematosus and cardiovascular system involvement [2].
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PMID:[Cardiovascular involvement in systemic lupus erythematosus: report of two cases]. 1287 81

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

We report here a case of a 3-week-old infant with a lung disease of unknown origin who underwent diagnostic fiber-optic bronchoscopy. During the procedure, she developed unilateral pulmonary edema. Factors that contributed to this complication are discussed along with means to reduce its occurrence.
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PMID:Unilateral negative-pressure pulmonary edema in an infant during bronchoscopy. 1512 95

Acute respiratory failure is a common complication of drug abuse. It is more likely to develop in the setting of chronic lung disease or debility in those with limited respiratory reserve. Drugs may acutely precipitate respiratory failure by compromising respiratory pump function and/or by causing pulmonary pathology. Polysubstance overdoses are common, and clinicians should anticipate complications related to multiple drugs. Impairment of respiratory pump function may develop from central nervous system (CNS) depression (suppression of the medulla oblongata, stroke or seizures) or respiratory muscle fatigue (increased respiratory workload, metabolic acidosis). Drug-related respiratory pathology may result from parenchymal (aspiration-related events, pulmonary edema, hemorrhage, pneumothorax, infectious and non-infectious pneumonitides), airway (bronchospasm and hemorrhage), or pulmonary vascular insults (endovascular infections, hemorrhage, and vasoconstrictive events). Alcohol, cocaine, amphetamines, opiates, and benzodiazepines are the most commonly abused drugs that may induce events leading to acute respiratory failure. While decontamination and aggressive supportive measures are indicated, specific therapies to correct seizures, metabolic acidosis, pneumothorax, infections, bronchospasm, and agitation should be considered. Drug-related respiratory failure when due to CNS depression alone may portend well, but in patients with drug-related significant pulmonary pathology, a protracted course of illness may be anticipated.
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PMID:Acute respiratory failure from abused substances. 1529 19

Seven years ago, Pediatric Cardiology published the first version of a review article outlining the various medications used in the field of heart diseases in children. This article is an update and expansion to what we have previously presented. Therapeutic intervention, both surgical and through cardiac catheterization, has enabled cure and palliation of an increasingly expanding spectrum of diseases at earlier ages and with more complex lesions. Refinement of these procedures includes more advanced tools as well as the support of an expanding armament of pharmacopoeia used to stabilize and support patients before, during, and after such procedures. In addition to updating previously published data regarding inotropes, antiarrhythmics, vasodilators, diuretics, sedatives, and analgesics as well as a variety of miscellaneous medications, this article describes the use of pulmonary medications frequently needed in patients with congestive heart failure, pulmonary edema, and chronic lung disease. We also describe the difficult management of withdrawal as a result of use of sedatives and analgesics. The most recent recommendation for subacute bacterial endocarditis prophylactic antibiotic regimens is also described.
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PMID:The pediatric cardiology pharmacopoeia: 2004 update. 1554 23

Pulmonary veins have been seen primarily as conduit vessels; however, over the past two decades, a large amount of evidence has accumulated to indicate that pulmonary veins can exhibit substantial vasoactivity. In this review, the role of veins in regulation of the pulmonary circulation, particularly during the perinatal period and under certain pathophysiological conditions, is discussed. In the fetus, pulmonary veins contribute a significant fraction to total pulmonary vascular resistance. At birth, the veins as well as the arteries relax in response to endothelium-derived nitric oxide and dilator prostaglandins, thereby assisting in the fall in pulmonary vascular resistance. These effects are oxygen dependent and modulated by cGMP-dependent protein kinase. Under chronic hypoxic conditions, pulmonary veins undergo remodeling and demonstrate substantial constriction and hypertrophy. In a number of species, including the human, pulmonary veins are also the primary sites of action of certain vasoconstrictors such as endothelin and thromboxane. In various pathological conditions, there is an increased synthesis of these vasoactive agents that may lead to pulmonary venous constriction, increased microvascular pressures for fluid filtration, and formation of pulmonary edema. In conclusion, the significant role of veins in regulation of the pulmonary circulation needs to be appreciated to better prevent, diagnose, and treat lung disease.
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PMID:Role of veins in regulation of pulmonary circulation. 1564 May 20


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