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)

Methotrexate may cause pulmonary side effects. Two cases of methotrexate-induced fibrosing alveolitis are reported. One of the patients died from perforated gastric ulcer, the other was successfully treated with systemic steroids. The pulmonary side effects of methotrexate are reviewed. The most common clinical manifestation is fibrosing alveolitis. Pulmonary fibrosis and acute, non-cardiogenic pulmonary oedema are rare.
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PMID:[Methotrexate induced pulmonary disease]. 226 58

Between February 1988 and December 1989, 15 combined heart-lung, 2 double lung and 5 single lung transplants were performed at our institution for end stage lung disease. The indication for heart-lung transplantation was primary lung disease with associated secondary heart failure in 11 cases, diffuse pulmonary disease with extensive adenopathy of the hilum in 2 cases and profuse and antibiotic-resistant tracheobronchial infection due to Pseudomonas in 2 cases. A double lung transplant was performed in 2 patients with hypertensive emphysema. The indication for a single lung transplantation was emphysema in 2 cases and pulmonary fibrosis in 3 cases; in this last indication, transplantation should be performed on the right side with a slight lengthening of the main bronchus to avoid the side-effects of mediastinal shift. There were 2 early deaths, 7 secondary deaths (from the 2nd to the 5th month) due to viral or bacterial infectious complications, and 1 late death in the 7th month (infection due to a syncitial virus). All 12 surviving patients have an excellent functional result; the size of the tracheal or bronchial anastomosis ranges from 85% to 100% of normal. From this experience, we conclude that specificity and severity of lung hazards are mainly related to bronchial infection, dependence on steroids and pleural adhesions. Moreover, posttransplant pulmonary oedema, mucociliary dysfunction and the differential diagnosis between rejection and infection require careful endobronchial suction and periodical sampling.
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PMID:Lung and heart-lung transplantation for end-stage lung disease. The Bordeaux Lung and Heart-Lung Transplant Group. 236 Oct 20

To know the pathogenesis of the lung fibrosis after ARDS, we investigated the role of PMN-elastase after endotoxin-induced pulmonary edema in awake sheep with chronic lung lymph fistulas. The permeability of the pulmonary circulation increased 2 hours after endotoxin injection. Four hours after endotoxin injection, WBC migrated to the lung interstitium and the number of WBC in BALF increased. Endotoxin increased PMN-elastase in plasma and lymph whereas the level of alpha-1-protease inhibitor (alpha-1-PI) did not change. The activity of alpha-1-PI measured by trypsin inhibitory capacity was zero in the exudative phase. The level of PMN-elastase in lymph was significantly higher 1 week after endotoxin injection than baseline levels. Histologically, pulmonary fibrosis developed 1 week after endotoxin injection. These results suggest that inflammatory mediators released from PMN play an important part in progress to the fibrotic phase after ARDS.
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PMID:[Pulmonary fibrosis after endotoxin-induced permeability edema]. 279 51

A 71-year-old man with a long-standing history of rheumatoid arthritis required methotrexate treatment since 1986, with a total dose of 210 mg. In April 1987, before arthroplastic surgery, methotrexate was discontinued. Four weeks later a syndrome of fever, dry cough, shortness of breath, and diffuse air-space consolidations on the chest radiograph evolved. An antibiotic therapy had no beneficial effect, and a bronchoscopy yielded no pathogens. An open lung biopsy led to the diagnosis of methotrexate-induced pneumonitis. This is the first report of a case where methotrexate-induced pneumonitis developed several weeks after cessation of the treatment. Methotrexate can cause four types of pulmonary adverse reactions: pneumonitis, pulmonary edema, pulmonary fibrosis, and pleuritis. Possible pathogenetic mechanisms, symptoms, treatment, and prognosis are discussed.
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PMID:Methotrexate-induced pneumonitis: appearance four weeks after discontinuation of treatment. 280 69

The radiologic appearance of atypical cardiogenic pulmonary edema (ACPE) is presented in 10 cases admitted from 1983 to 1985, with age ranges from 74 to 89, and with diagnosis of ischemic heart disease, with myocardial infarction in 50% of them. Clinically they had asthenia, adynamia and anorexia in 80%, cough and weight loss in 50%. All of them had tachycardia, pulmonary rales and 50% pericardial rub. ECG showed in 80% anterior subepicardial ischemia, 60% posteroinferior subepicardial ischemia, 60% bifascicular block, and 50% left anterior fascicular block. Chest films were interpreted at first as pulmonary fibrosis in 90% of the cases with superior lobe involvement in 50%. Heart enlargement was present in 50%. A chronic lung disease was disclosed on clinical and pulmonary physiological grounds. It is concluded that asthenia, adynamia and anorexia were atypical manifestations of heart failure in the elderly. Silent myocardial infarction was observed in half of our patients and it was complicated with pericardial involvement in 50%. Irregular distribution of fluids in pulmonary edema was attributed to anatomic changes in elder lung. These atypical behaviour of pulmonary edema, has been misinterpreted on radiologic basis with pulmonary infection, tumours, metastasis or fibrosis. Those radiologic changes disappeared or improved in 72 hrs. with treatment of left ventricular failure.
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PMID:[Radiologic characteristics of cardiogenic pulmonary edema in the elderly]. 296 66

Noncardiogenic pulmonary edema is an uncommon but serious complication of falciparum malaria. A case of fatal noncardiogenic pulmonary edema complicating falciparum malaria is presented in which the unfavorable outcome resulted from rapidly developing pulmonary fibrosis, documented through open-lung biopsy. Possible mechanisms of lung injury in falciparum malaria include: impaired perfusion and tissue hypoxia in the pulmonary microcirculation caused by reduced effective circulating volume; abnormal autonomic effects on the lung resulting from reduced blood flow in the central nervous system; immunologic injury to alveolar-capillary structures; and morphologic changes in the surface membranes of infected erythrocytes leading to sequestration of parasitized erythrocytes in vascular beds and pulmonary capillary damage. That pulmonary involvement in falciparum malaria is usually associated with high-grade parasitemia, concurrent cerebral involvement, and delay in institution of antimalarial therapy emphasizes the importance of early diagnosis and treatment.
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PMID:Noncardiogenic pulmonary edema and pulmonary fibrosis in falciparum malaria. 354 68

In patients with subacute toxic reactions from paraquat poisoning (death within 11 to 41 days), the extent of lipid peroxidation, expressed as serum malondialdehyde level, was 2.7-fold higher (12.33 +/- 4.42 nmole/mL) before pulmonary fibrosis than that in normal controls (4.55 +/- 1.23 nmole/mL). The extent of lipid peroxidation in patients with acute toxic reactions (death within one to three days) was not elevated; these patients died of pulmonary edema and hemorrhage (acute respiratory distress), liver failure, renal failure, and adrenal necrosis. Remarkable high levels of paraquat (greater than 5 mg/L) were found in the urine, serum, and tissues of patients with acute toxic reactions; a small amount of paraquat was found in the serum or urine of patients with subacute toxic reactions five to 11 days after ingestion. Patients who survived had no elevation in lipid peroxidation. Administration of vitamin E (100 to 4,000 mg/day from the first hospital day) had no effect on survival.
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PMID:Further studies of lipid peroxidation in human paraquat poisoning. 396 49

Three patients unconscious when rescued from drowning had radiographic studies of their lungs carried out after several hours, or on the following day. The findings had to be interpreted as pulmonary oedema. The most seriously affected patient showed the picture of massive acute interstitial oedema on the second day. After initial regression, coarse shadows developed, indicating the alveolar form of pulmonary oedema. The sputum contained candida, but there was no evidence of pulmonary candidiasis. In two patients there were transient signs of limited atelectases. Two patients were re-examined after five years. There were no features which could be interpreted as a consequence of the drowning episode. The radiographic appearances showed minor changes which could be due to mild pulmonary fibrosis.
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PMID:[Radiological appearances in the near-drowned (author's transl)]. 621 60

The intraperitoneal administration of either butylated hydroxytoluene (BHT) +/- thoracic X-irradiation, or cyclophosphamide, and intravenous injection of oleic acid, resulted in lung injury and repair in BALB/c mice which could be assessed in unanesthetized animals by changes in respiratory rate (RR) using a total body plethysmograph. Studies with BHT +/- X-rays, and cyclophosphamide found that the RR right before sacrifice (2 weeks after BHT and 3 weeks after cyclophosphamide) correlated well (r = 0.19) with the degree of pulmonary fibrosis as measured by changes in hydroxyproline content. However, prior to this timepoint, there was a peak and trough in respiratory rate response that could not be correlated with the time course of fibrosis development in the BHT-X-ray model. In an effort to determine the influence of pulmonary edema and lung cell proliferation on respiratory rate changes, an agent (oleic acid) capable of producing lung injury followed by a high level of cellular proliferation with only minimal development of fibrosis was studied. These studies showed that good correlations were found on day 3 following injection (day of peak increase in respiratory rate) between respiratory rate and either lung wet weight (r = 0.81) or the degree of cellular proliferation as measured by the incorporation of thymidine into pulmonary DNA (r = 0.80). Liver (carbon tetrachloride) and kidney (mercuric chloride) toxicants, and starvation produced decreases or no change in RR.
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PMID:Effect of lung, liver, and kidney toxicants on respiratory rate in the mouse. 622 16

The relative in vitro and in vivo toxicity of several types of manufactured fibrous glass insulation and crocidolite asbestos was investigated to aid in selection of a suitable glass fiber for subsequent use in inhalation exposures. The in vitro cytotoxicity to pulmonary alveolar macrophages of small glass fibers from microfiber insulation (count median diameter (CMD) approximately 0.1-0.2 micrometer) was greater than that of the larger fibers from household insulation (CMD approximately 2.4 micrometers). To screen for in vivo pulmonary toxicity, 2-21 mg of glass or asbestos fibers were administered in divided doses to male Syrian hamsters by intratracheal instillation. Animals were sacrificed at 1, 3.5 and 11 months following initial administration of material. One type of glass microfiber [count median diameter (CMD) approximately 0.1 micrometer] caused deaths from pulmonary edema at early times after instillation. High levels of asbestos, a second glass microfiber (CMD approximately 0.2 micrometer) and one type of household insulation fiber (CMD 2.3 micrometers) all resulted in increase in total collagen and mild pulmonary fibrosis at later times after instillation, although microfiber insulation produced a greater response than household insulation. Asbestos insulation produced the greatest response. A five-day inhalation exposure to a high level of glass microfibers deposited in lung less than 10 percent of the lowest instilled amount which elicited indications of lung injury. This amount did not produce significant biological changes at 1 to 12 months after exposure.
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PMID:In vitro and in vivo response after exposure to man-made mineral and asbestos insulation fibers. 631 89


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