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)

Thrombotic thrombocytopenic purpura is a rare disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever and renal dysfunction. in six of seven consecutive patients with thrombotic thrombocytopenic purpura seen in an eight month period, respiratory impairment was present. Respiratory dysfunction was characterized by tachypnea, hypoxemia nad infiltrates on chest roentgenogram. Five patients required mechanical ventilation. Two patients had cardiogenic pulmonary edema, but they remained hypoxemic despite treatment for pulmonary edema and maintenance of normal pulmonary capillary wedge pressure for more than 36 hours. Four patients died and autopsies revealed pulmonary edema, hemorrhage and hyaline thrombi. Pathologic examination of the heart also showed hyaline thrombi. Information from out patients with thrombotic thrombocytopenic purpura implicates respiratory dysfunction as a component of this disease as well as the classically described pentad. Cardiogenic and noncardiogenic pulmonary edema and possibly bleeding into the lung contributed to pulmonary impairment.
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PMID:Respiratory dysfunction in thrombotic thrombocytopenic purpura. 56 25

Septic shock carries a high mortality. It is manifest haematologically by thromobocytopaenia and other coagulation disturbances. The radiological manifestations are various degrees of pulmonary oedema, usually affecting the lower zones, without evidence of pulmonary hypertension. Radiological signs are always preceded on accompanied by thrombocytopaenia.
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PMID:The pulmonary manifestations of septic shock. 86 23

The sequence of ultrastructural changes of bovine platelets during the fatal course of East Coast fever was swelling; formation of vacuoles, pseudopodia, and indentations; then thrombocytorrhexis and degranulation; and finally, thrombocytolysis. These changes led to thrombocytopenia and release of serotonin, resulting in petechiations and pulmonary edema.
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PMID:Ultrastructure of blood platelets in cattle with East Coast fever. 126 40

A Thai female patient infected with P. falciparum had 80 per cent P. falciparum infected red cells at ring stage in the peripheral blood smear. The complications included anemia, thrombocytopenia, acute renal failure and pulmonary edema. A marked decrease in platelets number, low hemoglobin, low hematocrit and decreased red blood cell count were detected. More than 70 per cent of total platelets detected in the blood smear were binding to parasitized red blood cells. The number of binding platelets declined with decreasing per cent parasitized red cells. It was also noted that some platelets (10-20%) adhered to nonparasitized red cells. An increased number of large lymphocytes was shown by increased numbers of large unstained cells (LUC) by H* 1 automated analyzer. The peripheral blood smear showed abnormal binding of platelets to the infected red cells more frequently than to non infected red cells and free platelets on the day of high parasitemia. This abnormal phenomena was related to the number of platelets in the circulation. When the parasitized red cells were not detected in the blood smear, the number of platelets in the circulation had returned to normal.
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PMID:An unusual adhesion between red-cells and platelets in falciparum malaria. 140 64

Monoclonal antibody against human tumor necrosis factor alpha (TNF MAb) prevents death induced by intravenous gram-negative bacteria or lipopolysaccharide (LPS) in primates. Although these studies have demonstrated that TNF plays a prominent role in the development of lethal septic shock, exploration of dose-response relationships and possible mechanisms of protection have been limited. We addressed these questions in a series of experiments conducted in E. coli-challenged pigs. First, we determined that TNF MAb neutralized the cytotoxic activity found in septic pig plasma and in culture media from pig monocytes incubated with LPS. Second, we demonstrated that pretreatment with TNF MAb promotes survival, in a dose-dependent fashion, in an otherwise lethal E. coli bacteremic pig model. The results of the survival study highly correlate (r = 0.96, P < 0.01) the presence of TNF in the circulation with mortality. In an additional series of physiologic monitoring experiments designed to delineate possible mechanisms of protection, the authors demonstrate that TNF MAb pretreatment abrogates the prolonged leukopenia, thrombocytopenia, and microvascular leakiness resulting from intravenous bacterial challenge and maintains arterial blood pressure while diminishing pulmonary edema. These findings may provide a mechanism whereby neutralization of TNF systemically affords protection against the lethal sequelae of bacteremia.
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PMID:Efficacy of monoclonal antibody against human recombinant tumor necrosis factor in E. coli-challenged swine. 144 53

A technique is described for the intratracheal aerosolization of endotoxin into the rat. Using a miniaturized nozzle within the tracheal lumen to optimize uniform distribution 0.5 ml of an endotoxin solution (7 mg/kg) was aerosolized and dispersed throughout the lung. Time course studies of pulmonary function and histological changes revealed marked functional and morphological changes by 24 h. Histopathologic changes consisted of widespread pulmonary oedema and a diffuse neutrophilic alveolitis. At the same time, there were significant decreases in tidal volume, minute ventilation and lung compliance. Haematologic changes were also seen, including profound thrombocytopaenia and leukopaenia together with an increased haematocrit, indicating systemic effects in this model. Bronchoalveolar lavage (BAL) at 24 h revealed significant increases in BAL protein, erythrocytes and neutrophils. The functional, cytological and histological changes observed after endotoxin challenge mimic those seen in the Adult Respiratory Distress Syndrome in humans and can thus be used as a model to compare the efficacy of a variety of therapeutic interventions for this syndrome.
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PMID:Intratracheal aerosolization of endotoxin in the rat: a model of the adult respiratory distress syndrome (ARDS). 154 44

Seventeen patients with chemotherapy-resistant metastatic sarcoma were treated with whole body hyperthermia (WBH) combined simultaneously with 1-3-Bis(2-chloroethyl)-1-nitrosourea (BCNU). All of the patients had chemotherapy resistant metastases to major organ sites. Patients were heated to 41.8-42.0 degrees C for 2 h using an insulated blanket heating technique. Two patients (12%) experienced partial responses (PR). In addition, four objective tumour responses (OR) lasting more than 4 months were documented. One patient with previously rapidly growing chondrosarcoma pulmonary metastases experienced stable disease (SD) for 38 months from the onset of treatment. Median survival of seven patients with responding tumours (PR, OR and SD) compared with 10 patients with progressive disease was 15 versus 2 months, respectively. Cumulative thrombocytopenia was a therapy-limiting toxicity of the combined treatment, and occurred in six of seven patients. Acute toxicities attributable to WBH alone included transient thrombocytopenia in all patients, non-cardiogenic pulmonary oedema in two patients, and mild hypotension in five patients. Acute granulocytosis was observed in all patients. No treatment related deaths occurred. These data suggest that WBH combined with chemotherapy is associated with disease response in patients with chemotherapy-resistant, widely disseminated sarcoma metastases.
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PMID:Chemotherapy resistant sarcoma treated with whole body hyperthermia (WBH) combined with 1-3-bis(2-chloroethyl)-1-nitrosourea (BCNU). 160 34

Platelet-activating factor (PAF) is a glycerophospholipid known for its unusual potent vasoactive and proinflammatory activities. The present study examined whether PAF might serve as a priming factor in endotoxin-induced tumor necrosis factor-alpha (TNF alpha) synthesis, cardiovascular shock, and lung injury in anesthetized rats. Intravenous infusion of PAF (1 pmol/kg/min for 60 minutes, n = 5) alone or endotoxin (0.1 micrograms/kg i.v. bolus, n = 5) failed to alter blood pressure, serum TNF alpha and thromboxane B2, platelet and leukocyte count, and hematocrit, nor was lung histology, myeloperoxidase activity, and water content changed. In contrast, the combined administration of PAF and endotoxin markedly elevated serum TNF alpha (1,359 +/- 362 pg/ml, n = 5, p less than 0.01) and thromboxane B2 (43 +/- 5 pg/100 microliters, n = 8, p less than 0.01) along with hypotension, hemoconcentration, leukopenia, and thrombocytopenia. Most notably, the combined regimen caused neutrophil aggregation, adhesion, and accumulation into the lung parenchyma along with platelet-fibrin deposits in postcapillary venules, pulmonary edema, and increased lung myeloperoxidase activity. The role of PAF in this process was confirmed by 1) the prevention of the priming effect by pretreatment with the PAF antagonist BN 50739 (n = 5), and 2) the failure of lyso-PAF, the cardinal nonactive PAF-metabolite, to prime for endotoxin-induced production of TNF alpha (n = 4). These data suggest that PAF could serve as a key mediator in priming for endotoxin-induced tissue injury, especially the typical pulmonary pathophysiology of adult respiratory distress syndrome, a severe pathological outcome of septic shock, burns, and multiple organ injury.
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PMID:Priming by platelet-activating factor of endotoxin-induced lung injury and cardiovascular shock. 164 75

The incidence of severe falciparum malaria is increasing in the developed countries and mortality remains high despite progress in intensive care management and schizonticide treatment. Many authors emphasize the importance of exchange transfusion (EXT) in the most severe cases. We studied 21 cases (34 +/- 12 years, 6 females; SAPS: 8.4 +/- 3.7) of severe malaria (according to WHO criteria) consecutively admitted to ICU between 1985 and 1990: 3 patients underwent EXT. Twenty were febrile above 39 degrees C, 10 had cerebral malaria, 14 hepatic impairment, 8 acute renal failure, 5 pulmonary oedema. Nine patients required mechanical ventilation, 1 haemodialysis, 1 intracranial pressure monitoring. Mean parasitemia was 13%, 16 patients had thrombocytopenia less than 50 x 10(9)/l, 3 anemia less than 7 g/dl and 3 leucopenia less than 2.8 x 10(9)/l. Nineteen received quinine i.v., 1 mefloquine, 1 chloroquine. Sixteen patients received blood products transfusion, 3 were treated by EXT in addition. Twenty were cured and discharged from hospital without sequelae (mean stay: 14 days); 4 had nosocomial infection, 1 a splenic infarction. One patient (17-years-old; SAPS: 17; parasitemia: 7.8%) died 12 h after admission from non-cardiogenic pulmonary oedema with multi-organ failure. The literature and this study lead us to propose EXT in patients with unfavourable evolution after conventional treatment rather than in all the patients with a parasitemia above 10% at admission. A randomized study to compare conventional treatment in ICU with or without EXT is necessary.
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PMID:Severe falciparum malaria (21 cases). 179 87

A case of toxic epidermolysis (TE) with a fatal outcome is reported. It occurred after administration of 500 mg griseofulvin twice daily in a 19-year-old female patient. She developed the first skin lesions on the sixth day of treatment. All the body surface was involved, except for the scalp. Several complications arose in the course of the disease, thrombocytopaenia, lymphocytopaenia, rhabdomyolysis, and non cardiogenic pulmonary oedema. Death occurred as a result of multiple organ failure following septic shock associated with adult respiratory distress syndrome. The pathogenesis of these complications and the major therapeutic difficulties encountered are discussed. The involvement of griseofulvin in TE has only been reported once before. The arguments in favour of its involvement in the present case are discussed.
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PMID:[Fatal Lyell's syndrome caused by griseofulvin]. 219 42


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