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)

The preoperative pulmonary evaluation of organ transplant candidates involves the diagnosis of unexplained pulmonary infiltrates or symptoms, interpretation of pulmonary function abnormalities, and an assessment of surgical risk. Pretransplant pulmonary considerations in patients with end-stage hepatic diseases relate primarily to hypoxemia from poorly understood intrapulmonary vascular dilatations, mechanical dysfunction, and states of increased extravascular lung water. Except in severe cases, however, these generally do not prohibit liver transplantation, and even are likely to improve after transplant surgery. Early postoperative complications may be categorized as those expected from extensive intra-abdominal surgery that requires significant volume resuscitation, which typically are managed in the usual manner for those clinical situations. As immunosuppression begins to have an effect, the LTx recipient becomes susceptible to the same opportunistic infectious organisms (with their frequent pulmonary involvement) that cause significant morbidity and mortality in recipients of other solid organ transplants. Because many of the immunosuppressive agents also are the same, noninfectious side effects such as pulmonary edema and malignancy also are similar. As with all immunocompromised patients, prophylaxis, when possible, persistent infection surveillance, and an aggressive diagnostic and therapeutic approach help decrease the impact of pulmonary dysfunction in LTx recipients.
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PMID:Pulmonary complications of liver transplantation. 866 93

We tested whether NG-nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of NO synthesis, can prevent interleukin-2 (IL-2)-induced capillary leakage. Healthy C3H/HeJ female mice were treated with: nothing; IL-2 (10 injections; 35,000, 15,000, or 7,500 Cetus U i.p. every 8 h); IL-2 + L-NAME (0.01, 0.1, 0.5, and 1 mg/ml of drinking water starting 1 day before IL-2 therapy and ending with IL-2 therapy); or L-NAME alone. In the first series of experiments, mice were killed 1 h after last IL-2 injection to measure pleural effusion, and water content of the lungs, spleen, and kidney (markers of capillary leakage), as well as NO2- + NO3- levels in the serum and pleural effusion. In the two additional series, the survival of treated mice was followed. All doses of IL-2-induced capillary leak syndrome as indicated by pleural effusion, pulmonary edema, and fluid retention in the spleen and kidney. NO production was positively correlated with manifestation and severity of this syndrome. NO2- + NO3- levels in the pleural effusion were directly related to IL-2 dose, and L-NAME treatment reduced both the NO production and severity of capillary leakage, excepting fluid retention in the kidney. However, L-NAME therapy prevented IL-2-induced mortality only when combined with a middle range IL-2 dose (15,000 U/injection). In summary, oral L-NAME therapy effectively prevented IL-2-induced capillary leakage in healthy mice, suggesting its potential value as a supplement in IL-2-based immunotherapy of cancer and infectious diseases.
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PMID:NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, ameliorates interleukin-2-induced capillary leak syndrome in healthy mice. 868 Jun 49

We report three cases of drug-induced hemolytic uremic syndrome (HUS). Three patients with advanced gastrointestinal cancer underwent a curative operation and adjuvant chemotherapy with Mitomycin C (MMC), 5FU and Ara-C. Later, progressive anemia, thrombocytopenia, renal dysfunction and elevation of serum LDH were recognized. A diagnosis of HUS was made. As they had no symptoms of infectious diseases or relapse of cancer, the cause of HUS was thought to be MMC. Treatment with antiplatelet drugs and fresh frozen plasma was effective for two patients. However, one patient died of pulmonary edema.
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PMID:[Three cases of drug-induced hemolytic uremic syndrome]. 871 31

The fumonisins (FBs) are a group of closely related mycotoxins that are prevalent in maize. They were isolated from strains of Fusarium moniliforme (Sheldon), which were implicated in the aetiology of human oesophageal cancer in the Transkei, South Africa. Their discovery explained the cause of equine encephalomalacia, or "hole in the head" syndrome, when it was found by feeding trials in horses that they elicited the disease. Subsequently, they were found to cause hepatic cancer in rats and pulmonary oedema in pigs, with most animal species tested showing liver and kidney damage. FB1 is the most important of the group and, although poorly absorbed from the gastrointestinal tract, its action is at the cellular level, affecting sphingolipid metabolism. Ceramides derived from sphingosine metabolism are cell regulatory factors affecting, among other things, DNA synthesis. Because FB1 has a close molecular resemblance to sphinganine, it interferes with ceramide biosynthesis and, hence, the processes that it regulates, which is thought to explain its carcinogenic properties. Studies on the FBs are still at a relatively early stage, but it is already clear that they play an important role in animal mycotoxicoses and, by implication, in human disease. A more positive aspect is that they will be used in elucidating the role of sphingolipids in cellular regulation.
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PMID:Fumonisins, mycotoxins of increasing importance: their nature and their effects. 884 66

Previously, we showed that nitric oxide (NO) plays a major role in the pathogenesis of IL-2-induced capillary leak syndrome in healthy or mammary adenocarcinoma-bearing C3H/HeJ mice. NO synthase (NOS) inhibitors, such as NG-nitro-L-arginine methyl ester (L-NAME) reduced all the manifestations of IL-2-induced capillary leakage, without compromising the antitumor effects of IL-2. The present study was carried out on healthy C3H/HeJ mice subjected to one or two 4-day rounds of systemic IL-2 therapy with or without oral L-NAME therapy to: (a) identify the tissue source of NOS activity and NOS protein induced by IL-2 therapy; (b) identify histologically the nature of the structural damage to the lungs associated with IL-2 therapy-induced pulmonary edema; and (c) evaluate the effects of additional L-NAME therapy on the above-mentioned parameters. Results revealed that IL-2 therapy in healthy mice resulted in the expression of inducible NOS in numerous tissues including the endothelium and muscles of the anterior thoracic wall as well as splenic macrophages. One round of IL-2 therapy resulted in high levels of inducible NOS (iNOS) activity in the anterior thoracic wall accompanied by pleural effusion. After two rounds of IL-2 therapy, there was neither pleural effusion nor high iNOS activity in the thoracic wall. IL-2-induced pulmonary edema after one round of therapy correlated to both a significant rise in NO production measured in the serum and structural damage to the lungs and its capillaries. Addition of the NOS inhibitor L-NAME totally eradicated NOS activity but not necessarily iNOS expression. It also reduced IL-2-induced pulmonary edema and pleural effusion, restrained the rise in the levels of NO metabolites (nitrites and nitrates) in the serum and pleural effusion, and significantly restored the structural integrity of the lungs after one round of therapy. Thus, NOS inhibitors may be beneficial adjuncts to IL-2 therapy for cancer and infectious diseases.
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PMID:The role of active inducible nitric oxide synthase expression in the pathogenesis of capillary leak syndrome resulting from interleukin-2 therapy in mice. 901 Apr 49

Interleukin 12 (IL-12) activates natural killer and T cells with the secondary synthesis and release of interferon-gamma (IFN-gamma) and therefore enhances a Th1- or cell-mediated immune response. The immunostimulatory property of IL-12 may be used clinically in cancer and viral diseases. Safety studies in rodents and primates demonstrated a rather small therapeutic window with hepato- and splenomegaly, myelodepression, and lung edema. Investigations in mutant mice deficient for the IFN-gamma receptor (IFN-gamma R-/-) revealed that both the biologic and toxic effects are indirect and largely due to IL-12-induced IFN-gamma. The significance of these findings for the safety in man needs to be explored.
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PMID:Interleukin-12: role of interferon-gamma in IL-12 adverse effects. 907 24

Sphingolipids are highly bioactive compounds that participate in the regulation of cell growth, differentiation, diverse cell functions, and apoptosis. They are present in both plant and animal foods in appreciable amounts, but little is known about their nutritional significance. Recent studies have shown that feeding sphingomyelin to female CF1 mice treated with a colon carcinogen (1,2-dimethylhydrazine) reduced the number of aberrant colonic crypt foci; longer-term feeding also affected the appearance of colonic adenocarcinomas. Therefore, dietary sphingolipids should be considered in studies of the relationships between diet and cancer. Sphingolipids have also surfaced as important factors in understanding the mechanism of action of a recently discovered family of mycotoxins, termed fumonisins. Fumonisins are produced by fungi commonly found on maize and a few related foods, and their consumption can result in equine leukoencephalomalacia, porcine pulmonary edema and a number of other diseases of veterinary animals and, perhaps, humans. A cellular target of fumonisins is the enzyme ceramide synthase, and disruption of sphingolipid metabolism by fumonisins has been established by studies with both cells in culture and animals that have consumed these toxic mycotoxins. These findings underscore the ways in which sphingolipids and agents that affect sphingolipid utilization should be given consideration in selecting animal diets for nutritional and toxicological studies.
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PMID:Importance of sphingolipids and inhibitors of sphingolipid metabolism as components of animal diets. 916 47

Whole-body hyperthermia (WBH) is a well-described investigational adjunct to systemic chemotherapy for the treatment of advanced malignancies. The hemodynamic consequences of this physiologic state may include tachycardia, which can produce acute myocardial ischemia in patients with coronary artery disease. Ischemic heart disease is currently considered a contraindication to WBH. We chose to investigate the consequences of using a new beta 1-adrenergic antagonist, esmolol, to attempt to control the tachycardia associated with WBH. After institutional approval and patient consent, nine consecutive patients with normal cardiac function presenting for WBH with carboplatin infusion were studied. Along with standard monitors, radial arterial and oximetric thermodilution pulmonary artery catheters were placed. Patients were sedated and heated in a radiant warmer (Enthermics). Spontaneous ventilation was maintained and hemodynamic data were gathered at 37 degrees C, and at 41.8 degrees C (before, during and after esmolol infusion). Heart rate and cardiac output increased (by 46% (p = 0.001) and 35% (p = 0.04) respectively) while mean arterial pressure and systemic vascular resistance fell (by 18% (p = 0.02) and 44% (p = 0.006) respectively) during hyperthermia. Heart rate was significantly reduced during esmolol administration (mean dose 180 micrograms/kg/min) in the absence of changes in cardiac index and calculated oxygen delivery. Ventricular filling pressures and stroke work were unchanged. No heart failure, pulmonary edema, or other adverse event was observed. Hemodynamic changes seen during esmolol administration were completely reversed 15 min after the infusion was stopped. We conclude that the administration of moderate doses of esmolol is safe for this population of patients undergoing WBH, and that this technique raises the question of whether patients with ischemic heart disease could safely undergo WBH.
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PMID:The use of esmolol in whole-body hyperthermia: cardiovascular effects. 922 10

There are frequently respiratory complications with cancer particularly in primary lung carcinoma. Among these are bronchopulmonary infections with or without endobronchial obstruction, carcinomatous lymphangitis, thromboembolic disease and haemorrhagic disease as well. Radiotherapy and chemotherapy may induce various respiratory complications which diagnosis can be of varying shades of difficulty. The classical post radiation pneumonitis occurring exclusively in the field of radiation hardly poses any problem unless it could be masking a recurrence. Certain clinical manifestations address very difficult problems of differential diagnosis by their lack of specificity and by their often unforeseeable character (except for bleomycin fibrosis which is perfectly dose dependent). Moreover patients often have multiple treatments and the identification of the single responsible agent becomes very difficult. We will not discuss here the infectious or secondary haemorrhagic complications of radiotherapy or chemotherapy but rather the anaphylactic manifestations, diffuse interstitial pneumonia with lymphocytic alveolitis or fibrosis, eosinophilic pneumonia, non-cardiogenic pulmonary oedema, bronchiolitis obliterans with organising pneumonia and the rare pulmonary vascular disorders such as pulmonary veno-occlusive disease.
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PMID:[Radiation- and chemically-induced respiratory manifestations]. 948 Apr 78

Although percutaneous ethanol injection is widely used to treat hepatic tumors, this technique has not been applied to lung tumors. We performed a preliminary experiment with percutaneous ethanol injection into the rabbit lung, and evaluated the local and systemic effects of absolute ethanol injection on pulmonary structures in order to assess the feasibility and safety of this technique as a local treatment for human lung tumors. Percutaneous injection of absolute ethanol into the rabbit lung was performed under CT guidance. The volume of ethanol injected ranged from 0.6 to 1.0 ml (approximately 0.2-0.5 ml/kg). Follow-up CT scans were performed 1, 2, 7 and 30 days after the injection. The animals were killed at intervals (range: 3 h-30 days), and the lung was examined histologically. The ethanol was well tolerated and did not induce significant systemic side-effects. All doses induced necrosis in the injected lung, but none was lethal. Although ethanol spilling into the thoracic cavity induced effusion and pleuritis, these reactions were manageable. Alcohol injection produced an area of necrosis surrounded by pulmonary edema associated with polymorphonuclear cells invasion within 24 h; moreover, granulation change, epithelial regeneration, and alveolar septal fibrosis had appeared by one week. The necrosis was sometimes multifocal, probably due to transbronchial spread of the injected ethanol. In conclusion, the feasibility and safety of absolute ethanol injection were confirmed. Neither severe systemic side effects nor lethal extensive necrosis were observed with injected ethanol; however, an unexpected side effect, multifocal necrosis, was seen. The latter reaction suggests that careful observation and care would be essential after alcohol injection into the lung.
Jpn J Cancer Res 1998 Jan
PMID:Preliminary study of percutaneous alcohol injection into the lung. 951 Apr 81


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