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

We studied systemic anaphylaxis induced by the administration of 200 mug of horseradish peroxidase into 11 anesthetized rabbits known to be producing anti-horseradish peroxidase antibodies only of the IgE class. Ventilatory changes included a transient, abrupt decrease in breathing frequency followed by increased minute ventilation; lung mechanical changes included decreased dynamic lung compliance and increased total pulmonary resistance; cardiovascular changes included pulmonary hypertension, systemic hypotension, and, frequently, a transient bradycardia. Recovery from these physiologic changes took place within 60 min. After recovery, the administration of 2 mg of horseradish peroxidase into 6 of the rabbits induced a second reaction indistinguishable from the first with respect to ventilatory and circulatory alterations; however, lung mechanical changes were less prominent. No histologic evidence of pulmonary edema or intraluminal plugging of the pulmonary edema or intraluminal plugging of the pulmonary circulation was observed by light microscopy. Although the first anaphylactic reaction was accompanied by disappearance of stainable basophils from the circulating blood, the second reaction occurred despite the absence of circulating basophils. These studies characterize further the effects of antigen challenge in rabbits producing detectable concentrations of IgE, but not other classes of antibody to the antigen.
 ...
PMID:IgE-induced respiratory and circulatory changes during systemic anaphylaxis in the rabbit. 98 86

Of 113 methyl isocyanate (MIC)-exposed subjects studied initially at Bhopal, India, 79, 56, 68, and 87 were followed with clinical, lung function, radiographic, and immunologic tests at 3, 6, 12, 18, and 24 months. Though our cohort consisted of subjects at all ages showing a varied severity of initial illness, fewer females and young subjects were seen. Initially all had eye problems, but dominant symptoms were exertional dyspnea, cough, chest pain, sputum, and muscle weakness. A large number showed persistent depression mixed with anxiety, with disturbances of personality parameters. The early radiographic changes were lung edema, overinflation, enlarged heart, pleural scars, and consolidation. The persistent changes seen were interstitial deposits. Lung functions showed mainly restrictive changes with small airway obstruction; there was impairment of oxygen exchange. Oxygen exchange improved at 3-6 months, and spirometry improved at 12 months, only to decline later. The expiratory flow rates pertaining to large and medium airway function improved, but those for small airways remained low. There were changes of alveolitis in bronchoalveolar lavage fluid on fiber optic bronchoscopy, and in 11 cases positive MIC-specific antibodies to IgM, IgG, and IgE were demonstrated. On follow up, only 48% of the subjects were clinically stable, while 50% showed fluctuations. Thirty-two percent of the subjects had lung function fluctuations. Detailed sequential behavior over 2-4 years was predicted for dyspnea, forced vital capacity, maximum expiratory flow rate (0.25-0.75), peak expiratory flow rate, VO2, and depression score. A model for clinical behavior explained a total variance of 52.4% by using the factors of cough, PCO2 and X-ray zones in addition to above five parameters. The behavior of the railway colony group (1640 patients) revealed a similar pattern of illness. When this observed pattern of changes was transferred to the affected Bhopal city sections (with an equitable age-sex distribution), our model results were again validated. Thus the picture of MIC-induced disease seems similar despite the differences for age-sex and initial severity of illness in our cohort and in the population of Bhopal city as predicted by our model.
 ...
PMID:Sequential respiratory, psychologic, and immunologic studies in relation to methyl isocyanate exposure over two years with model development. 139 63

Immunopathological studies of SIDS share the problems of all necropsy based studies of this syndrome: the extent of autolytic changes in the material under study; and the lack of appropriate controls. Despite these problems, several studies have been performed on serum, bronchoalveolar lavage, and pulmonary tissue. Many of these studies have been inspired by the modified anaphylaxis hypothesis, based on the experiments of Coombs and coworkers. Lightly anaesthetised guinea-pigs, which had been sensitised to cows' milk protein, were shown to die after intratracheal challenge. Studies of serum IgE concentrations in SIDS initially indicated raised specific IgE for Dermatophagoides pteronyssinus, Aspergillus fumigatus, and bovine beta-lactoglobulin, but subsequent studies have not sustained these findings. Raised immunoglobulin concentrations in bronchoalveolar lavage fluid have been found in association with SIDS but this probably reflects plasma leakage rather than local secretion. Immunocytochemical analysis of lavage cells performed by the same group revealed no major difference between SIDS cases and controls, although these were limited to four cases. To date, there have been no comprehensive studies of the inflammatory cell content of the pulmonary parenchyma in SIDS. In our own studies, we have examined the mast cell and eosinophil populations in the lungs of 49 cases of infants with SIDS and in 33 infants dying of non-pulmonary causes in the first 18 months of life. We found no difference in mast cell numbers between the groups but there was a striking excess of eosinophils in the lungs of infants dying of SIDS. Because eosinophils can secrete oxygen free radicals and cytotoxic cationic proteins, we regard this as evidence of a potential mechanism for the pulmonary oedema that is characteristic of SIDS. A viral infection which might otherwise have been trivial could therefore prove fatal.
 ...
PMID:Immunopathology of SIDS. 147 58

This "syndrome" has been observed in 4 of 23,935 in-patients registered in the years 1974-1987 in the Comprehensive Hospital Drug Monitoring (Bern/St. Gallen), with 6 reactions. Signs of an attack of bronchial asthma, laryngeal or pulmonary edema or a (heart-)circulatory event were not observed. Each patient was cyanotic and 3 had the feeling of impending death. The eliciting drugs were penicillin-G (twice) and cefazolin (once), given i.v.; iron dextran i.m. (once); pitressin tannate i.m. (once) and dicobalt edetate (Kelocyanor) i.v.(once). In each case the reaction started during or shortly after injection of the drug; the duration of the reaction in 5 of these events was 20-80 minutes. The pathomechanism could be a special form of anaphylactic reaction with acute pulmonary hypertension, comparable to IgE-induced anaphylaxis in the rabbit or aggregate anaphylaxis in the monkey or the dog. Further observations are needed for more detailed study.
 ...
PMID:[Acute severe dyspnea as a side effect of drugs. Report from the CHDM (Comprehensive Hospital Drug Monitoring)]. 212 Jul 71

Systemic mast cell disease (SMCD) is a rare disease often associated with symptoms of general malaise, pruritus, diarrhea, vomiting, fever, urticaria pigmentosa, hepatosplenomegaly and lymphadenopathy. We reported a case of SMCD associated with cutaneous xanthoma and serum hyper IgE. Skin biopsy revealed xanthomas and diffuse infiltration of mast cells in the dermis. The association of SMCD with xanthoma was reported in the literature for only one case. The hyper IgE could be due to the defect of IgE receptors on the cell membrane of mast cells of dysfunction of T and/or B cell. Any of the treatment using H1 and H2 receptor blockade, disodium cromoglycate, adrenocorticosteroid or chemotherapy (VEPA) were not effective. The patient died of pulmonary edema and multiple organ failure 7 months after the diagnosis was established. The crush method for the cytological examination of bone marrow was considered more useful than smear method for the diagnosis of SMCD.
 ...
PMID:[Systemic mast cell disease associated with cutaneous xanthomas and markedly elevated serum IgE]. 224 20

Fifty-three subjects with positive skin prick test results to cat extract and rhinoconjunctival symptoms on exposure to cat dander were enrolled in a double-blind, placebo-controlled study of oral cat immunotherapy. Responses were assessed by development of symptoms and nasal blockage on exposure to an apartment contaminated with cat dander, by titrated skin prick tests, and by cat-specific IgG and IgE. A total cumulative dose of 2.5 x 10(6) allergy units or 436 U Fel d I were administered over a period of 3 months. Both groups of subjects had significantly fewer symptoms on exposure to cat dander during the course of the study, but there was no significant difference between active and placebo groups. There were no significant changes in either group in nasal blockage, skin prick test results, or specific IgG levels. Both groups had significant increases in cat-specific IgE, but there were no differences between groups. Subjects receiving active treatment had a slight excess of gastrointestinal complaints. Two subjects receiving active treatment experienced systemic symptoms: one had pulmonary edema, and the other had persistent asthma and urticaria, which may have represented reactions to the treatment. We conclude that oral cat immunotherapy with the preparation and doses used in this study is not effective.
 ...
PMID:Safety and efficacy of oral immunotherapy with standardized cat extract. 830 83

In a murine ear-swelling model, we demonstrated a unique hypersensitivity response and defined it as early-type hypersensitivity (ETH). ETH was characterized by increased vasopermeability and edematous change that occurred within 1 h at the site of Ag challenge. In this study, intranasal challenge with Dermatophagoides farinae (Df) on Df-sensitized BALB/c mice induced an ETH response in the lungs. The lung ETH was manifested by an increase in wet lung weight, production of TNF-alpha in bronchoalveolar lavage fluids, and hyperemia and edematous change around vessels of small airways 1 h after Ag provocation. The challenged animals subsequently developed airway inflammation, beginning with a neutrophilic infiltrate which was followed by lymphocytes and eosinophils. The Df-induced eosinophilia was Ag-specific and maximal at 48 h after challenge. At this time, the trachea from sensitized mice also exhibited hyperreactivity to carbachol. Pretreatment with anti-CD4+ mAb significantly decreased the recruitment of eosinophils in bronchoalveolar lavage fluids. An enhanced expression of pulmonary endothelial vascular cell adhesion molecule-1 was noted as early as 6 h after challenge. Anti-Df Abs of IgG class, but not IgE class, were detected in Df-immunized mice at the time of challenge. Furthermore, Df challenge induced a stronger eosinophil response in BALB/c mice (H-2d) than in B10.BR (H-2k) mice. B10.BR mice also did not exhibit pulmonary edema or ETH of ear swelling 1 h after challenge. These data suggest that an ETH-associated 1 h pulmonary edematous change was induced by intranasal challenge of Df in Df-sensitized mice, and that the ETH might contribute to the development of subsequent pulmonary inflammation and eosinophilia.
 ...
PMID:Early-type hypersensitivity-associated airway inflammation and eosinophilia induced by Dermatophagoides farinae in sensitized mice. 859 45

Although fulminating non-cardiogenic pulmonary edema following cardiopulmonary bypass is not a new phenomenon, the exact cause and pathogenesis are still unknown. The causative agent of this potentially lethal syndrome was hypothesized to be either protamine or blood products. There was no evidence that an antibody-mediated reaction plays a role and patients were reported to have negative skin tests. We report, for the first time, a patient who presented with fulminating non-cardiogenic pulmonary edema after repeated protamine administration with a subsequent positive skin test to protamine. Specific IgG antibodies to protamine were also found; however, the level was in the range of that of exposed non-reacting controls. IgE antibodies could not be detected.
 ...
PMID:Protamine-induced fulminating non-cardiogenic pulmonary edema following cardiopulmonary bypass. 881 45

We have used mice rendered deficient for nitric oxide synthase 2 (NOS2) production to study the role of inducible nitric oxide (NO) in the pathogenesis of allergic airways disease. Using a model with OVA as aeroallergen, we show that the manifestations of disease, including infiltration of inflammatory cells, particularly eosinophils, loss of structural integrity of the airway walls, microvascular leakage, pulmonary edema, and airway occlusion are markedly less severe in the NOS2 mutants than in wild-type animals. Indeed, NOS2-deficiency resulted in a 55-60% reduction in both circulatory and pulmonary eosinophil numbers following aeroallergen treatment, although eosinophil maturation or efflux from the bone marrow was not suppressed. There were no obvious differences in levels of airway hyperreactivity recorded in OVA-treated wild-type and NOS2-deficient mice. Interestingly, the suppression of allergic inflammation was accompanied by marked increases in T cell production of IFN-gamma but not by any obvious reduction in the secretion of either IL-4 or IL-5, nor by major changes in the IgG1 and IgE OVA-specific serum Ig profiles in the mutants. The markedly enhanced production of IFN-gamma in NOS2-/- mice was apparently responsible for the suppression of both eosinophilia and disease, as in vivo depletion of this factor restored allergic pathology in these animals. Our data indicate that NOS2 promotes allergic inflammation in airways via down-regulation of IFN-gamma activity and suggest that inhibitors of this molecule may represent a worthwhile therapeutic strategy for allergic diseases including asthma.
 ...
PMID:Inhibition of allergic airway inflammation in mice lacking nitric oxide synthase 2. 988 18

A rare and strong adverse reaction to contrast media (mdc) i.v. injected to carry out an abdominal vessels' angiography is reported. The patient suffered from non cardiogenic pulmonary edema and hypoxia. Chest X-ray detected the same radiological patterns of ARDS: in contrast alveolar edema became insignificant in 5 days. Serum immunocomplexes levels were high in the early phase of the reaction. Serum IgE, C3 and C4 were within the normal ranges. The case can be considered strongly significative because of the rarity of this syndrome; moreover, the early monitoring detected some data which could contribute to the knowledge of the physiopathology of contrast media adverse reaction. Overall, the presence of an immunological disease can increase the risk for adverse reactions to contrast media.
 ...
PMID:[Acute pulmonary edema from contrast media. A clinical case]. 1047 47


1 2 Next >>