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

Pulmonary edema complicating heroin overdosage is a well recognized entity and regarded as the major mechanism contributing to death in heroin addicts. It's pathogenesis is unknown, several mechanisms are discussed: hypoxia-induced increase of pulmonary capillary permeability, depressed myocardial contractility, centrally induced respiratory depression, primary toxic effects on the alveolar capillaries and acute anaphylactic shock. The present study included opiate-related deaths (n=23) and a control group of sudden cardiovascular deaths (n=12) to verify the hypothesis, that defects of the alveolar capillary membranes and/or an acute anaphylactic reaction leads to pulmonary congestion, edema and hemorrhages. Lung specimens were obtained from these 35 autopsies of persons autopsied in the Institute of Forensic Medicine, University of Bonn, in 1997 and 1998. All specimens were examined with hematoxylin-eosin, prussian blue and investigated with immunohistological methods using primary antibodies against collagen IV, laminin and IgE. Defects of the basal laminae of the alveoli were found, demonstrated by laminin and collagen IV, and the number of IgE-positive cells was counted in both groups. There was an increased but not significant number of IgE-positive cells in the heroin-group and defects of the epithelial and endothelial basal laminae were found in both groups without significant differences.
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PMID:Pulmonary edema in fatal heroin overdose: immunohistological investigations with IgE, collagen IV and laminin - no increase of defects of alveolar-capillary membranes. 1080 97

There is increasing evidence that inflammatory mechanisms other than atopy or eosinophilic inflammation may be involved in the pathogenesis of asthma. The mechanisms associated with non-atopic (non-IgE) or neutrophil-mediated asthma are poorly investigated. Non-atopic airway inflammation and hyperresponsiveness was induced in mice by skin sensitization with dinitrofluorobenzene (DNFB) followed by intra-airway challenge with dinitrobenzene sulfonic acid (DNS). Acute bronchoconstriction and mast cell activation were observed shortly after challenge. Increased levels of the major mast cell mediator, TNF-alpha, were found in the bronchoalveolar lavage fluid of DNFB-sensitized. Mast cells play a key role in the early release of TNF-alpha since mast-cell-deficient WBB6F1-W/Wv mice did not show an increase in TNF-alpha release after DNFB-sensitization and DNS challenge compared to their ++ littermates. Features of the late-phase pulmonary reaction included mononuclear and neutrophilic cell infiltration, pulmonary edema, in vitro tracheal hyperreactivity and in vivo airway hyperresponsiveness. These characteristics bear marked similarity with those observed in non-atopic asthmatic patients. Therefore, this model can be used to further study the mechanisms potentially responsible for the development of non-IgE-mediated asthma.
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PMID:Murine model for non-IgE-mediated asthma. 1552 66

A case of acute onset non-cardiogenic pulmonary edema induced by hydrochlorothiazide (HCT) is presented. Rapid recovery was obtained with supportive therapy. Leukopenia was evident during the acute phase, with rapid recovery parallel to the clinical improvement, suggesting pulmonary sequestration of granulocytes. Immunological studies including lymphocyte stimulation test with HCT and measurement of specific IgG and IgE to HCT elicited negative results. The pathogenesis of this type of reaction remains to be elucidated.
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PMID:Immunological studies in a case of hydrochlorothiazide-induced pulmonary edema. 1643 12

Caffeic acid phenethyl ester (CAPE) is an active component of honeybee propolis extracts. It has several positive effects, including anti-inflammatory, anti-oxidation, anti-cancer, anti-bacterial, anti-viral, anti-fungal, and immunomodulatory effects. In particular, the suppressive effect of NF-kappaB may disrupt a component of allergic induction. The principal objective of this experimental study was to evaluate the effects of CAPE on the active systemic anaphylaxis induced by ovalbumin (OVA) challenge in mice. Mice were intraperitoneally sensitized and intravenously challenged with OVA. Histopathological analysis, nuclear factor (NF)-kappaB activation, and the plasma levels of histamine and total IgE after allergen challenge were evaluated. After challenges, all of the sham-treated mice developed anaphylactic symptoms, increased plasma levels of histamine and OVA-specific IgE, marked vascular leakage, NF-kappaB activation, platelet-activating factor (PAF) production, and histological changes including pulmonary edema and hemorrhage in the renal medullae within 20 min. By way of contrast, a reduction in the plasma levels of histamine and OVA-specific IgE and an inhibition of NF-kappaB activation and PAF release were observed in the CAPE-treated mice. In addition, a significant prevention of hemoconcentration and OVA-induced pathological changes were noted. These results indicate that CAPE demonstrates an anti-allergic effect, which may be the result of its protective effects against IgE-mediated allergy.
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PMID:Evaluation of anti-allergic properties of caffeic acid phenethyl ester in a murine model of systemic anaphylaxis. 1788 25

Release and activation of pro-inflammatory mediators are among the most important induced factors that are involved in the scorpion envenomation pathogenesis. Inflammatory response and lung reactivity were studied in mice following subcutaneous injection with Androctonus australis hector (Aah) venom. Venom immunodetection in lungs and sequestered cell population in the airways were determined. Cytokines, cellular peroxidase activities (eosinophil peroxidase, myeloperoxydase), and IgE antibodies were also assessed. Immunohistochemical study revealed a positive detection of the Aah venom in the alveolar wall, venule lumens, and inside inflammatory cells. Severe lung edema associated with rapid inflammatory response was observed after animal envenomation. Lung neutrophilia and eosinophilia were accompanied with IL-4, IL-5 release, and IgE synthesis. In conclusion, high cytokine levels, recruitment of inflammatory cells (eosinophils and neutrophils), and increased IgE concentration may contribute to the exacerbation and maintenance of the induced inflammatory response in lungs by scorpion venom. These results lead to the better understanding of this induced pathogenesis and could help the physicians to take care of envenomed patients.
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PMID:Lung immunoreactivity and airway inflammation: their assessment after scorpion envenomation. 2154

Adverse reactions to radiographic contrast media are relatively rare and occur with a frequency of 0.02-0.04%. We describe a case of isolated pulmonary oedema after computed tomography of the coronary arteries in a 51 year-old man. Initially anaphylaxis was suspected, but due to the clinical picture together with lack of response to treatment with adrenaline and lack of increase in the serum tryptase concentration an IgE mediated mechanism was less likely. The patient responded to non-invasive ventilation over three days. The mechanism behind the reaction is unknown.
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PMID:[Pulmonary oedema subsequent to radiographic contrast in a computed tomography of the coronary arteries]. 2256 93

Vitexin is an important component of various medicinal plants frequently used to treat asthma, such as Crataegus spp., Vitex spp., Passiflora spp., and Echinodorus spp. However, there is no information about the vitexin potential as anti-asthmatic. The aim of the present work was to evaluate the anti-hypersensitive activity of vitexin in a murine ovalbumin (OVA)-induced allergic asthma model. Mice were sensitized to OVA by i.p. injection on days 1st and 10th, followed by a daily challenge with OVA using a nebulizer, from days 19th to 24th. Vitexin or dexamethasone were orally administered 1h before each OVA challenge. Vitexin attenuates migration induced by OVA-hypersensitivity of eosinophil, neutrophil, and mononuclear cells in bronchoalveolar lavage fluid (BALF). Histological analysis of the lungs shows that vitexin suppressed leukocyte infiltration, mucus production and pulmonary edema. Increases in Th2 cytokines in BALF in OVA-induced asthma is also attenuated by vitexin, as well as plasma levels of IgE. Overall, these results suggest that vitexin can suppress OVA-induced allergic inflammation in mice and provide a strong rationale for further developing vitexin as a candidate treatment for allergic hypersensitivity. These data corroborate the popular use of vitexin-rich plants for asthma treatment.
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PMID:Vitexin inhibits inflammation in murine ovalbumin-induced allergic asthma. 2909 59

BACKGROUND Hypereosinophilic syndrome (HES) is defined as hypereosinophilia with eosinophil mediated organ damage or dysfunction, provided that other causes of organ damage have been excluded. CASE REPORT An 83-year-old female presented with worsening dyspnea for 3 weeks. She was initially diagnosed with bronchitis and prescribed oral antibiotics along with prednisone taper. However, her dyspnea continued to worsen requiring hospitalization. Physical examination was significant for signs of volume overload. Laboratory investigations were notable for leukocytosis with eosinophilia, elevated BNP (brain natriuretic peptide) and troponin. Electrocardiogram (ECG) showed normal sinus rhythm with non-specific ST-T wave changes. Computed tomography (CT) scan of the chest showed pulmonary edema, bilateral peripheral ground glass opacities, and pleural effusions. Transthoracic echocardiogram (TTE) revealed an ejection fraction (EF) of 45%. She was diagnosed with NSTEMI (non-ST-elevation myocardial infarction) with new onset heart failure; appropriate management was initiated. Left heart catheterization did not show any significant obstructive lesions. Presence of peripheral ground glass opacities on the CT chest scan and eosinophilia raised suspicion for HES. Thorough HES workup was done, all tests came back negative except for elevated serum IgE level. Cardiac biopsy returned positive for eosinophilic myocarditis. Bone marrow biopsy showed 20% eosinophils. Positron emission tomography (PET) scan did not show any hypermetabolic lesions to suggest malignancy. The patient was managed for idiopathic HES with high dose steroids resulting in significant clinical improvement. CONCLUSIONS About 40% of patient with HES manifest cardiac involvement, and one quarter of patients with HES have pulmonary involvement with variable radiologic findings. Steroids remain the mainstay treatment for idiopathic HES.
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PMID:Idiopathic Hypereosinophilic Syndrome in an Elderly Female: A Case Report. 3090 63


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