Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The feline model of respiratory hypersensitivity induced by intraperitoneal injection of ovalbumin has been studied. IgE serum antibodies were present for 3-10 weeks following sensitization, with maximum titers occurring between 50 and 70 days. Similarly, peak passive cutaneous anaphylaxis reactions occurred between 50 and 70 days. Alveolar macrophages, obtained by tracheal lavage at 65 days after sensitization, produced elastase like and collagenase-like secretions 48 h after challenge with ovalbumin in culture. Macrophages from nonsensitized cats did not produce these secretions. It is hypothesized that reaginic antibodies and sensitized alveolar macrophages, such as those found in the cat model, may be responsible in part for the destruction of lung tissue found in long-term respiratory diseases, similar to fibrosing alveolitis and pulmonary emphysema in man.
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PMID:Increase in serum IgE levels of ovalbumin-sensitized cats and the detection of elastase and collagenase activities in secretions of sensitized feline alveolar macrophages challenged in vitro. 19 42

1. Histamine in small doses caused systemic depressor responses in horses, whereas greater doses caused biphasic effects. All doses of 5-hydroxytrypt-amine (5-HT) were pressor and all doses of bradykinin depressor. All three active substances raised pulmonary artery pressure and lowered central venous pressure. 5-HT reduced ventilation volume. Histamine caused brief apnoea followed by hyperpnoea only.2. Acute anaphylaxis in the horse was accompanied by a severe systemic arterial depressor response, a pressor response in the pulmonary artery and vena cava, and alternating phases of apnoea and dyspnoea.3. During anaphylaxis, profound haemoconcentration, leucopoenia, thrombocytopoenia and hyperkalaemia were in evidence. Early during anaphylactic shock (2 to 4 min) there were profound increases in plasma histamine (five to six-fold) and plasma kinin activity (four to five-fold). Plasma 5-HT concentrations were reduced initially but recovered. Later in anaphylaxis (10 to 20 min) whole blood histamine concentration fell significantly. This coincided with the most profound period of leucopoenia.4. No significant differences were observed in histamine concentration in any of five tissues between six ponies subjected to anaphylaxis and six controls. Mast cell numbers were not reduced but mast cells were more metachromatic (pink) and there was spilling of mast cell granules.5. Gross pathological changes were noted mainly in the lungs which were extensively oedematous and congested. Inflamed, congested and oedematous areas in the large colon and caecum were seen, and the kidneys, spleen and liver were engorged. Alveolar emphysema, peribroncheolar oedema (containing mononuclear cells and neutrophils) were recorded. Alveoli contained erythrocytes.
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PMID:Acute systemic anaphylaxis in the horse. 476 91

The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response, appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. The insidious and probably most important human lung disease due to particles is bronchiolar obstruction and obliteration, producing progressive impairment of air flow. The responsible particle is the complex combination of poorly digestive lipids and complex carbohydrates with active chemicals which we call cigarette smoke. More research is needed to perfect, correct and quantify our preliminary picture of the pathogenesis of lung disease by particles, but a useful start has been made.
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PMID:Particles causing lung disease. 637 14

Anaphylactic shock was produced in guinea-pigs by sensitizing them with oval albumin and challenging them with an intracardial dose (rapid shock) or intraperitoneal dose (slow shock) of the same protein 4 weeks later. The animals died within 5 min or 30 min, respectively. Blood for biochemical assays was taken by cardiac puncture and tissue samples were excised for histamine assay and histological studies. High concentrations of histamine (4-5 times the control values) were measured in the animals which died rapidly, but not in the others, whereas the histamine content of the stomach wall and lungs was decreased both in rapid and slow shock. Plasma cortisol was low in the rapid shock group. Plasma free fatty acids were high in both groups, but glucose only in the slow shock group. The lungs were distended, indicating bronchial obstruction. Occasional platelet agglutinations were seen in the lung veins. The most promising signs regarding the diagnosis of death from anaphylaxis were the high plasma histamine values and acute emphysema.
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PMID:Histamine, cortisol and organ changes in fatal anaphylactic shock in guinea-pigs. 670 65

Bronchial asthma remains a significant cause of mortality at all ages, despite the increased understanding of its pathogenesis and the range of drugs available for its treatment. Changes in therapeutic management can influence death rates and constant surveillance, combined with high-quality post mortem investigations, is essential. Disease severity, poor disease management and adverse psychosocial circumstances are all risk factors for asthma mortality. Bronchial asthma causes characteristic histological changes in the mucosa of the airways which are present even before the clinical diagnosis of asthma can be made. These include fibrous thickening of the lamina reticularis of the epithelial basement membrane, smooth muscle hypertrophy and hyperplasia, increased mucosal vascularity and an eosinophil-rich inflammatory cell infiltrate. In addition, mucoid plugging of the airway lumen is frequently associated with fatal asthma. The recognition of these changes can allow the diagnosis of asthma to be made for the first time at autopsy, in those cases where asthma goes undiagnosed in life. Acute severe asthma may be accompanied by pneumothorax and surgical emphysema of the mediastinum. Disorders which may mimic asthma include pulmonary embolism, chronic obstructive pulmonary disease and anaphylaxis, but careful post mortem examination and appropriate investigations should reveal the true cause of death.
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PMID:Asthma deaths; persistent and preventable mortality. 1287 25

Asphyxia, not an uncommon cause of sudden death, may result from numerous etiologies. Foreign-body aspiration and strangulation are 2 extrinsic causes. Airway obstruction may also be caused by laryngeal edema, asthma, infection, or anaphylaxis. Chronic causes of asphyxia include musculoskeletal diseases (eg, muscular dystrophy, amyotrophic lateral sclerosis), neurologic disorders (eg, myasthenia gravis, multiple sclerosis), respiratory disease (eg, emphysema, chronic bronchitis), or tumors. The manner of death in cases of asphyxiation may be natural, accidental, homicide, or suicide. For the death investigator, determining the cause and manner of death can often be quite challenging. We report here 2 cases of an esophageal fibrovascular polyp causing sudden asphyxial death, review of the literature, and discussion of other differential diagnoses in the case of asphyxial death.
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PMID:Sudden death due to asphyxia by esophageal polyp: two case reports and review of asphyxial deaths. 1612 Oct 86

The distribution profile of infiltrated mast cell-subpopulations and eosinophils in the lung and heart sections of the patients who died of severe allergic hyperresponsiveness, was investigated. Four study groups were designed comprising 9 cases who died in systemic anaphylaxis (Group I), 10 asthmatic individuals whose death were assigned to acute and severe bronchial asthma (Group II), 10 asthmatic cases who died from non-immunological diseases (Group III). Twenty consecutive autopsies of non-allergic subjects who died of unnatural causes (Group IV) served as control group in this study. Utilizing antibodies against human tryptase and chymase and a double immunohistochemical staining method, we distinguished successfully all three subsets of mast cells (MC), MC-TC (containing both tryptase and chymase), MC-T (containing only tryptase) and MC-C (containing only chymase) types, subdivided on the basis of the protease compositions of their secretory granules. In order to immunostaining eosinophils, we used antibody to major basic protein as a marker. We also measured postmortem blood tryptase, specific and total serum IgE. The intriguing finding of this study was the marked differences of cellular composition in the lung between fatal anaphylaxis and asthma death. Significant augmentation of MCs infiltrated in lung and heart sections of anaphylaxis patients and drastic infiltration of bronchial eosinophils in asthmatic death and consequent release of their related inflammatory mediators might explain the differential expression of the associated symptoms in these two groups. The anaphylactic deaths did show neither emphysema nor significant mucous bronchial secretions whereas all asthmatic deaths did. The degree of pulmonary congestion and edema was also more severe in anaphylaxis. This corresponded with the histological findings and the location and number of mast cell-subsets and eosinophils in the different compartments of the lungs. We have demonstrated that the third type of mast cell MC-C is only found in the lungs in anaphylactic deaths. The practical consequence of our study will be that it is now possible to confirm a suspicion of anaphylaxis death not only by measurements of serum mast cell tryptase, but also by immunohistochemical methods.
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PMID:Differential accumulation of pulmonary and cardiac mast cell-subsets and eosinophils between fatal anaphylaxis and asthma death: a postmortem comparative study. 1708 16

This report details the pathological and radiological findings in a rare case of massive subcutaneous emphysema. A 74-year-old male presented with sudden onset dyspnea and facial swelling following a fall. His symptoms were refractory to treatments for anaphylaxis, which was suspected clinically, and he quickly succumbed. Autopsy, including post mortem CT scan revealed the underlying etiology to be multiple rib fractures with rupture of the parietal pleura, bilateral pneumothoraxes and massive subcutaneous emphysema involving the face, torso and upper limbs. Multiple frothy air bubbles were observed throughout the mediastinal adipose tissues on internal examination. Our findings echo those of rare previous reports and show how subcutaneous emphysema may, in rare circumstances, mimic anaphylaxis.
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PMID:Massive subcutaneous emphysema mimicking anaphylaxis - pathological and radiological correlations. 3131 86