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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In immunological investigations in hypersensitivity pneumonia some have a diagnostic value for the clinician but many others are essentially of interest in research and in analysing the pathophysiology. Unfortunately, skin tests with the responsible antigens are often positive in patients but also in exposed subjects without the lung disease. Studies on peripheral blood require a search for IgE immediate hypersensitivity which is rarely positive and above all a search for precipitating antibodies by the different standard tests available: there again, positive findings occur often enough in exposed but asymptomatic subjects; the sensibility and specificity of cell-mediated hypersensitivity tests seem much more reliable. The study of cell populations in broncho-alveolar lavage fluid generally shows an inverted T4:T8 lymphocyte ratio; a functional analysis seems to show a high degree of lymphocyte activation, which may be of T4 or T8 phenotype whilst cytotoxic lymphocyte activity would be exclusively found in the patients and not in asymptomatic exposed subjects. The provocation test, as long as it is positive, is one of the firmest elements in a diagnosis, above all if one takes care to couple this with a study of the lavage. Finally, the satisfaction of the immuno-histological criteria is currently rarely required to confirm the presence of hypersensitivity pneumonitis.
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PMID:[Immunological studies in hypersensitivity pneumopathies]. 329 29

Complete absence of the C1r portion of the first component of complement was found in a 2 1/2-year-old boy of Puerto Rican origin who presented with a staphylococcal liver abscess. His medical history also included two episodes of pneumonia complicated by a pneumatocele and empyema, purulent staphylococcal lymphadenitis, recurrent otitis media, and pneumococcal bacteremia. The C1s component of complement was 50% of normal, and C4 was elevated. Other immunologic tests, including nitroblue tetrazolium test, and IgE were normal. This is the tenth patient reported with C1r deficiency. The patient differs from other reported patients with C1r deficiency in that he presented with a liver abscess, an infection that has not been reported in patients with complement deficiencies, and in that he has an apparent susceptibility to staphylococcal infection.
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PMID:Recurrent infections and staphylococcal liver abscess in a child with C1r deficiency. 331 73

We describe a case of eosinophilic pneumonia in which plasma cells appeared in bronchoalveolar lavage fluid (BALF). A 49-year-old man presented with wheezing, lung infiltrates, peripheral eosinophilia, and extremely high IgE levels in serum and BALF. A differential count of BALF revealed 56.6 percent lymphocytes and 1.3 percent plasma cells. The appearance of plasma cells suggests local maturation of B cells and represents a morphologic proof of local production of immunoglobulins. The increased number of lymphocytes suggests their role in B cell differentiation via the lymphokine network.
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PMID:Plasma cells in the bronchoalveolar lavage fluid of a patient with eosinophilic pneumonia. Morphologic proof of local production of antibodies. 333 39

We studied a patient with relapsing idiopathic chronic eosinophilic pneumonia. Each one of four attacks observed during a 4-year period was characterized by dyspnea, wheezing, peripheral blood eosinophilia, elevated serum IgE levels, and pulmonary infiltrates. Glucocorticoid therapy caused prompt resolution of symptoms and disappearance of blood eosinophilia and pulmonary shadowing. Electron microscopy and tissue immunofluorescence studies for major basic protein documented extensive eosinophil degranulation and the presence of free granules within the pulmonary microvasculature. In addition, exfoliation of the alveolar lining cell was observed in association with a clustering of free intact and disintegrating extracellular eosinophil granules against a denuded basement membrane. These findings suggest a cytotoxic potential of the eosinophil at the level of the pulmonary parenchyma in a case of idiopathic chronic eosinophilic pneumonia.
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PMID:Ultrastructural and immunohistochemical evidence for release of eosinophilic granules in vivo: cytotoxic potential in chronic eosinophilic pneumonia. 355 78

The Hyper IgE syndrome is a rare disease consisting of recurrent sinusitis and pneumonia, pneumatoceles, chronic dermatitis, and elevated serum levels of IgE. The primary radiographic abnormalities are recurrent alveolar lung disease and pneumatoceles. Pneumothorax may occasionally occur as in one of our cases. Other causes of pneumatoceles are usually easily excluded by the history and other clinical data. Pulmonary scintigraphy and computed tomography may add information valuable to the management of these patients.
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PMID:Hyperimmunoglobulinemia E syndrome: pulmonary imaging considerations. 372 44

Five patients with eosinophilic lung diseases and blood hypereosinophilia (PIE syndrome) were investigated clinically and by bronchoalveolar lavage (BAL). Comparative studies on blood and alveolar eosinophils were carried out after purification and selection of eosinophil subpopulations according to their density. A predominant 'hypodense' alveolar eosinophil population was found in BAL fluids of active chronic eosinophilic pneumonia (CEP). In addition, supernatants of alveolar macrophages obtained from CEP are able to enhance spontaneously the generation of eosinophil oxygen metabolites. Such eosinophil stimulation emphasizes a probable tissue cell cooperation. In addition, BAL permitted the study of membrane immunological markers on eosinophilic inflammatory cells endowed with migratory properties. An increase in eosinophils carrying surface IgE was demonstrated in alveolar cells from PIE Syndrome particularly with hypodense eosinophils from CEP patients. Although no specific stimulus is known at the present time, this work underlines the potential implication of IgE-mediated hypersensitivity processes in the pathogenesis of eosinophilic lung diseases.
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PMID:Eosinophilic lung disease: immunological studies of blood and alveolar eosinophils. 395 85

Among 586 children with asthma, 484 (82%) were found to have IgE-mediated ("extrinsic") asthma, and seventy-two (12%) non-IgE ("intrinsic") asthma. The remaining 30 patients (6%) were classified as "intermediate", as they had serum IgE within or above serum IgE levels of healthy children but no allergy to common allergens. During a three-year study period, the seventy-two patients with intrinsic asthma as opposed to 84 patients with extrinsic asthma had significantly more hyperinflation of the lungs, more episodes of acute hospital admissions due to asthma and/or pneumonia, more elevated serum IgG and IgM, and more cultures from secretions of lower airways of Haemophilus influenzae and pneumococci. Further, although treated with corticosteroids, eleven of the children with intrinsic asthma showed progressive disease, judged from fixed and/or declining forced vital capacity followed by signs of lung fibrosis on repeated pulmonary X-rays. It is emphasized that children with intrinsic asthma may represent an entity of childhood asthma, in some cases with severe progression of disease within a few years.
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PMID:Non-IgE-mediated asthma in children. 405 Apr 18

The cell populations in the alveoli are exposed to the environment and react differently to each type of challenge (mineral particles, toxic gases, infections, antigenic substances. . .). Amongst the best studied of these irritant factors is tobacco smoke which in the long term leads to a number of changes both in the distribution of alveolar cells and also their function and morphology. Amongst acute and sub-acute pathogens, bacterial infections produce a rapid poly-morpho-nuclear neutrophilia and then a lymphocytosis; oxygen and oxidising agents in general lead to a neutrophilia which amplifies the pulmonary parenchymal changes related to the release of toxic metabolites of oxygen. The inhalation of antigenic substances also disturbs the behaviour of alveolar cells: activation of macrophages in the presence of allergy in those sensitized to IgE and immediate attraction of neutrophils preceding a T lymphocyte alveolitis in hypersensitivity pneumonia. It is possible to categorise several patterns of reaction in intra-pulmonary cells when challenged by some insult, a direct cytotoxic action, the accumulation of inflammatory cells and immunological competence corresponding to the concept of "a neutrophil alveolitis" or a "T cell alveolitis" with the development of emphysematous lesions. An understanding of the cellular make-up present in the alveoli when reacting to an external pathogen enables a better approach to the pathophysiological mechanisms in question.
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PMID:[Local cellular response to stress of the lower lung]. 687 51

A six year old female presented with a recent history of pyoderma gangrenosum involving her legs and arms associated with an episode of Mycoplasma-like pneumonia. This was followed by Aspergillus osteomyelitis involving her left ulna and right femur. Both the skin lesions and the osteomyelitis responded to prolonged treatment with antifungal and antibiotic agents. Investigation of this patient revealed (1) an elevated serum IgE (4,800 units/ml), (2) defect in neutrophil chemotaxis that appeared to be due to immune complexes, (3) an abnormal nitroblue tetrazolium (NBT) result (0 percent stimulated and unstimulated), and (4) depressed mitogen responses to concanavalin A, phytohemagglutinin, and pokeweed mitogen, negative results of intradermal skin tests, and negative dinitrochlorobenzene (DNCB) sensitization. The patient's clinically unaffected sibling had similar findings except for a positive DNCB response. In both children, intracellular bacterial killing of catalase-positive and negative organisms was normal. Kindred studies revealed widespread T-cell abnormalities consistent with autosomal dominant inheritance. Tissue typing studies showed that affected siblings shared the A1, B8, DR3 haplotype. This kindred is unique in that both the proband and the sibling have abnormalities of both the hyper-IgE syndrome and chronic granulomatous disease.
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PMID:Combined neutrophil and T-cell deficiency: initial report of a kindred with features of the hyper-IgE syndrome and chronic granulomatous disease. 697 28

We described three cases of eosinophilic pneumonia of unknown aetiology investigated clinically and by lung biopsy. The illnesses lasted between six and 20 weeks and consisted of cough, dyspnoea, malaise, and in two cases prolonged pyrexia. All had blood eosinophilia and chest radiographs showing widespread bilateral shadowing; in two cases this had a characteristic peripheral distribution. One patient recovered spontaneously and the other two responded to steroids, with disappearance of pyrexia within 12 hours and radiological clearing within 14 days. Lung function tests during the acute illness showed volume restriction or gas transfer defects or both in two cases. After remission all three showed abnormalities if small airways function. Lung biopsies performed during the acute illness were examined histologically and by transmission electron microscopy, and in two cases by immunofluorescence. There was both intra-alveolar and interstitial eosinophilic pneumonia with bronchiolitis obliterans, microgranulomata, and a vasculitis. Electron microscopy showed numerous eosinophils, many degranulated, and macrophages with phagocytosed eosinophilic granules and intracytoplasmic inclusions. In one case IgM, IgG, and IgA were demonstrated in the bronchial walls and interstitium. No IgE or complement was present. We believe that eosinophil granules are responsible for the tissue damage and fever and suggest mechanisms for this and for the response to steroid therapy.
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PMID:Chronic eosinophilic pneumonia. 700 96


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