Immunoglobulin levels and electron microscopy in eosinophilic pneumonia

Five cases of acute eosinophilic pneumonia have been studied. High levels of Immunoglobulin E (IgE) occurring during the acute episode fell to normal during naturally occurring or corticosteroid-induced remission. Severe restriction of ventilation with marked impairment of pulmonary gas exchange and...

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Veröffentlicht in:The American journal of medicine 1978-01, Vol.64 (3), p.529-536
Hauptverfasser: McEvoy, J.D.S., Donald, K.J., Edwards, R.L.
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Sprache:eng
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Zusammenfassung:Five cases of acute eosinophilic pneumonia have been studied. High levels of Immunoglobulin E (IgE) occurring during the acute episode fell to normal during naturally occurring or corticosteroid-induced remission. Severe restriction of ventilation with marked impairment of pulmonary gas exchange and severe hypoxemia during the acute episodes were followed by residual abnormalities of carbon monoxide gas transfer after clinical roentgenologic resolution had occurred. Light microscopy of lung biopsy specimens obtained in the acute phase showed a characteristic pattern of aggregation and rupture of eosinophils in the lung with interstitial edema, mild interstitial fibrosis and minimal alveolar epithelial cell response. Electron microscopy showed eosinophils rupturing in the interstitial tissue with active ingestion of eosinophil granules by macrophages. Massive hydropic change in interstitial macrophages and endothelial cells with edema of adjacent interstitial tissue was the striking ultrastructural lesion. There was also ultrastructural evidence of intravascular leukocyte rupture, platelet aggregation and coagulation in pulmonary vessels. Immunofluorescent studies of lung biopsy tissue did not show evidence of immunoglobulins G (IgG), A (IgA), M (IgM), E (IgE) or complement but one did show fibrin. The findings suggest that eosinophilic pneumonia is a reagin-mediated hypersensitivity pneumonitis. The role of eosinophil lysis in the pathogenesis of the intracellular and extracellular edema, local coagulation in pulmonary vessels and residual fibrosls warrants further investigation.
ISSN:0002-9343
1555-7162
DOI:10.1016/0002-9343(78)90248-6