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Allergic Bronchopulmonary Aspergillosis*: Model of Bronchopulmonary Disease with Defined Serologic, Radiologic, Pathologic and Clinical Findings from Asthma to Fatal Destructive Lung Disease FREE TO VIEW

Paul A. Greenberger, M.D.; Roy Patterson, M.P., F.C.C.P.
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Reprint requests: Dr. Greenberger, Allergy-Immunology Section, 303 East Chicago Avenue, Chicago 60611


Copyright 1987, by the American College of Chest Physicians


Chest. 1987;91(6_Supplement):165S-171S. doi:10.1378/chest.91.6_Supplement.165S
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Abstract

Allergic bronchopulmonary aspergillosis (ABPA) complicates asthma and results in immunologic lung destruction. Respiratory failure or fatalities from end-stage fibrotic lung disease have occurred in patients in the third and fourth decades of life. Allergic bronchopulmonary aspergillosis may be confirmed in patients with varying severity of asthma from minimal to corticosteroid-dependent and has been reported to occur in approximately 10 percent of patients with cystic fibrosis. It has been documented in infants and children, the geriatric patient with asthma, in the presence of a normal chest roentgenogram, in the corticosteroid-dependent asthmatic patient, and on a familial basis. The pathogenesis of ABPA is unclear, but may be related to the array of immunologic abnormalities Including: 1) elevation of total serum IgE, not all of which is directed to Aspergillus fumigatus (Af); 2) elevated serum IgE-Af, IgG-Af and IgA-Af; 3) precipitating antibodies to Af; 4) hyperreactivity of peripheral blood basophils to Af and other molds; and 5) sensitized lymphocytes. Research in ABPA should be multidisciplinary and initially should include investigators in allergy-immunology, mycology, pulmonary, and epidemiology.


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