Allergic bronchopulmonary aspergillosis. Model of bronchopulmonary disease with defined serologic, radiologic, pathologic and clinical findings from asthma to fatal destructive lung disease

P. A. Greenberger, R. Patterson

Research output: Contribution to journalReview articlepeer-review

46 Scopus citations

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 immunological 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.

Original languageEnglish (US)
Pages (from-to)165S-171S
JournalCHEST
Volume91
Issue number6
DOIs
StatePublished - 1987

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine
  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Allergic bronchopulmonary aspergillosis. Model of bronchopulmonary disease with defined serologic, radiologic, pathologic and clinical findings from asthma to fatal destructive lung disease'. Together they form a unique fingerprint.

Cite this