Abstract
Allergic bronchopulmonary aspergillosis (ABPA) is a Th2 hypersensitivity lung disease in response to Aspergillus fumigatus that affects asthmatic and cystic fibrosis (CF) patients. Sensitization to A. fumigatus is common in both atopic asthmatic and CF patients, yet only 1-2% of asthmatic and 7–9% of CF patients develop ABPA. ABPA is characterized by wheezing and pulmonary infiltrates which may lead to pulmonary fibrosis and/or bronchiectasis. The inflammatory response is characterized by Th2 responses to Aspergillus allergens, increased serum IgE and eosinophilia. A number of genetic risks have recently been identified in the development of ABPA. These include HLA-DR and HLA-DQ, IL-4 receptor alpha chain (IL-4RA) polymorphisms, IL-10-1082GA promoter polymorphisms, surfactant protein A2 (SP-A2) polymorphisms, and cystic fibrosis transmembrane conductance regulator gene (CFTR) mutations. The studies indicate that ABPA patients are genetically at risk to develop skewed and heightened Th2 responses to A. fumigatus antigens. These genetic risk studies and their consequences of elevated biologic markers may aid in identifying asthmatic and CF patients who are at risk to the development of ABPA. Furthermore, these studies suggest that immune modulation with medications such as anti-IgE, anti-IL-4 and/or IL-13 monoclonal antibodies may be helpful in the treatment of ABPA.
Highlights
Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease due to bronchial colonization by Aspergillus fumigatus that occurs in susceptible patients with asthma and cystic fibrosis (CF)
Classic Diagnostic Criteria (i) Acute or subacute clinical deterioration not attributable to another etiology (ii) Total serum IgE concentration greater than 1000 IU/mL unless patient is receiving corticosteroid therapy (iii) Immediate cutaneous reactivity to Aspergillus fumigatus while the patient is not being treated with antihistamines or in vitro presence of serum IgE antibody to A. fumigatus (iv) Precipitating antibodies or serum IgG antibody to A. fumigatus (v) New or recent abnormalities on chest radiography or chest CT that have not cleared with antibiotics and standard physiotherapy
If patient is taking steroids, repeat when steroid treatment is discontinued. (iii) Immediate cutaneous reactivity to Aspergillus fumigatus while the patient is not being treated with antihistamines or in vitro presence of serum IgE antibody to A. fumigatus (iv) One of the following: (a) precipitins to A. fumigatus or in vitro documentation of IgG antibody to A. fumigates, or (b) new or recent abnormalities on chest radiography or chest CT that have not cleared with antibiotics and standard physiotherapy of airway walls
Summary
Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease due to bronchial colonization by Aspergillus fumigatus that occurs in susceptible patients with asthma and cystic fibrosis (CF). The first published description of ABPA as an entity came from the United Kingdom in 1952 [1], while the first cases in the United States were reported a decade later [2, 3]. ABPA affects approximately 1-2% of asthmatic patients and 7–9% of CF patients [4,5,6]. If unrecognized or poorly treated, ABPA leads to airway destruction, bronchiectasis, and/or pulmonary fibrosis, resulting in significant morbidity and mortality
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