Abstract
Allergic bronchopulmonary aspergillosis (ABPA) is a pulmonary disorder, occurring mostly in asthmatic and cystic fibrosis patients, caused by an abnormal T-helper 2 lymphocyte response of the host to Aspergillus fumigatus antigens. ABPA diagnosis is defined by clinical, laboratory and radiological criteria including active asthma, immediate skin reactivity to A. fumigatus antigens, total serum IgE levels>1000 IU/mL, fleeting pulmonary parenchymal opacities and central bronchiectases that represent an irreversible complication of ABPA. Despite advances in our understanding of the role of the allergic response in the pathophysiology of ABPA, pathogenesis of the disease is still not completely clear. In addition, the absence of consensus regarding its prevalence, diagnostic criteria and staging limits the possibility of diagnosing the disease at early stages. This may delay the administration of a therapy that can potentially prevent permanent lung damage. Long-term management is still poorly studied. Present primary therapies, based on clinical experience, are not yet standardized. These consist in oral corticosteroids, which control acute symptoms by mitigating the allergic inflammatory response, azoles and, more recently, anti-IgE antibodies. The latter two are used as a steroid-sparing agent to prolong the remission stage of the disease. Anti-IgE antibodies also have immunomodulatory properties. At present, the only way to bypass these limits and allow for an early diagnosis, is to assume ABPA in all patients with difficult-to-control asthma or cystic fibrosis. They should then be screened for sensitization to A. fumigatus antigens and, if positive, monitored more closely. Future controlled studies are needed to standardize present therapy, standardize cut-off values of various investigations, define the role of different novel immunomodulatory therapies, define the role of novel assays (such as recombinant A. fumigatus antigens and CCL17) and confirm new diagnostic and staging criteria.
Highlights
Allergic bronchopulmonary aspergillosis (ABPA) is an immunological pulmonary disease resulting from a hypersensitivity to Aspergillus antigens, to Aspergillus fumigatus (A. fumigatus)
A positive Skin Prick Test (SPT) for A. fumigatus is due to IgE-mediated response to A. fumigatus antigens and it is considered the gold standard screening for ABPA
SPT is highly sensitive for A. fumigatus IgE mediated response (90%) but is not specific to ABPA: up to 40% of patients without ABPA can demonstrate a sensitization to A. fumigatus antigens [29]
Summary
Allergic bronchopulmonary aspergillosis (ABPA) is an immunological pulmonary disease resulting from a hypersensitivity to Aspergillus antigens, to Aspergillus fumigatus (A. fumigatus). Agarwal et al [23] established that ABPA diagnosis should first be formulated by the presence of two obligatory criteria — positivity of skin prick test and/or elevated serum IgE to A. fumigatus and total serum IgE levels >1000 IU/mL and at least two of three “other criteria” including precipitins or IgG antibodies to A. fumigatus, radiological pulmonary findings consistent with ABPA, and total eosinophil count >500 cells/μL (in patients not treated with steroids) [23]. The diagnostic criteria for CF-ABPA patients are reviewed extensively and most recently in the CF Foundation Consensus Conference (CFFCC) statement where ABPA is suggested in case of clinical deterioration (worsening cough, exercise intolerance or wheezing, increased sputum and decline in pulmonary function test, not attributable to another etiology) This should lead to skin testing for A. fumigatus (a wheal >3 mm in diameter is considered positive) and measurement of total serum IgE levels (suggestive of ABPA if >1000 IU/mL for patients not treated with systemic corticosteroids). Patients with difficult to control ABPA symptoms are identified by stage 5, while stage 6 includes patients with widespread bronchiectases or fibrosis [23]
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