Differentials
Asthma exacerbation
SIGNS / SYMPTOMS
Although mucus production may increase with asthma, brown mucus plugs and hemoptysis are unlikely.
INVESTIGATIONS
Skin test for sensitivity to Aspergillus fumigatus: negative.
Serum total IgE: in nonallergic asthma, not elevated (tested when the patient is not taking systemic corticosteroids as these decrease IgE levels).
Aspergillus-specific IgE and IgG: not elevated.
Non-ABPA infectious exacerbation of cystic fibrosis
SIGNS / SYMPTOMS
Clinically there is no differentiating sign or symptom.
INVESTIGATIONS
Serum total IgE: not elevated.
Aspergillus-specific IgE and IgG: not elevated.
Chest x-ray: no new infiltrates from baseline.
Skin test for sensitivity to A fumigatus: negative.
Chronic eosinophilic pneumonia
SIGNS / SYMPTOMS
Similar clinical features to ABPA.
Asthma accompanies or precedes the illness in 50% of cases.[24]
Occurs predominantly in women and nonsmokers; cases have been reported after radiation therapy for breast cancer.[36][37]
INVESTIGATIONS
Chest x-ray: bilateral peripheral or pleural-based infiltrates, described as the photographic negative of pulmonary edema, are virtually pathognomonic for chronic eosinophilic pneumonia (CEP).
Lung biopsy: CEP is characterized by interstitial and alveolar eosinophils and histiocytes. Fibrosis is minimal, and bronchiolitis obliterans organizing pneumonia is a commonly associated finding.[24]
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
SIGNS / SYMPTOMS
Vasculitic disorder as opposed to an allergic condition.
Often includes sinusitis as a clinical manifestation, whereas sinusitis rarely occurs with ABPA.[38][39][40]
The skin and cardiovascular, GI, and nervous systems may also be involved. Skin symptoms include palpable purpura, petechiae, or granulomatous nodules. Cardiovascular symptoms include pericarditis, heart failure, and myocardial infarct. GI symptoms include diarrhea, pain, bleeding, and colitis.
INVESTIGATIONS
Chest x-ray: commonly shows transient and patchy opacities without lobar or segmental distribution.[40]
Lung biopsy: eosinophilic infiltrates, an eosinophilic vasculitis (especially of the small arteries and veins), interstitial and perivascular necrotizing granulomas, and areas of necrosis.[39][40]
Hypereosinophilic syndromes (HES)
SIGNS / SYMPTOMS
HES are associated with marked peripheral eosinophilia and potential involvement of diverse organs such as the heart, GI tract, lungs, brain, and skin.[41]
Although 40% of HES patients have pulmonary manifestations, they also have signs and/or symptoms of end-organ dysfunction (not limited to the respiratory tract). Cardiac manifestations of eosinophilic myocarditis are the major cause of morbidity and mortality. Neurologic manifestations of cerebral thromboemboli, encephalopathy, and neuropathy may be presenting symptoms. Colitis and gastritis may occur from eosinophil infiltration of gut mucosa. Common skin manifestations are eczema, hives, and angioedema.
INVESTIGATIONS
Molecular testing for the FIP1L1/PDGFR-alpha mutation: may be positive for a genetic variant of HES.[42]
Bone marrow evaluation: demonstrates increased eosinophils and eosinophil precursors or may confirm a myeloproliferative process.[41]
Blood eosinophilia: HES has ≥1500/microliter present on at least 2 occasions in the absence of any other cause. In ABPA the cause is hypersensitivity to the Aspergillus mold, whereas in HES no etiology is found.
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