Allergic bronchopulmonary aspergillosis - CHEST Publications ...

Table 1—Studies Describing the Prevalence of AH and/or ABPA in Patients with Bronchial Asthma Over the Last
Two Decades*
Study/Year Type of Study
Type of Skin
Test Type of Antigen
Attapattu 31 /1991 Prospective Intradermal Commercial (Bencard
Allergie; Munich,
Germany)
Eaton et al 33 /2000
Kumar and Gaur
Prospective Prick Commercial (Hollister-
Stier Laboratories)
34 /
2000
Base was performed for relevant studies published from
1952 to 2008. A total of 250 articles were reviewed for the
purpose of this article.
Epidemiology of ABPA
Aspergillus hypersensitivity (AH) is defined by the
presence of an immediate-type cutaneous hypersensitivity
to A fumigatus antigens, and it is the first step
in the development of ABPA. 24 Only a minority of
patients with AH develop the complete clinical
picture of ABPA. 25 The population prevalence of
ABPA in asthma, generally referred to as 1 to
2%, 5,13,26,27 is based on the inference of only three
studies (one peer-reviewed and two non–peer-reviewed
studies). 28,29 In the only peer-reviewed
study, 28 14 patients with allergic bronchopulmonary
mycosis were identified from a total of 1,390 new
referrals in a catchment area population of half a
million, estimating a period prevalence of just above
1%. The other two non–peer-reviewed questionnaire-based
studies suggested a maximum prevalence
of ABPA of 1% in the United States. 29 In a
recent metaanalysis, 30 we demonstrated a prevalence
of AH and ABPA in asthma of 28% and 12.9%,
respectively. The limitation noted in this review was
that all the studies were performed in specialized
clinics and may not be representative of the general
population. Thus the exact population prevalence of
ABPA remains speculative but is likely to be fairly
Criteria Used for
Diagnosis of ABPA
Major (A/R/T/E/P)
Minor (C)
Prevalence of AH
in Asthma (n/N)
Prevalence of ABPA
in Asthma (n/N)
58/134 8/134
Major (A/R/T/E/P/
I/C/S)
47/255 9/35
Prospective Intradermal Locally prepared Major (A/R/T/E/P/
I/C/S)
Minor (C/S/B)
47/200 32/200
Al-Mobeireek et al 20 / Prospective Prick Commercial (Soluprick;
12/53
2001
ALK Laboratories;
Wallingford, CT)
Maurya et al 35 /2005 Prospective Intradermal Locally prepared Major (A/R/T/E/P/
I/C/S)
Minor (C/S)
30/105 8/105
Agarwal et al 23 /2007 Prospective Intradermal Commercial (Hollister- Major (A/R/T/E/P/ 291/755 155/755
Stier Laboratories) I/C/S)
Minor (S/B)
Prasad et al 36 /2008 Prospective Intradermal Not available Major (A/R/T/E/P/
I/C/S)
Minor (C/S/B)
74/244 18/244
* Criteria for ABPA: Major (A asthma, R radiologic opacities, T immediate positive skin test, E eosinophilia, P precipitins to A
fumigatus, I IgE elevated, C central bronchiectasis, S specific IgG/IgE to A fumigatus); Minor (C sputum cultures of A fumigatus,
S type III skin test positivity, B brownish black mucus plugs).
high in patients attending asthma clinics. Table 1
summarizes the prevalence of ABPA in patients with
asthma reported in various studies 20,23,31–36 over the
last two decades. The prevalence of ABPA in patients
admitted with acute severe asthma is even
higher. In a recent study of 57 patients with acute
severe asthma admitted in the respiratory ICUs, we
demonstrated the prevalence of AH and ABPA to be
around 51% and 39%, respectively. 37 The occurrence
of AH and ABPA was significantly higher in patients
with acute asthma compared to the outpatient bronchial
asthma (around 39% and 21%, respectively). 23
Pathogenesis of ABPA
The susceptibility of asthmatic patients to develop
ABPA is not fully understood (Fig 1). Some authors
have reported that exposure to large concentrations
of spores of A fumigatus may cause ABPA. 16,38–41
Environmental factors are not considered the main
pathogenetic factors because not all asthmatics develop
ABPA despite being exposed to the same
environment. In a genetically predisposed individual42–54
(Table 2), inhaled conidia of A fumigatus
persist and germinate into hyphae with release of
antigens that compromise the mucociliary clearance,
stimulate and breach the airway epithelial barrier,
and activate the innate immunity of the lung. 55–58
This leads to inflammatory cell influx and a resultant
early- and late-phase inflammatory reaction. 59,60 The
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