|Year : 2019 | Volume
| Issue : 2 | Page : 63-69
Allergic bronchopulmonary aspergillosis: Indian scenario
Rajendra Prasad1, Rishabh Kacker1, Nikhil Gupta2
1 Department of Pulmonary Medicine, Era's Lucknow Medical College and Hospital, Era University, Lucknow, Uttar Pradesh, India
2 Department of Medicine, Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
|Date of Submission||27-Dec-2019|
|Date of Acceptance||06-Jan-2020|
|Date of Web Publication||28-Jan-2020|
Dr. Rajendra Prasad
Department of Pulmonary Medicine, Era's Lucknow Medical College and Hospital, Era University, Lucknow, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Aspergillus is ubiquitous, occurring in mycelial form and grows at 15-530C and humid conditions. Pulmonary aspergillosis is a clinical spectrum of lung disease caused by the fungus Aspergillus. ABPA is the commonest disease among allergic bronchopulmonary mycoses. The exact prevalence of ABPA is not known but contemporary estimates suggested that ABPA complicates 1 to 11% of all chronic cases of bronchial asthma. The basic underlying immuno-pathophysiologic process in ABPA is a hypersensitivity reaction to fungus in the bronchial tree. Patients are usually atopic with previous history of bronchial asthma. The onset is insidious with constitutional symptoms like anorexia, fatigue, weight loss, headache, generalized aches and pains, and low-grade fever. It is characterized by repeated episodes of exacerbation with periods of remission, if untreated may progress to fibrotic lung disease. Patients with chronic fibrotic disease may present with cyanosis, corpulmonale and respiratory failure. Radiologically fleeting shadows are characteristic of ABPA. Bronchiectasis, centrilobular nodules and mucoid impaction are main features of ABPA seen in CT scan thorax. Oral corticosteroid remains the cornerstone for the treatment of ABPA. Optimization of baseline asthma therapy is essential. Early diagnosis and proper treatment may alter the prognosis of disease and further prevent end stage lung fibrosis.
Keywords: Allergic bronchopulmonary aspergillosis, diagnosis, treatment
|How to cite this article:|
Prasad R, Kacker R, Gupta N. Allergic bronchopulmonary aspergillosis: Indian scenario. Indian J Allergy Asthma Immunol 2019;33:63-9
|How to cite this URL:|
Prasad R, Kacker R, Gupta N. Allergic bronchopulmonary aspergillosis: Indian scenario. Indian J Allergy Asthma Immunol [serial online] 2019 [cited 2021 Apr 21];33:63-9. Available from: https://www.ijaai.in/text.asp?2019/33/2/63/276956
| Introduction|| |
Aspergillus is ubiquitous, occurring in mycelial form, which is thermo tolerant and grows at 15°C–53°C, the optimum being 37°C–40°C and humid conditions. It is present in the environment, decaying vegetation, fallen leaves, mulch, water, saunas, basements, crawl spaces, bedding, and some foodstuffs and even in marijuana.
Pulmonary aspergillosis is a clinical spectrum of lung disease caused by the fungus Aspergillus. The classification of pulmonary aspergillosis includes saprophytic aspergillosis in the form of pulmonary aspergilloma, immune disease in the form of allergic bronchopulmonary aspergillosis (ABPA), IgE mediated asthma, hypersensitivity pneumonitis, allergic Aspergillus sinusitis (AAS) and infectious disease in the form of invasive and semi-invasive pulmonary aspergillosis. One of the latest study also categorised aspergillosis related respiratory disorders into upper and lower respiratory tract disorders. ABPA is the commonest disease among allergic bronchopulmonary mycoses. ABPA is a hypersensitivity immunological lung disorder caused by species of the dimorphic fungus Aspergillus, commonly Aspergillus fumigatus (about 95%) and rarely by Aspergillus flavus, Aspergillus niger, Aspergillus oryzae, Aspergillus sydowi, Aspergillus terreus, Aspergillus glaucus, Aspergillus nidulans, and Aspergillus clavatus'. Other fungi such as Candida, Helminthosporium, Curvularia, Drechslera, Pseudallescheria boydii, and Fusarium vasinfectum have also been found to cause an identical syndrome. Clinically manifesting as chronic asthma, recurrent pulmonary infiltrates, and bronchiectasis.,,,,,,,, The condition has immunologic features of immediate hypersensitivity (Type I), antigen-antibody complexes (Type III), and eosinophil-rich inflammatory cell responses (Type IVb), based on the revised Gell and Coombs classification of immunologic hypersensitivity., The First case of ABPA was reported in England  in 1952 and in India  in 1971. Since then, a number of cases have been reported from all over the world. Concomitant occurrence of ABPA and AAS is now being increasingly recognised which is also called as “sinobronchial allergic mycosis” syndrome. ABPA is commonly associated in patients with chronic bronchial asthma and cystic fibrosis but can also occur in non-asthmatics. A new phenotype of asthma has been described recently, namely severe asthma with fungal sensitization (SAFS). SAFS can be conceptualized as a continuum of fungal sensitization, with asthma at one end and ABPA at the other. It is diagnosed by the presence of SAFS, and exclusion of ABPA.
| Prevalence of Allergic Bronchopulmonary Aspergillosis|| |
ABPA has long been reported to be common in U. K. where it is the cause of 50%–80% of cases of the pulmonary eosinophilia. The exact prevalence of ABPA is not known but contemporary estimates suggested that ABPA complicates 1%–11% of all chronic cases of bronchial asthma.,,,,,,,, Many case series of ABPA were reported from India.,,, A very recent study from India, however, found a higher prevalence of Aspergillus sensitization (39.5%) and ABPA (27%) in 564 patients with asthma. Alok Nath et al. in their latest study on 350 patients found the prevalence of Aspergillus hypersensitivity (AH) and ABPA to be 35.1% and 21.7%, respectively. The condition is being increasingly recognized and the estimated prevalence rates in recent publications have been reported ranging from 5.9% to 20.5% for ABPA and 38%–43% for AH., Prevalence data from this part of the country are sparse.
| Immunopathology of Allergic Bronchopulmonary Aspergillosis|| |
ABPA patients are atopic with history of chronic asthma. The basic underlying immuno-pathophysiologic process in ABPA is a hypersensitivity reaction to fungus in the bronchial tree. In susceptible individuals after inhalation of fungal spores in the bronchi, fungi germinate and form vegetative elements (hyphae). Local immunologic reactions and stagnation of tenacious sputum in bronchial airways favor the trapping of fungal spores and further colonization. Antigenic substance of the fungus stimulates formation of IgE, IgG, and IgA antibodies. ABPA is immunologically classified as it gives both Type I (immediate) and Type III (Arthus, antigen-antibody immune complex) hypersensitivity reactions. Type I reaction is IgE mediated and responsible for accumulation of eosinophils, bronchospasm, edema leading to acute symptoms of diseases. Type III reaction results in polymorph aggregation, inflammation of bronchial and peribronchial tissues and is responsible for the radiological features of ABPA. Recently, possible role of Type IVb , hypersensitivity reaction has also been observed in patients with ABPA and the presence of parenchymal granuloma and mononuclear cell infiltration seen on histopathology. Long-standing involvement of the bronchial tree leads to bronchiectasis, fibrosis, lung contraction, and lobar shrinkage.
| Clinical Presentation|| |
Patients are usually atopic with previous history of bronchial asthma. The onset is insidious with constitutional symptoms like anorexia, fatigue, weight loss, headache, generalized aches and pains, and low-grade fever. The frequency and severity of symptoms of underlying asthma are not fully controlled with usual anti-asthmatic therapy. It is characterized by repeated episodes of exacerbation with periods of remission, if untreated may progress to fibrotic lung disease. It may occur at any age but usually in the age group of 20–40 years. Patients with chronic fibrotic disease may present with cyanosis, corpulmonale, and respiratory failure. However, symptoms have little or no relationship to severity or chronicity of the disease, as one-third patients may be relatively asymptomatic in spite of extensive radiological shadows.
Golden-brown rubbery flecks or plugs of sputum production is characteristic and has been reported in 5%–54% of cases. These plugs consist of fungal hyphae with eosinophils and mucous. Cough, breathlessness and wheezing are the common symptoms seen in ABPA. Hemoptysis has been reported in 34%–85% of cases, while pleuritic chest pain may be present in 50% of cases. In one of his study author found that hemoptysis is found in 28.6% of patients. Chronic cases of ABPA may rarely present with symptoms of bronchiectasis. On clinical examination of chest, wheezing and diffuse crepitations are the common findings but tachypnea, cyanosis, features of cor pulmonale and sometimes hypertrophic osteoarthropathy may be seen. The disease is often incorrectly diagnosed as tuberculosis, bronchiectasis and bacterial pneumonia. Almost half of the ABPA patients are initially misdiagnosed as pulmonary tuberculosis.
| Diagnostic Approach|| |
ABPA is suspected in any patient with asthma with lung shadows on chest skiagram and peripheral blood eosinophilia. All the features are not necessary to diagnose ABPA. The important diagnostic criteria are the presence of recurrent pulmonary infiltrates, peripheral blood eosinophilia and positive skin test to Aspergillus antigen. Criteria for diagnosis of SAFS include History of poorly controlled asthma (>500 μg/day of fluticasone or the equivalent, near continuous oral corticosteroids for >6 months, or >2 oral steroid tapers per year. Total serum IgE <1000 IU/ml, Positive immediate skin test reactivity to A. fumigatus, elevated specific serum IgE to A. fumigatus or absence of serum precipitins (by gel diffusion) and elevated specific serum IgG to A. fumigatus and No radiographic evidence of bronchiectasis or infiltrates.
| Radiological Features|| |
Radiological features in patients of ABPA may be transient (acute) or permanent (chronic). Transient shadows may clear with or without steroid therapy and are mainly due to pulmonary infiltrates and stagnation of secretions in damaged bronchi., Transient shadows are perihilar infiltrates mimicking adenopathy, air fluid levels from dilated central bronchi filled with fluid and debris. Parenchymal abnormalities are more common and present in 80%–90% patients of ABPA as ill-defined homogenous shadows without evidence of loss of volume which may be of 5–15 mm in size or more as massive/lobar in extent, may be unilateral or bilateral, more in upper lobes, resolve (fleeting/migratory shadows) often after expectoration of bronchial plugs but tends to recur in same/other places. Sometimes pulmonary shadows mimic carcinoma.
Fleeting shadows are characteristic of ABPA, author in one of his study found 66.7% patients had fleeting shadows. Author described “walking pneumonia” as a clue to diagnosis of ABPA. Bronchial abnormalities occur in 50%–70% of episodes of acute ABPA consists of tramline, parallel lines and ring shadows which represents normal or abnormal bronchial wall. The impacted bronchus may appear as full wine glass having an open upper end with tapering lower end, gloved finger 2–3 centimeter long and 5–8 mm wide, and inverted V, Y or toothpaste shadows. Gloved-finger shadows are due to distally occluded bronchi filled with secretions. Tram lime shadows are the thickened walls of undilated bronchi, so the distance between lines is that of a normal bronchus while parallel lines shadows represent walls of bronchiectatic bronchi, the distance between walls is greater than normal. Permanent (chronic) changes reflect histological abnormalities secondary to repeated acute episodes of ABPA, and are often associated with physiologic abnormalities. Rarely cavitations, local emphysema, pulmonary fibrosis or contracted upper lobe, honeycombing, collapse due to mucous impaction, and spontaneous pneumothorax  are recognized, even total collapse of lung has been reported.
Conventional tomography has been shown to be more sensitive than the plain chest radiograph. Computerized tomography might be useful in the assessment of extent of disease. High resolution computed tomography (HRCT) is a sensitive noninvasive technique for the recognition of ABPA. Proximal bronchiectasis is due to deposition of immune complex in proximal airways. Bronchiectasis, centrilobular nodules and mucoid impaction are main features of ABPA. proximal bronchiectasis with ABPA may be seen in 40% patients  and characterized by string of pearls and signet ring appearance as described by Webb, et al. proximal bronchiectasis (in 2nd, 3rd, 4th order large bronchi) is an important diagnostic feature of ABPA with normal small bronchi and bronchioles.
Radiological classification of allergic bronchopulmonary aspergillosis
Serological ABPA (ABPA-S) (mild), ABPA-central bronchiectasis (ABPA-CB) (moderate), and ABPA-CB-other radiologic findings (ORF). In ABPA-S all the diagnostic features of ABPA are present except evidence of proximal bronchiectasis on HRCT. It is believed that patients with ABPA-S have milder clinical course and less severe immunological findings when compared to ABPA-CB. In ABPA-CB all findings of ABPA including proximal bronchiectasis on HRCT present however in ABPA-CB-ORF all findings of ABPA and CB along with other radiological features such as pulmonary fibrosis, bleb, bullae, pneumothorax, parenchymal scarring, emphysematous change, multiple cyst, fibrocavitory lesions, Aspergilloma, ground glass appearance, collapse, mediastinal lymph node, pleural effusion and pleural thickening. Newly proposed radiological classification of ABPA based on computed tomography chest findings, categorizes ABPA as ABPA-S, ABPA with bronchiectasis, ABPA with high attenuation mucus and ABPA with chronic pleuropulmonary fibrosis.
| Laboratory Investigations|| |
- Peripheral blood eosinophilia (usually 1000–3000/m 3), leucocytosis and raised ESR in acute episodes and sputum contain eosinophils in most of the cases
- Serological tests: Increase in total IgE and specific IgE and IgG precipitating antibodies (in 70%) against A. fumigatus., Both total and specific IgE levels are high during development of pulmonary infiltrates and decrease after remission. The total IgE levels are >1000 IU/ml may be as high as 20,000 IU/ml in acute cases except in cases that are in remission or on steroids therapy. Precipitating antibodies against A. fumigatus are present in most of cases of ABPA with pulmonary infiltrates and diminished after steroid therapy 
- Skin test: Positive skin tests (Type 1 and Type 3) are more reliable than precipitin tests. Immediate type 1, skin reaction is positive in most of the cases but also positive in 25% of asthmatics without ABPA. Late onset (Type 3) erythema and edema occur usually after 4–6 h and reaches at peak within 8 h and subsides by 24 h due to deposition of IgE, IgM, IgA and complement components
- Sputum smear and culture for Aspergillus: Nearly two-third of patients of ABPA show positive smear and culture for Aspergillus, Positive culture with Aspergillus species in sputum has been reported in 58% cases of ABPA 
- Pulmonary function test: Is neither sensitive nor specific and does not help to define the extent of disease or exclude it, during remission patient may have normal lung function even in presence of bronchiectasis. The status depends upon the stage at which they are performed. Acute and chronic pulmonary function changes in ABPA have been described. In acute episodes obstructive changes are observed, while during irreversible stages with bronchiectasis and fibrosis restrictive changes are found. In chronic-cases diffusion capacity is reduced.
[TAG:2]Classical Diagnostic Criteria for Allergic Bronchopulmonary Aspergillosis (Rosenberg et al. 1977)[/TAG:2]
Bronchial asthma, Radiological pulmonary infiltrates, Immediate skin test positivity to A. fumigatus antigen, Elevated total serum IgE, Precipitating antibodies against A. fumigatus antigen, Peripheral blood eosinophilia, Elevated serum IgE and IgG against A. fumigatus and Central/proximal bronchiectasis with normal tapering of distal bronchi.
History of expectorating golden brown plugs in sputum, Positive sputum smear and culture for Aspergillus species, Late Type III (Arthus) skin reactivity to A. fumigatus.
The presence of six of eight major criteria makes the diagnosis almost certain.
Latest criteria do not differentiates in major and minor, eight diagnostic criteria are laid down to detect ABPA suggested by Patterson et al. 1997 as follows:
Asthma (mild or severe) or cystic fibrosis, Immediate cutaneous reactivity to Aspergillus antigen, Current or previous pulmonary infiltrates, Elevated total IgE concentration (>l mg/L), Precipitin antibodies to A. fumigatus, Peripheral blood eosinophilia, Elevated serum IgE and/or IgG-against A. fumigatus and Proximal bronchiectasis.
| Staging of Allergic Bronchopulmonary Aspergillosis|| |
Five stages of allergic bronchopulmonary aspergillosis has been described according to Patterson et al.
- Acute stage: Symptomatic presenting with fever, sputum production and symptoms of asthma. High level of serum IgE and eosinophilia, with radiological pulmonary infiltrates. Steroids are indicated to achieve remission
- Remission stage: Control of respiratory symptoms, radiological clearing, decline in IgE levels and eosinophilia. Steroids are not required in this stage
- Exacerbation stage: Occurs when patient presents all features of acute stage or when there is a twofold rise in the total serum IgE levels. Radiological study shows appearance of new infiltrates. Management requires induction of remission with steroids. Maintenance steroids are not necessary
- Steroid Dependent Asthma: Patient is symptomatic suffering from asthma and needs long-term steroids. Lab investigations present rise in serum IgE. Radiology is variable
- Fibrosis: Dyspnea and other manifestations of fibrotic lung disease with irreversible obstructive and/or restrictive pulmonary functions are present, Serum IgE level is variable. High IgE levels may reflect continued activity. Radiological study shows pulmonary fibrosis. Management requires long-term steroid that may not reverse these changes completely. Cor pulmonale, respiratory failure and death may occur.
Recently, new clinical staging of ABPA by International Society for Human and Animal Mycology  has been proposed:
- Stage 0 Asymptomatic: Patient fulfills GINA definition of controlled asthma, patient fulfills the diagnostic criteria of ABPA, and has not been previously diagnosed to have ABPA
- Stage 1 Acute: Patient has uncontrolled asthma, fulfils the diagnostic criteria for ABPA and not previously diagnosed to have ABPA
- Stage 1a With mucoid impaction: Meets all the criteria and there is documented mucoid impaction on chest radiograph, CT chest or bronchoscopy
- Stage 1b Without mucoid impaction: Meets all the criteria and there is no documented mucoid impaction on CT chest or bronchoscopy
- Stage 2 Response: Clinical improvement (resolution of constitutional symptoms, improvement in asthma control), major radiological improvement and IgE decline by ≥25% of baseline at 8 weeks
- Stage 3 Exacerbation: Clinical and/or radiological deterioration associated with an increase in IgE by ≥50%
- Stage 4 Remission: Sustained clinicoradiological improvement with IgE levels remaining at or below baseline for ≥6 months on or off therapy other than systemic glucocorticoids
- Stage 5a Treatment-dependent ABPA: If patient has relapse on two or more consecutive occasions within 6 months of stopping treatment or has worsening of clinical, radiological, or immunological parameters on tapering oral steroids/azoles
- Stage 5b Glucocorticoid-dependent asthma: If the patient requires oral or parenteral glucocorticoids for control of asthma while the activity of ABPA is controlled as reflected by IgE levels and chest radiograph
- Stage 6 Advanced ABPA: Presence of type II respiratory failure and/or cor pulmonale with radiological evidence of fibrotic findings consistent with ABPA on HRCT of the chest after excluding reversible causes of acute respiratory failure.
| Treatment of Allergic Bronchopulmonary Aspergillosis|| |
Oral corticosteroid remains the cornerstone for the treatment of ABPA. The goal of therapy is to achieve symptom resolution, clearance of radiographic infiltrates, and establishment of a stable baseline serum level of total IgE. There are two dose schedules of oral glucocorticoid therapy, low dose and high dose. In low dose oral glucocorticoid therapy, Prednisolone 0.5 mg/kg/d is given for 2 wk, then on alternate day for 6–8 weeks and then tapered 5–10 mg every 2 weeks and then discontinued. In high dose glucocoticoid therapy Prednisolone 0.75 mg/kg is given for 6 weeks, followed by 0.5 mg/kg for 6 weeks, then taper 5 mg every 6 weeks to continue for a total of atleast 6–12 months. Higher dose and prolonged use of steroids associated with better outcome. During the acute episode, usual starting dose of prednisone is 0.5 mg/kg daily for 2 weeks then reduced to an alternate day regime for 2–3 months, after that it should be tapered off in next 2–3 months. Repeat chest X-ray in 1 month should demonstrate clearing of the infiltrates. The total serum IgE level also regresses along with the infiltrates. The failure of the total serum IgE level to decrease suggests continuation of active disease and requires additional corticosteroids.
Following successful infiltrate clearing there is a reduction in total serum IgE and remission of the patient's symptoms. The total serum IgE level, chest x ray, absolute eosinophil count should then be followed at 6–8 weeks intervals regularly. The goal of glucocorticoid therapy is not normalization of total S. IgE but reduction in total S. IgE by 35%–50% from baseline that defines remission by 6 weeks Serial total serum IgE levels are important for follow-up care. A sudden doubling of total serum IgE levels over baseline usually heralds activity of disease. Such activity can be aborted or even prevented with increased dose of prednisone at the time when the elevated level of IgE is noted.
Patients who have remission of ABPA may discontinue prednisone. The remission may last for years or may be permanent. In patients with recurrent flares of ABPA or in those with severe persistent asthma, long-term corticosteroid therapy may be necessary to control their symptoms. Patients in the fibrotic stage of ABPA may have increased sputum volume as a result of infection. Measures such as postural drainage and antibiotics may be useful, but with deterioration, exercise tolerance decreases and oxygen therapy may be needed.
Optimization of baseline asthma therapy is essential with inhaled corticosteroid and β2-agonists. In addition, prophylactic measures should be instituted when indicated to prevent the adverse effects of long-term corticosteroid treatment such as osteoporosis. Thus, patients who will be taking prednisolone for more than 2–3 months should be considered for bone mineral density analysis to direct commencement of calcium/Vitamin D supplementation with or without bisphosphonates.
| Role of Antifungal Drugs|| |
Pooled analysis showed that itraconazole could significantly decrease IgE levels by >25% when compared to placebo, reduction in steroid dose by ≥50%; increase in exercise tolerance by ≥25%, improvement of ≥25% in results of spirometry, resolution of pulmonary opacities but failed to reach statistical but did not cause significant improvement in lung function but did not cause significant improvement in lung function., Itraconazole modified the immunologic activation associated with ABPA and improve clinical outcome at least over the period of 16 wks. A decline in exacerbation rates was also seen. At present, itraconazole should be limited in cases where oral steroids are contraindicated or refused by patients. In patients requiring high doses of oral steroid, itraconazole may allow reduction in steroid doses, but should not replace the need of steroid; the major concern being no long term trials and adrenal supression with itraconazole. Thus long term trials are required before firm recommendation can be made for the use of itraconazole in ABPA. The use of omalizumab in ABPA has been associated with improvement in symptoms, reduction in exacerbations and asthma hospitalizations, improvement in lung function and reduction in dose of oral steroids. Recently voriconazole has also been tried in the treatment of ABPA.,,
| Conclusion|| |
Presently ABPA is one of the important emerging immunologically mediated respiratory diseases, commonly presenting in patients of asthma. It should be highly suspected in patients presenting with history of asthma, peripheral blood eosinophilia, recurrent pneumonitits or transient (fleeting) pulmonary infiltrates mimicking pulmonary tuberculosis. In such suspected patients, detailed evaluations are needed to prove the diagnosis. Early diagnosis and proper treatment may alter the prognosis of disease and further prevent end stage lung fibrosis.
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| References|| |
Binder RE, Faling LJ, Pugatch RD, Mahasaen C, Snider GL. Chronic necrotizing pulmonary aspergillosis: A discrete clinical entity. Medicine (Baltimore) 1982;61:109-24.
Shah A, Panjabi C. Allergic bronchopulmonary aspergillosis: A perplexing clinical entity. Allergy Asthma Immunol Res 2016;8:282-97.
Greenberger FA, Patterson R. Diagnosis and management of allergic bronchopulmonary aspergillosis. Ann Allergy 1986;56:444.
Greenberger PA. Allergic bronchopulmonary aspergillosis. J Allergy Clin Immunol 2002;110:685-92.
Rosenberg M, Patterson R, Mintzer R, Cooper BJ, Roberts M, Harris KE. Clinical and immunologic criteria for the diagnosis of allergic bronchopulmonary aspergillosis. Ann Intern Med 1977;86:405-14.
Greenberger PA, Patterson R, Ghory A, Arkins JA, Walsh T, Graves T, et al
. Late sequelae of allergic bronchopulmonary aspergillosis. J Allergy Clin Immunol 1980;66:327-35.
Patterson R, Greenberger PA, Radin RC, Roberts M. Allergic bronchopulmonary aspergillosis: Staging as an aid to management. Ann Intern Med 1982;96:286-91.
Patterson R, Greenberger PA, Halwig JM, Liotta JL, Roberts M. Allergic bronchopulmonary aspergillosis. Natural history and classification of early disease by serologic and roentgenographic studies. Arch Intern Med 1986;146:916-8.
Patterson R, Greenberger PA, Lee TM, Liotta JL, O'Neill EA, Roberts M, et al
. Prolonged evaluation of patients with corticosteroid-dependent asthma stage of allergic bronchopulmonary aspergillosis. J Allergy Clin Immunol 1987;80:663-8.
Greenberger PA, Patterson R. Allergic bronchopulmonary aspergillosis and the evaluation of the patient with asthma. J Allergy Clin Immunol 1988;81:646-50.
Greenberger PA, Miller TP, Roberts M, Smith LL. Allergic bronchopulmonary aspergillosis in patients with and without evidence of bronchiectasis. Ann Allergy 1993;70:333-8.
Greenberger PA. Clinical aspects of allergic bronchopulmonary aspergillosis. Front Biosci 2003;8:s119-27.
Rajan TV. The Gell-Coombs classification of hypersensitivity reactions: A re-interpretation. Trends Immunol 2003;24:376-9.
Geha RS, Sampson HA, Askenase PW. Allergy and hypersensitivity. In: Janeway CA, Travers P, Walport M, Shlomchik M J, editors. Immunobiology. New York, NY: Garland; 2001. p. 517-56.
Hinson KF, Moon AJ, Plummer NS. Broncho-pulmonary aspergillosis; a review and a report of eight new cases. Thorax 1952;7:317-33.
Shah JR. Allergic bronchopulmonary aspergillosis. J Assoc Physicians India 1971;19:835-41.
Venarske DL, deShazo RD. Sinobronchial allergic mycosis: The SAM syndrome. Chest 2002;121:1670-6.
Hoshino H, Tagaki S, Kon H, Shibusa T, Takabatake H, Fujita A, et al
. Allergic bronchopulmonary aspergillosis due to Aspergillus niger
without bronchial asthma. Respiration 1999;66:369-72.
Agarwal R. Severe asthma with fungal sensitization. Curr Allergy Asthma Rep 2011;11:403-13.
McCarthy DS, Pepys J. Allergic bronchopuimonary aspergillosis, clinical immunology and clinical features. Clin Allergy 1971;1:261-86.
Henderson AH, English MP, Vecht RJ. Pulmonary aspergillosis. A survey of its occurrence in patients with chronic lung disease and a discussion of the significance of diagnostic tests. Thorax 1968;23:513-8.
Schwartz HJ, Greenberger PA. The prevalence of allergic bronchopulmonary aspergillosis in patients with asthma, determined by serologic and radiologic criteria in patients at risk. J Lab Clin Med 1991;117:138-42.
Eaton T, Garrett J, Milne D, Frankel A, Wells AU. Allergic bronchopulmonary aspergillosis in the asthma clinic. A prospective evaluation of CT in the diagnostic algorithm. Chest 2000;118:66-72.
Adiseshan N, Simpson J, Gandevia B. The association of asthma with Aspergillus
and other fungi. Aust N
Z J Med 1971;1:385-91.
Donnelly SC, McLaughlin H, Bredin CP. Period prevalence of allergic bronchopulmonary mycosis in a regional hospital outpatient population in Ireland 1985-88. Ir J Med Sci 1991;160:288-90.
AI-Mobeireek AF, Gad EI-Rab MO, AI-Hedaithy SS, Alasali K, Al-majed S, Joharjy I. Allergic bronchopulmonary mycosis in patients with asthma: Period prevalence at a university hospital in Saudia Arabia. Respir Med 2001;95:341-7.
Maurya V, Gugnani HC, Sarma PU, Madan T, Shah A. Sensitization to Aspergillus
antigens and occurrence of allergic bronchopulmonary aspergillosis in patients with asthma. Chest 2005;127:1252-9.
Prasad R, Garg R, Sanjay, Dixit R. A study on prevalence of allergic bronchopulmonary aspergillosis in patients of bronchial asthma. The Internet Journal Of Pulmonary Medicine 2008;9:2.
Khan ZU, Sandhu RS, Randhawa HS, Menon MP, Dusaj IS. Allergic bronchopulmonary aspergillosis: A study of 46 cases with special reference to laboratory aspects. Scand J Respir Dis 1976;57:73-87.
Chetty A, Bhargava S, Jain RK. Allergic bronchopulmonary aspergillosis in Indian children with bronchial asthma. Ann Allergy 1985;54:46-9.
Shah A, Bhagat R, Panchal N, Jaggi OP, Khan ZU. Allergic bronchopulmonary aspergillosis with middle lobe syndrome and allergic Aspergillus
sinusitis. Eur Respir J 1993;6:917-8.
Behera D, Guleria R, Jindal SK, Chakrabarti A, Panigrahi D. Allergic bronchopulmonary aspergillosis-a retrospective study of 35 cases. Ind J Chest Dis All Sci 1994;36:173-9.
Agarwal R, Gupta D, Aggarwal AN, Behera D, Jindal SK. Allergic bronchopulmonary aspergillosis: Lessons from 126 patients attending a chest clinic in north India. Chest 2006;130:442-8.
Nath A, Khan A, Hashim Z, Patra JK. Prevalence of Aspergillus
hypersensitivity and allergic bronchopulmonary aspergillosis in patients with bronchial asthma at a tertiary care center in North India. Lung India 2017;34:150-4.
] [Full text]
Agarwal R, Gupta D, Aggarwal AN, Saxena AK, Chakrabarti A, Jindal SK. Clinical significance of hyperattenuating mucoid impaction in allergic bronchopulmonary aspergillosis: An analysis of 155 patients. Chest 2007;132:1183-90.
Attapattu MC. Allergic bronchopulmonary aspergillosis in a chronic asthmatic. Ceylon Med J 1983;28:251-3.
Sa firstein BH, D'Souza MF, Simon G, Tai EH, Pepys J. Five-year follow-up of allergic bronchopulmonary aspergillosis. Am Rev Respir Dis 1973;108:450-9.
Prasad R, Garg R, Sanjay, Shukla AD. Allergic bronchopulmonary aspergillosis: A review of 42 patients from a tertiary care center in India. Lung India 2009;26:38-40.
] [Full text]
McCarthy DS, Simon G, Hargreave FE. The radiological appearances in allergic bronchopulmonary aspergillosis. Clin Radiol 1970;21:366.
Goldberg B. Radiological appearance in pulmonary aspergillosis. Clin Radiol 1962;13:106.
Prasad R, Garg R, Sanjay. Walking pneumonia in a patient of bronchial asthma: A clue to the diagnosis of allergic bronchopulmonary aspergillosis. Pulmon 2007;9:120-23.
Menon MP, Das AK. Allergic bronchopulmonary aspergillosis (Radiological aspect). Ind J Chest Dis 1977;19:157-69.
Ricketti AJ, Greenberger PA, Glassroth J. Spontaneous pneumothorax in allergic bronchopulmonary aspergillosis. Arch Intern Med 1984;144:151-2.
Ellis RH. Total collapse of the lung in aspergillosis. Thorax 1965;20:118-23.
Ward S, Heyneman L, Lee MJ, Leung AN, Hansell DM, Müller NL. Accuracy of CT in the diagnosis of allergic bronchopulmonary aspergillosis in asthmatic patients. AJR Am J Roentgenol 1999;173:93742.
Neeld DA, Goodman LR, Gurney JW, Greenberger PA, Fink JN. Computerized tomography in the evaluation of allergic bronchopulmonary aspergillosis. Am Rev Respir Dis 1990;142:12005.
Webb WR, Muller NL, Naidich DP, editors. High-Resolution CT of the Lung. 2nd
ed. New York: Lippincot-Raven Publishers; 1996. p. 234-41.
Scadding J. The bronchi in Allergic aspergillosis. Scand J Respir Dis 1967;48:372-.
Kumar R. Mild, moderate, and severe forms of allergic bronchopulmonary aspergillosis: A clinical and serologic evaluation. Chest 2003;124:890-2.
Agarwal R, Chakrabarti A, Shah A. Allergic bronchopulmonary aspergillosis: Review of literature and proposal of new diagnostic and classification criteria. Clini Exp Allergy 2013;43:850-73.
Greenberger PA. Allergic bronchopulmonary aspergillosis and fungoses. Clin Chest Med 1988;9:599-608.
Wang JL, Patterson R, Rosenberg M, Roberts M, Cooper BJ. Serum IgE and IgG antibody activity against Aspergillus fumigatus
as a diagnostic aid in allergic bronchopulmonary aspergillosis. Am Rev Respir Dis 1978;117:917-27.
Lmbeau SA, Imbeau SA, Nichols D, Flaherty D, Dickie H, Reed C. Relationships between prednisolone therapy, disease activity, and the total IgE level in allergic bronchopuimonary aspergillosis. J Allergy Clin lmmunol 1978;62:91.
Malo JL, Hawkins R, Pepys J. Studies in chronic allergic bronchopulmonary aspergillosis. 1. Clinical and physiological findings. Thorax 1977;32:254-61.
Fink JN. Therapy of allergic bronchopulmonary aspergillosis. Indian J Chest Dis Allied Sci 2000;42:221-4.
Agarwal R. Allergic bronchopulmonary aspergillosis. Chest 2009;135:805-26.
Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. American College of Rheumatology Task Force on Osteoporosis Guidelines. Arthritis Rheum 1996;39:1791-801.
Tucker RM, Haq Y, Denning DW, Stevens DA. Adverse events associated with itraconazole in 189 patients on chronic therapy. J Antimicrob Chemother 1990;26:561-6.
Mulliez P, Croxo C, Roy-Saint Georges F, Darras A. Allergic broncho-pulmonary aspergillosis treated with voriconazole. Rev Mal Respir 2006;23:93-4.
Bandrés Gimeno R, Muñoz Martínez MJ. Prolonged therapeutic response to voriconazole in a case of allergic bronchopulmonary aspergillosis. Arch Bronconeumol 2007;43:49-51.
Erwin GE, Fitzgerald JE. Case report: Allergic bronchopulmonary aspergillosis and allergic fungal sinusitis successfully treated with voriconazole. J Asthma 2007;44:891-5.