|Year : 2021 | Volume
| Issue : 1 | Page : 47-53
Allergic bronchopulmonary aspergillosis misdiagnosed as other respiratory diseases: Case-based approach
Rajendra Prasad1, Harshita Rani1, Huda Shamim1, 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||25-Jan-2022|
|Date of Decision||26-Jan-2022|
|Date of Acceptance||26-Jan-2022|
|Date of Web Publication||13-Apr-2022|
Dr. Rajendra Prasad
A-28, Sector J, Aliganj, Lucknow - 226 024, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Allergic bronchopulmonary aspergillosis (ABPA) is a complex clinical entity resulting from an allergic immune response to Aspergillus fumigatus and most often occurring in a patient with asthma. Here in this article, we are reporting several cases of ABPA misdiagnosed as other respiratory diseases.
Keywords: Allergic bronchopulmonary aspergillosis, Aspergillus fumigatus, walking pneumonia
|How to cite this article:|
Prasad R, Rani H, Shamim H, Kacker R, Gupta N. Allergic bronchopulmonary aspergillosis misdiagnosed as other respiratory diseases: Case-based approach. J Intern Med India 2021;15:47-53
|How to cite this URL:|
Prasad R, Rani H, Shamim H, Kacker R, Gupta N. Allergic bronchopulmonary aspergillosis misdiagnosed as other respiratory diseases: Case-based approach. J Intern Med India [serial online] 2021 [cited 2023 Sep 30];15:47-53. Available from: https://www.upjimi.org/text.asp?2021/15/1/47/343032
| Introduction|| |
Aspergillus is a ubiquitous fungi, which occurs most commonly in mycelial form, is thermo-tolerant with optimal temperature for growth being 37–40C favoring humid conditions. Allergic bronchopulmonary aspergillosis (ABPA) is a complex clinical entity resulting from an allergic immune response to Aspergillus fumigatus and most often occurring in a patient with asthma or cystic fibrosis. ABPA is defined by a constellation of clinical, laboratory, and radiographic criteria that include active asthma, serum eosinophilia, an elevated total immunoglobulin E (IgE) level, fleeting pulmonary parenchymal opacities, bronchiectasis, and evidence for sensitization to A. fumigatus by skin prick testing. It mimics various common respiratory diseases. This article aims to report the several cases of ABPA with variable presentation which mimics other respiratory diseases in my 45 years of clinical experience.
A case of allergic bronchopulmonary aspergillosis mimicking tuberculosis
A 28-year-old male presented with complaints of breathlessness since childhood and he presented with exacerbation. He had a history of intake of antitubercular drugs from private clinician 15 years back for 6 months and he was already taking inhaled salbutamol along with oral bronchodilators for bronchial asthma. Chest X-ray showed diffuse parenchymal shadows in both lungs [Figure 1.1]. High-resolution computed tomography (HRCT) of the thorax showed bilateral central bronchiectasis [Figure 1.2]a and [Figure 1.2]b. His eosinophil count ranged from 8% to 12% on different occasions and total IgE was also raised (6,516.8 IU/mL). Specific IgE against A. fumigatus was elevated (38.6 kUA/L). Specific immunoglobulin G (IgG) against A. fumigatus was also raised (170 U/mL). Skin prick test (type 1) was also positive for A. fumigatus. The patient was diagnosed with a case of ABPA. The patient was put on oral prednisolone 0.5 mg/kg body weight daily for 2 weeks which was tapered off to 0.5 mg/kg body weight alternate day for the next 2 weeks and then tapered to maintenance dose for another 3 months [Figure 1.3]. The patient was advised to take regular proper asthma medication and for follow-up regularly.
A case of allergic bronchopulmonary aspergillosis presenting as pneumonia
A 32-year-old female came to our hospital with complaints of recurrent cough with expectoration, breathlessness for 20 years, and hemoptysis on and off for 5 years. She was diagnosed with a case of pulmonary tuberculosis (TB) and had received seven courses of antitubercular drugs without any response. Sputum smear was negative for acid-fast bacilli (AFB) and GeneXpert was also negative for Mycobacterium tuberculosis. General physical examination was within the normal limits. Examination of the respiratory system showed bilateral ronchi. Total IgE was raised (2,256 IU/mL). IgE specific for A. fumigatus (200 kUA/L) and IgG for Aspergillus were raised (65 U/mL). Skin prick test (Type 1) was also positive for A. fumigatus. Chest X-ray in 2008 and HRCT thorax showed bilateral homogeneous shadows and bilateral central bronchiectasis respectively [Figure 2.1] and [Figure 2.2]. Chest X-ray in 2016 showed clearing of bilateral shadows [Figure 2.3]. HRCT thorax showed bilateral central bronchiectasis [Figure 2.4]. The patient was diagnosed with a case of ABPA. The patient was then treated with oral corticosteroids with a dose of 0.5 mg/kg body weight for 2 weeks and 0.5 mg/kg body weight alternate day for 3 months and showed marked improvement in clinical, laboratory, and radiographic findings. The patient is on maintenance dose of steroids along with inhaled corticosteroids (LABA + ICS) and doing fairly well.
A case of allergic bronchopulmonary aspergillosis mimicking multidrug-resistant tuberculosis
A 22-year-old male, nonsmoker presented with complaints of cough and episodic breathlessness for 7 years, recurrent hemoptysis for 6 months, loss of appetite, and generalized weakness for 6 months. Sputum for AFB was negative, and based on chest X-ray in 2003, he was given anti-tubercular drug for 6 months (2 hEZ/4HR) regularly from a private practitioner without any response [Figure 3.1]. The patient had a bout of hemoptysis and deteriorated radiologically after 6 months and patient was suspected as multidrug-resistant-TB but sputum for AFB was negative on three occasions. He had also received bronchodilators and oral steroids off and on [Figure 3.2]. On routine blood investigation, eosinophils were raised (30%); absolute eosinophilic count was raised (3,710/mm3). Total IgE was 34,220 IU/mL. Serum IgG against A. fumigatus (118 U/mL) and Serum IgG against A. fumigatus (21.50 U/mL) were raised. HRCT thorax showed evidence of consolidation with central bronchiectasis [Figure 3.3]a and [Figure 3.3]b. The patient was diagnosed with a case of ABPA and was given oral steroids 0.5 mg/kg body weight daily for 2 weeks followed by 0.5 mg/kg body weight alternate day for 6 weeks. All the shadows cleared in 8 weeks duration. The patient was also given treatment for asthma (LABA + ICS) regularly.
A case of allergic bronchopulmonary aspergillosis with high-density mucus impaction mimicking mass lesion
A 36-year-old male presented with complaints of breathlessness since early childhood, cough with expectoration for 4 months, hemoptysis on and off for 15 days, fever, and chest pain right side since 10 days. The patient had received anti-tubercular treatment for 3 months and was on inhaled bronchodilators for 5 years. On general examination, clubbing was present. Chest X-ray showed multiple nodular shadows in the right middle zone [Figure 4.1]. Computed tomography (CT) thorax showed high-attenuated mucus plugs in the right middle lobe. Routine blood investigation showed eosinophil count 7%. Total IgE was raised (3,400 IU/mL) and both specific IgE (58 IU/mL) and IgG (113 IU/mL) against A. fumigatus were elevated. Fiber-optic bronchoscopy showed lot of mucus plugs in right middle lobe. The patient was diagnosed as ABPA with high density mucus impaction [Figure 4.2]a, [Figure 4.2]b, [Figure 4.2]c, [Figure 4.2]d. The patient was put on oral prednisolone 0.5 mg/kg body weight daily for 2 weeks which was tapered off to 0.5 mg/kg body weight alternate day for next 2 weeks as there was clinical and radiological improvement [Figure 4.3] and then tapered to maintenance dose for another 4 months [Figure 4.4].
Allergic bronchopulmonary aspergillosis presenting as a pulmonary mass
A 38-year-old male, known case of asthma for 15 years, presented with cough with expectoration, shortness of breath, chest tightness, and fever for 15 days. There was no history of hemoptysis, expectoration of brownish black mucus plugs or loss of weight or appetite. On general physical examination, the patient had respiratory rate of 24 breaths/min without any use of accessory muscles of respiration. Expiratory polyphonic rhonchi were audible over bilateral lung fields. Other systemic examination was normal. The patient was prescribed antibiotics and was suspected to have pulmonary mass by other clinicians on the basis of chest radiograph for which he was referred to our center. The chest radiograph [Figure 5.1] showed an irregular shaped opacity in right lower zone mimicking pulmonary mass. HRCT of thorax showed homogenous opacity in right lower lobe resembling pulmonary mass [Figure 5.2] and central bronchiectasis [Figure 5.3]. Laboratory investigations showed the absolute eosinophil count of the patient was raised (1,120 cells/mm3), total serum IgE of the patient was elevated (6,121 kUA/L). Aspergillus-specific IgG was elevated (156.80 U/mL) and Aspergillus-specific IgE was elevated (37.30 kUA/L) and immediate A. fumigatus skin prick test was positive (Type I). Patient was diagnosed with ABPA. Patient was treated with oral corticosteroids with a dose of 0.5 mg/kg body weight for 2 weeks and 0.5 mg/kg body weight alternate day for 3 months and showed marked improvement in clinical, laboratory, and radiographic findings [Figure 5.4].
A case of allergic bronchopulmonary aspergillosis presenting as collapse right upper lobe
A 23-year-old female presented with history of breathlessness since childhood, recurrent nasal blockage since 3 years for which she underwent functional endoscopic sinus surgery 1 year back. Patient presented with exacerbation of breathlessness. Chest X-ray and contrast enhanced computerized tomography thorax showed collapse of right upper lobe [Figure 6.1] and [Figure 6.2]. Routine blood investigation showed peripheral eosinophilia (15%). Total IgE was elevated (2,248 IU/mL). Specific IgE (24 IU/mL) and IgG against Aspergillus was elevated (24.78 IU/mL). Spirometry was done which showed obstructive airway disease. Patient was diagnosed as ABPA presenting with collapse. Patient was put on oral prednisolone 0.5 mg/kg body weight daily for 2 weeks which was tapered off to 0.5 mg/kg body weight alternate day for next 2 weeks and then tapered to maintenance dose for another 4 months. Patient was advised to take regular asthma medication (LABA + ICS) and for follow-up regularly. Collapse disappeared after 1 month of treatment with oral steroids [Figure 6.3] and [Figure 6.4]. Patient improved clinically and her total IgE came down to 640 IU/mL.
| Discussion|| |
ABPA is a complex immune hypersensitivity reaction that manifests when the bronchi become colonized by Aspergillus, which causes chronic inflammation followed by bronchiectasis, fibrosis, and ultimately respiratory failure. Although there are 200 species of Aspergillus (A.), only few such as A. fumigatus, Aspergillus flavus, and Aspergillus niger have been reported to cause ABPA. The Rosenberg Patterson criteria are most widely used for diagnosis and include eight major and three minor criteria. The major criteria include asthma, roentgenographic evidence of pulmonary opacities, skin test positive for Aspergillus (Type 1 reaction) blood esonophilia, precipitating antibodies (IgG) against A. fumigatus in the serum, elevated serum IgE levels (>1000 IU/mL), central bronchiectasis, and elevated serum A. fumigatus-specific IgG and IgE. The minor criteria include the presence of Aspergillus in sputum, expectoration of brownish black mucus plugs, and delayed skin reaction to Aspergillus antigen (Type III reaction). If six of the eight major primary criteria are met, the diagnosis is made certain. Greenberger 1997 criteria do not differentiate into major and minor diagnostic criteria. Eight diagnostic criteria are laid down to detect ABPA. These criteria are 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.
Recently proposed diagnostic criteria for ABPA by International Society for Human and Animal Mycology include predisposing conditions like Bronchial asthma and cystic fibrosis. Obligatory criteria (both of which should be present) include Type I Aspergillus skin test positive or elevated IgE levels against A. fumigates and Elevated total IgE levels (>1000 IU/mL). Other criteria (at least two of three should be present) which include presence of precipitating or IgG antibodies against A. fumigatus in serum, radiographic pulmonary opacities consistent with ABPA and total eosinophil counts >500 cells/μL in steroid naıve patients. A wide spectrum of radiographic changes can be seen in patients with ABPA including transient migratory radiographic opacities secondary to eosinophilic pneumonia. These shadows were termed as “walking pneumonia., HRCT characteristically shows central bronchiectasis, mucus-filled bronchi, consolidation, and centri-lobular nodules. Other manifestations include segmental or lobar collapse, pleural effusion, and spontaneous pneumothorax. A characteristic radiographic finding in ABPA is high-attenuation mucus.
The presentation of ABPA as pulmonary masses (as seen in our one patient) is distinctly uncommon. These masses are usually attributed to mucus plugging of bronchi and distal accumulation of secretions, as seen in our patient or large bronchocele (mucus-filled dilated bronchi), which appear as masses but with no proximal obstruction. Another mechanism is probably inflammatory eosinophilic parenchymal consolidation without endobronchial involvement, appearing as pseudotumor. Eosinophilic organizing pneumonia due to adjoining intense bronchial inflammation led to pseudotumor formation. Although bronchoceles are classically seen in ABPA, reversible bronchoceles are almost pathognomonic of ABPA. The presence of hyperdense mucus is the most characteristic (if not pathognomonic) finding of ABPA and occurs in almost 19% of these patients. The high-attenuation calcium salts generally indicate chronicity and negate an acute event. In our patient, the quick disappearance of the mass after initiation of treatment indicates an acute event which dramatically responded to treatment. It is important to note that ABPA can also be diagnosed in patients without history of asthma unlike our cases. This is particularly important because in these patients, presence of a lung mass can lead to strong consideration of lung cancer as a diagnostic possibility and lead to invasive diagnostic procedures to establish an accurate diagnosis. ABPA can present as pulmonary mass lesion and must be considered in the differential diagnosis in patients presenting with history of asthma. High-attenuation density within these masses can help narrow the differential diagnosis. It is important to consider ABPA in the diagnostic algorithm of pulmonary masses because treatment with glucocorticoids is associated with excellent outcomes, as seen in our patient. Pulmonary infiltrates and segmental collapse are the usual radiological picture, it can rarely present as lung collapse as in one of our case. Parenchymal abnormalities, which have a predilection for upper lobes, include consolidation, collapse, and parenchymal scarring. Parenchymal lesions can extend up to the pleura. The collapse can be managed by aggressive pulmonary toileting to cause mobilization of secretions by physiotherapy, postural drainage, and/or bronchoscopy along with treatment with drugs such as corticosteroids and/or antifungal agents. Our patient was treated with oral steroids and responded well. Her collapse disappeared after 4 weeks of treatment.
| Conclusion|| |
With above case-based discussion, it can be concluded that if any patient with background history of bronchial asthma present with blood eosinophilia and various radiological abnormalities, ABPA should be suspected and further investigations should be done for the early diagnosis and treatment of ABPA.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
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| References|| |
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. Allergic bronchopulmonary aspergillosis and the evaluation of the patient with asthma. J Allergy Clin Immunol 1988;81:646-50.
Agarwal R, Chakrabarti A, Shah A, Gupta D, Meis JF, Guleria R, et al.
Allergic bronchopulmonary aspergillosis: Review of literature and proposal of new diagnostic and classification criteria. Clin Exp Allergy 2013;43:850-73.
Prasad R, Garg R, Sanjay. Walking pneumonia in a patient of bronchial asthma: A clue to the diagnosis of allergic bronchopulmonary aspergillosis. Pulmon 2007;9:120-3.
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]
Thompson BH, Stanford W, Galvin JR, Kurihara Y. Varied radiologic appearances of pulmonary aspergillosis. Radiographics 1995;15:1273-84.
Lemire P, Trepanier A, Hebert G. Bronchocele and blocked bronchiectasis. Am J Roentgenol Radium Ther Nucl Med 1970;110:687-93.
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