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Year : 2016  |  Volume : 30  |  Issue : 1  |  Page : 35-37

Allergic bronchopulmonary aspergillosis masquerading as malignancy in a nonasthmatic: A rare case report

Department of Pulmonary Medicine, T. N. Medical College, B. Y. L. Nair Hospital, Mumbai, Maharashtra, India

Date of Web Publication2-Aug-2016

Correspondence Address:
Jyotsna M Joshi
Department of Pulmonary Medicine, T. N. Medical College, B. Y. L. Nair Hospital, Mumbai - 400 008, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-6691.187567

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Allergic bronchopulmonary aspergillosis (ABPA) is a lung disease caused by hypersensitivity reaction to antigens of Aspergillus species of which Aspergillus fumigatus is the most common culprit. ABPA is most commonly diagnosed in patients with a history of uncontrolled bronchial asthma despite optimum treatment. ABPA is rarely diagnosed in nonasthmatics. Diverse radiological appearances are known in ABPA patients; however, whole lung collapse has been rarely reported. We report a case of ABPA in a 62-year-old female with no background history of asthma, initially suspected to have bronchogenic carcinoma of the right lung. After ruling out malignancy, the diagnosis of ABPA was established based on Rosenberg-Patterson criteria. Treatment with oral steroids for 6 months in tapering doses lead to clinical and radiological improvement and decrease in IgE levels. This case is unique as ABPA masquerading as malignancy causing a lung collapse in a nonasthmatic is a very rare presentation.

Keywords: Allergic bronchopulmonary aspergillosis, malignancy, mucoid impaction

How to cite this article:
Chaudhary A, Utpat K, Desai U, Joshi JM. Allergic bronchopulmonary aspergillosis masquerading as malignancy in a nonasthmatic: A rare case report. Indian J Allergy Asthma Immunol 2016;30:35-7

How to cite this URL:
Chaudhary A, Utpat K, Desai U, Joshi JM. Allergic bronchopulmonary aspergillosis masquerading as malignancy in a nonasthmatic: A rare case report. Indian J Allergy Asthma Immunol [serial online] 2016 [cited 2023 Mar 21];30:35-7. Available from: https://www.ijaai.in/text.asp?2016/30/1/35/187567

  Introduction Top

Allergic bronchopulmonary aspergillosis is an allergic immune response to aspergillus fumigatus antigens. It is commonly encountered in patients with asthma and cystic fibrosis. The disease is potentially progressive if not managed adequately. Early diagnosis and treatment with oral corticosteroids is of paramount importance to prevent the irreversible parenchymal damage and deterioration of lung functions. This case highlights the possibility of atypical presentation of ABPA and thus emphasizing the need for a high index of suspicion for its early recognition and management.

  Case report Top

A 62-year-old nonsmoker woman followed up to the outpatient department of our hospital with symptoms of 1-month duration of cough with mucoid expectoration, exertional dyspnea not associated wheeze, and few episodes of streaky hemoptysis. History suggestive of atopy was present in the form of allergic rhinitis in self. However, there was no history suggestive of bronchial asthma. Clinical examination revealed signs of volume loss with absent breath sound in the right hemithorax. Chest radiograph (CXR) revealed right opaque hemithorax with deviation of trachea to right [Figure 1]. Hence, a suspicion of malignancy (bronchogenic carcinoma) was considered. However, a contrast-enhanced computed tomography (CECT) of chest done 6 days later revealed a soft tissue causing obstruction of the right middle lobe bronchus and lower lobe bronchus with postobstructive consolidation [Figure 2] as against a complete lung collapse seen on CXR. Hence, in view of discordant CXR and CECT findings, possibility of differential diagnoses other than malignancy was considered, and the patient was evaluated further. Complete blood count revealed eosinophilia with absolute eosinophil count of 3740/mm 3 . Evaluation with serum IgE revealed increased levels of 18,100 Ku/l. Spirometry showed evidence of restrictive abnormality with ratio of forced expiratory volume (FEV) in first second (FEV1) to forced vital capacity (FVC) of 91%, FEV1 of 0.96 L (56% of predicted) and FVC of 1.05 L (51% of predicted) with no bronchodilator reversibility. Fiber-optic bronchoscopy was performed and showed mucous plugging in the right middle and lower lobe bronchus, which was suctioned and aspirated with instillation of normal saline. Biopsy revealed respiratory mucosa with underlying hypertrophied bronchial musculature with accompanying eosinophils and mucin but no evidence of malignancy. There was a significant symptomatic improvement and improvement in breath sounds after bronchoscopic removal of mucous plug. Repeat CXR showed residual patchy opacity in the right lower zone with clearing of rest of hemithorax. In view of history of atopy, peripheral eosinophilia, raised serum IgE, and allergic bronchopulmonary aspergillosis (ABPA) was considered the next differential diagnosis. For confirmation, the patient was evaluated with Specific IgE against Aspergillus fumigatus which was positive (18.0 kUA/L). The patient was initiated on therapy with oral steroids (prednisolone) 1 mg/kg/day for 4 weeks followed by tapering by 5 mg every week till a maintenance dose of 20 mg alternate day was reached and continued on the same for total duration of 6 months. The patient was also started on intranasal corticosteroids. One month after initiation of oral steroids, patient showed significant symptomatic improvement along with a reduction in peripheral eosinophilia to 1200/mm 3 with spirometry showing improvement in lung functions (FEV1 improved to 96% predicted and FVC 100% predicted). After completion of 6 months of therapy, patient was asymptomatic from respiratory point of view, and there was a significant reduction in eosinophilia from 3740/mm 3 at baseline to 432/mm 3 . Serum IgE reduced from 18100 Ku/L to 1255 Ku/L. CXR showed only a patchy opacity in the right lower zone. Spirometry showed improvement in FEV1 by 540 ml (FEV1 100% predicted) and in FVC by 1100 ml (FVC 114% predicted) as compared to baseline. Repeat CT thorax [Figure 3] at the end of therapy showed significant improvement with regression of the areas of postobstructive consolidation seen in the right middle and lower lobes with only residual proximal cystic bronchiectasis in the right middle and lower lobe. Currently, patient is in remission and is on regular 6 monthly follow-up.
Figure 1: Chest radiograph showing right opaque hemithorax with shift of trachea to right signifying right lung collapse

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Figure 2: Contrast-enhanced computed tomography thorax showing a soft tissue causing obstruction of the right middle lobe bronchus and lower lobe bronchus with postobstructive consolidation and bronchiectatic changes

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Figure 3: Computed tomography thorax showing residual proximal cystic bronchiectasis in the right middle and lower lobe

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  Discussion Top

ABPA is an immunological lung disorder caused by hypersensitivity to fungus A. fumigatus which usually presents with difficult to control asthma and recurrent pulmonary infiltrates. It is a common but frequently misdiagnosed [1] clinical condition requiring a high index of suspicion for its detection owing to its varied presentations. It is detected by a combination of clinical, radiological, and serological criteria. The criteria for diagnosis are the Rosenberg-Patterson criteria. [2],[3] Major criteria include history of uncontrolled bronchial asthma, X-ray evidence of fleeting pulmonary opacities, skin test positive for Aspergillus (Type 1 reaction), eosinophilia, precipitating antibodies (IgG) against Aspergillus 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).

Diverse radiological manifestations are known among ABPA patients. Common radiological presentations include finger in glove opacities representing mucoid impaction and proximal bronchiectasis, lobar/segmental collapse, focal consolidation, transient pulmonary infiltrates, band-like opacities, fibrosis, and cavities. Very rarely, whole lung collapses have been reported. [4] Airway mucus can have normal or high attenuation. In high-attenuation mucus, the concentration of ions such as calcium, iron, and manganese contributes to a Hounsfield density that can exceed that of surrounding skeletal muscle. [5] ABPA can be subdivided into ABPA-S (diagnosed serologically) and ABPA-CB (central bronchiectasis present radiologically). Central bronchiectasis is a hallmark finding although ABPA without bronchiectasis is also recognized. [6]

The pathophysiology of ABPA is allergic in nature, characterized by activation of eosinophils and elaboration of IgE. Hence, immunosuppression is the mainstay of the treatment. Most common modality of management is conservative medical treatment with oral corticosteroids for duration of 6-12 months. Potential role for newer antifungal azole medications as corticosteroid-sparing agents is still a topic of debate, but a few studies have suggested that antifungals may improve the long-term outcome in this potentially relapsing condition.

Although ABPA has been described historically to be associated with uncontrolled asthma, history of asthma can be missing at times. [7] Our patient was atopic; however, there was no history suggestive of asthma. We therefore emphasize that ABPA should be considered a differential diagnosis whenever dealing with a patient presenting with lung collapse even without a background history of an airway disease to avoid misdiagnosis. There has been a case reported in literature where patient underwent a lobectomy for a suspected malignancy and later was diagnosed to have ABPA. [8] Likewise, this unusual case also serves as a reminder for the treating physicians that ABPA can present with atypical clinical and radiological features.

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Conflicts of interest

There are no conflicts of interest.

  References Top

de Oliveira E, Giavina-Bianchi P, Fonseca LA, França AT, Kalil J. Allergic bronchopulmonary aspergillosis' diagnosis remains a challenge. Respir Med 2007;101:2352-7.  Back to cited text no. 1
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.  Back to cited text no. 2
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.  Back to cited text no. 3
Agarwal R. Allergic bronchopulmonary aspergillosis. Chest 2009;135:805-26.  Back to cited text no. 4
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;173:937-42.  Back to cited text no. 5
Rajkumar DP. Evaluation of allergic bronchopulmonary aspergillosis in patients with and without central bronchiectasis. J Asthma 2002;39:473-7.  Back to cited text no. 6
Patterson K, Strek ME. Allergic bronchopulmonary aspergillosis. Proc Am Thorac Soc 2010;7:237-44.  Back to cited text no. 7
Sánchez-Alarcos JM, Martínez-Cruz R, Ortega L, Calle M, Rodríguez-Hermosa JL, Alvarez-Sala JL. ABPA mimicking bronchogenic cancer. Allergy 2001;56:80-1.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3]


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