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CASE REPORT |
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Year : 1996 | Volume
: 42
| Issue : 2 | Page : 53-5 |
Allergic bronchopulmonary aspergillosis.
JL Oak, DR Yavgal, RR Chakore
Department of Medicine, Seth GS Medical College & KEM Hospital, Parel, Mumbai.
Correspondence Address: J L Oak Department of Medicine, Seth GS Medical College & KEM Hospital, Parel, Mumbai.
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 0009715302 
A 38 year old male was diagnosed to have allergic bronchopulmonary aspergillosis which responded remarkably to prednisolone therapy.
Keywords: Adult, Anti-Inflammatory Agents, Steroidal, therapeutic use,Aspergillosis, Allergic Bronchopulmonary, complications,diagnosis,drug therapy,Case Report, Dyspnea, etiology,Hemoptysis, etiology,Human, Male, Prednisolone, therapeutic use,Skin Tests, Tomography, X-Ray Computed,
How to cite this article: Oak J L, Yavgal D R, Chakore R R. Allergic bronchopulmonary aspergillosis. J Postgrad Med 1996;42:53 |
Allergic bronchopulmonary aspergillosis (ABIPA) is a complex hypersensitivity reaction to the presence of aspergillus colonising the bronchial tree. It has a rare occurrence[1]. It occurs almost exclusively in atopic asthmatic individuals, affecting bronchial wails and its peripheral parts of the lung. Due to abnormally thick mucus plugs in bronchial asthmatics, its fungal spores remain trapped in the bronchial lumen producing acute migratory infiltrates in the lung and then a variety of irreversible changes causing chronic dysfunction[2]. Cor pulmonale occurs in about 1 % of these patients.
A 38 yrs old male patient, florist by occupation presented with repeated episodes of breathlessness, cough with mucopurulent expectoration and wheezing since 4-5 yrs. Initially he used to have 3-4 attacks of acute episodic dyspnoea but since one year he was getting an attack every month. He had streaky haemoptysis tour times during one year. He had no history of fever, chest pain or weight loss. The patient had received antituberculous drugs two years ago for a period of one year but he had no clinical response. He was also taking bronchodilators whenever required.
On examination his vital parameters were normal. He had no cyanosis, clubbing or lymphadenopathy. His respiratory system examination revealed bilateral rhonchi. Rest of the systems were normal.
Blood investigations: Hb 14.5 gm %, T.WBC count 12,400/cmm. Polymorphs 47 %, Lymphocytes 27 %. Eosinophils 26 % (absolute eosinophils count was 3224), ESR 36 mm/hr, BUN 7 mg % and T. Proteins 7.1 gm %.
His serial X-rays from the year 1994 to 1997 were reviewed which showed patchy alveolar infiltrates in RUZ, LMZ, LLZ [Figure - 1], [Figure - 2] changing in pattern with proximal bronchiectasis.
HRCT of the chest revealed multiple rounded dilated bronchi with air fluid level showing central bronchiectasis [Figure - 3].
His sputum exam for AFB was negative on three occasions. His pulmonary function test showed reduced peaked expiratory flow rate, his ventilation reserve and timed vital capacities were normal. There was evidence of small airway obstruction. His serum IgG was 1490 ng/dl (N.R.: 800-1700 ng/dl) and serum IgE level was 9388 IU/ml (N.R.: 10-180 IU/ml).
Our patient had recurrent attacks of bronchospasm, peripheral eosinophilia, radiographs of chest showed fleeting infiltrates, proximal bronchiectasis and increased levels of IgE (> 1000 IU/ml), thus satisfying the primary criteria[3] of ABPA. The diagnosis of ABPA was made and the patient was subjected to skin testing. The skin testing for aspergillus showed immediate positive reaction. The patient was given a course of oral prednisolone 40 mg/day for a period of four weeks and then tapered. It produced a remarkable improvement.
The pathogenesis of ABPA is believed to involve the inhalation, trapping and subsequent germination of aspergillus spores and viscid secretion in the airways of an atopic individual. Aspergillus fumigatus is the most common cause. Following germination, the organism vegetate in the bronchial lumen and produce high concentration of the antigen. The host response with a high levels of IgE and IgG sets in motion a series of antigen-antibody reactions, resulting in infiltration with eosinophils and bronchial damage. Eosinophils in the blood and sputum is common, Direct examination of sputum plugs will often disclose hyphae and the fungal spores. A sputum culture, positive for aspergillus test does not always mean that the patient is suffering from allergic aspergillosis, since it can be found commonly in expectorated material. Hence Petterson and colleagues suggested primary criteria of ABPA[3].
In Britain, ABPA has been reported in 22% of hospitalised asthmatic patients[4],[5]. The physicians should suspect the syndrome in every patient with asthma with pulmonary infiltrates, which shift from one place to another. The mucus plugging causes segmental, lobar or total collapse of the lungs giving rise to 'tramline' shadows, 'gloved ring' shadows 6 or ring shadows due to inflammation and thickening of bronchial walls. In late, stage there is a loss of volume of upper lobes, honeycombing and extensive bronchiectasis.
:: References | |  |
1. |
Albelda SM, Talbot GH. Pulmonary Aspergillosis, in Pulmonary Disease and Disorders, 2nd Ed. Vol. 2. McGraw Hill Publication; 1988, pp 1639-1655. |
2. | Aslam PA, Estridge CE, Huges FA Jr. Aspergillosis of the lung - An eighteen years experience. Chest 1971; 59:28-32 |
3. | Ambastha V, Sharma OP. ‘Many Faces of Pulmonary Aspergillosis’. J Int Med 1994; Suppl.6:25-30. |
4. | Mc Carty DS, Pepys J. Allergic Bronchopulmonary Aspergillosis: Clinical Immunology. Clin Allergy 1971; 1:261-286. |
5. | Mc Carty DS, Pepys J. Pulmonary Aspergillosis: Clinical Immunology. Clin Allergy 1973; 3:57-65. |
6. | Mc Carty DS, Simon G, Hargreave FD. The radiological appearances in allergic bronchopulmonary Aspergillosis. Clin Radiol. 1970; 21:366-375.
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Figures
[Figure - 1], [Figure - 2], [Figure - 3]
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