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Tropical Pulmonary Eosinophilia

1991; Elsevier BV; Volume: 100; Issue: 2 Linguagem: Inglês

10.1378/chest.100.2.587c

1931-3543

Debidas Ray,

Chronic Obstructive Pulmonary Disease (COPD) Research

To the Editor: I read with keen interest the article on airway hyperreactivity in tropical pulmonary eosinophilia by Drs Chhabra and Gaur, which appeared in the May 1988 issue of Chest,1Chhabra SK Gaur SN Airway hyperreactivity in tropical pulmonary eosinophilia..Chest. 1988; 93: 1105-1106Crossref PubMed Scopus (5) Google Scholar as well as the comments on that article by Drs Chitkara and Donath, which appeared in the January 1990 issue of Chest.2Chitkara RK Donath J Tropical eosinophilia (letter)..Chest. 1990; 97: 253Abstract Full Text Full Text PDF Scopus (1) Google Scholar It was rightly pointed out in the latter communication that the presence of measurable hyperresponsiveness in tropical pulmonary eosinophilia (TPE) might indeed be useful in elucidating the pathogenesis. In addition to my findings in an article3Ray D Lung function in tropical eosinophilia..Indian J Chest Dis. 1974; 16: 363-373Google Scholar quoted in the letter by Drs Chitkara and Donath, we subsequently documented improvement in lung capacity in acute TPE within eight weeks following successful treatment with diethylcarbamazine.4Ray D Improvement of lung capacity in tropical pulmonary eosinophilia following diethyl carbamazine therapy..Lung India. 1983; 1: 153-154Google Scholar We also studied the bronchial response to inhaled isoprenahne in TPE and found that patients during the first episode of TPE of recent onset were on the whole unresponsive whereas those experiencing a relapse of the disease showed a significant response.5Ray D Bronchial response to inhaled isoprenaline in tropical pulmonary eosinophilia..Lung India. 1986; 4: 25-28Google Scholar The pathologic picture of TPE in the first few weeks is one of outpouring of histiocytes, soon followed by eosinophils in alveolar, interstitial, peribronchial, and perivascular spaces and eosinophilic infiltration of the bronchioles with edema of the walls and blocking of the lumen with shedding of mucous membrane and clumps of esoinophils.6Udwadia FE Joshi V A study of tropical eosinophilia..Thorax. 1964; 19: 548-553Crossref PubMed Scopus (17) Google Scholar We thought that these earliest changes in TPE may have acted as a mechanical hindrance to satisfactory bronchial response in our patients with primary TPE. It would be interesting to know whether either or both patients of Drs Chhabra and Gaur had any previous eosinophilic episode. If these two hyperreactive patients with acute illness were indeed studied during the first episode of TPE, then the more likely explanation for our finding would be that the bronchospasticity due to intense major basic protein activity and excessive release of leukotrienes7Gleich GJ Longering DA Immunology of eosinophilia..Annu Rev Immunol. 1984; 12: 429-459Crossref Scopus (146) Google Scholar is so severe in the patients with an acute attack of primary TPE that they, unlike those in relapse, may not show significant bronchial response to the 10 mg of aerosol isoprenaline commonly administered.