title: Persistent lower respiratory tract inflammation associated with interstitial lung disease in patients with tropical pulmonary eosinophilia following conventional treatment with diethylcarbamazine.
abstract: Tropical pulmonary eosinophilia (TPE) presents as an acute syndrome with dyspnea, fluffy infiltrates, and rounded opacities on the chest radiograph, reduced lung function, marked eosinophilia in the blood and lower respiratory tract, and high titers of specific IgE and IgG antifilarial antibodies. The standard therapy for TPE is a 3-wk course of diethylcarbamazine (DEC) following which there is almost always a marked improvement in all parameters. However, clinical observations suggest that the disease can persist despite DEC therapy and lead to chronic dyspnea with restrictive lung impairment. To evaluate the concept that DEC therapy is not completely "curative" for TPE, but rather leaves most individuals with a mild, chronic form of TPE defined by persistent inflammation of the lower respiratory tract, we evaluated 23 individuals an average of 12 +/- 2 months following a standard 3-wk course of diethylcarbamazine for acute TPE. In the majority there were mild, persistent symptoms referrable to the lung, chest X-ray abnormalities, blood eosinophilia, and elevated serum IgE and filarial specific IgG. On the average, lung function was consistent with the presence of chronic, mild interstitial lung disease. When the inflammatory cells from the lower respiratory tract were examined, there was a persistent eosinophilic alveolitis (TPE/post-DEC 1769 +/- 376 eosinophils/microliters epithelial lining fluid; normal subjects 256 +/- 38, p less than 0.02). Evaluation of the lower respiratory tract inflammatory cells recovered from the TPE/post-DEC-treated individuals demonstrated spontaneous release of exaggerated amounts of O2-. and H2O2 compared to normal subjects (p less than 0.05, both comparisons).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
authors.forename: W N
authors.initials: WN
authors.lastname: Rom
authors.forename: V K
authors.initials: VK
authors.lastname: Vijayan
authors.forename: M J
authors.initials: MJ
authors.lastname: Cornelius
authors.forename: V
authors.initials: V
authors.lastname: Kumaraswami
authors.forename: R
authors.initials: R
authors.lastname: Prabhakar
authors.forename: E A
authors.initials: EA
authors.lastname: Ottesen
authors.forename: R G
authors.initials: RG
authors.lastname: Crystal
mesh_terms: D000208:Acute Disease; D000328:Adult; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D004049:Diethylcarbamazine / Q000627:therapeutic use*; D004804:Eosinophils / Q000473:pathology; D005260:Female; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D007249:Inflammation / Q000473:pathology; D008297:Male; D011657:Pulmonary Eosinophilia / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D011658:Pulmonary Fibrosis / Q000209:etiology* / Q000473:pathology; D012137:Respiratory System / Q000473:pathology; D013481:Superoxides / Q000378:metabolism
chemical_list: D013481:Superoxides; D006861:Hydrogen Peroxide; D004049:Diethylcarbamazine