Acquired alpha 1-antitrypsin deficiency in tropical pulmonary eosinophilia.

dc.contributor.authorRay, Debidas
dc.contributor.authorHarikrishna, S
dc.contributor.authorImmanuel, Chandra
dc.contributor.authorVictor, Lalitha
dc.contributor.authorSubramanyam, Sudha
dc.contributor.authorKumaraswami, V
dc.date.accessioned2011-12-07T09:27:42Z
dc.date.available2011-12-07T09:27:42Z
dc.date.issued2011-07
dc.description.abstractBackground & objectives: Observation of an increased frequency of an intermediate deficiency of serum alpha1-antitrypsin (α1-AT) in patients with Tropical Pulmonary Eosinophilia (TPE) was earlier reported. Though the possibility of existence of an acquired deficiency was suggested, without phenotyping a hereditary α1-AT deficiency in TPE could not totally be ruled out. In this study, we have done Pi (Protease inhibitor) phenotyping to investigate the possibility of association of any heterozygous (or homozygous) α1-AT deficiency in patients with TPE. Methods: Serum a1antitrypsin (α1-AT) was measured in 103 patients (Group A) with TPE, 99 patients with pulmonary eosinophilia who had associated intestinal worm infestation (Group B) and 43 healthy volunteers who served as controls. In 19 α1-AT deficient patients (9 of Group A and 10 of Group B), α1-AT level was measured before and after treatment. In 58 patients with TPE and in 5 controls, phenotyping was done. Results: Fifteen patients of Group A and 16 from Group B showed intermediate α1-AT deficiency (150 mg % or less. None of the control subjects had α1-AT deficiency (<200 mg%). After treatment with DEC and/or deworming, in 19 patients there was a significant (P < 0.001) rise in α1-AT levels. Results of phenotyping showed that all had M1 or M2 allele and none had S or Z variant (either homozygous or heterozygous) thus ruling out any underlying genetic cause for the observed α1-AT deficiency. Interpretation & conclusions: The observed α1-AT deficiency may be due to the chronic inflammation in TPE and associated oxidative stress. However, in such α1-AT deficient patients with TPE and those with worm infested pulmonary eosinophilia, faecal α1-AT concentration and faecal α1-AT clearance should be routinely estimated to rule out the possibility of any intestinal protein loss.en_US
dc.identifier.citationRay Debidas, Harikrishna S, Immanuel Chandra, Victor Lalitha, Subramanyam Sudha, Kumaraswami V. Acquired alpha 1-antitrypsin deficiency in tropical pulmonary eosinophilia. Indian Journal of Medical Research. 2011 Jul; 134(1): 79-82.en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/135732
dc.language.isoenen_US
dc.source.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171921/en_US
dc.subjectα1-antitrypsinen_US
dc.subjectacquired deficiencyen_US
dc.subjecttropical pulmonary eosinophiliaen_US
dc.subjectphenotypingen_US
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshAlleles
dc.subject.meshAnimals
dc.subject.meshCase-Control Studies
dc.subject.meshDiethylcarbamazine --therapeutic use
dc.subject.meshElephantiasis, Filarial --epidemiology
dc.subject.meshFemale
dc.subject.meshFilariasis --epidemiology
dc.subject.meshHumans
dc.subject.meshMale
dc.subject.meshOxidative Stress
dc.subject.meshPulmonary Eosinophilia --complications
dc.subject.meshWuchereria bancrofti --isolation & purification
dc.subject.meshalpha 1-Antitrypsin --blood
dc.subject.meshalpha 1-Antitrypsin --genetics
dc.subject.meshalpha 1-Antitrypsin Deficiency --blood
dc.subject.meshalpha 1-Antitrypsin Deficiency --etiology
dc.subject.meshalpha 1-Antitrypsin Deficiency --genetics
dc.titleAcquired alpha 1-antitrypsin deficiency in tropical pulmonary eosinophilia.en_US
dc.typeArticleen_US
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