Serum C3d levels in tropical pulmonary eosinophilia

Background & objectives: Results of earlier studies to evaluate the possible role of complement system in tropical pulmonary eosinophilia (TPE) using classical methods like serum haemolyte component CH50, C3 and C4 levels were inconclusive. In this study we determined levels of serum C3d which is a catabolic fragment of C3, to find out any direct evidence of activation of the complement system in TPE. Methods: The study population consisted of 3 groups. Group A consisted of 37 patients with well characterized TPE. In group B, 26 patients with pulmonary eosinophilia had similar respiratory and haemotological features as in Group A but had associated worm infestation in stool. The control group consisted of 39 healthy volunteers. Serum C3d levels were determined by sandwich ELISA technique. Results: The serum C3d levels in TPE patients were not significantly different from those of the patients of group B or the normal controls. Interpretation & conclusions: Absence of significant change in serum C3d goes against the possibility of complement activation in TPE. Results of our study suggest that complement system is unlikely to play a pivotal role in pathogenesis of TPE

Acquired alpha 1-antitrypsin deficiency in tropical pulmonary eosinophilia

Background & 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