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A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma
Author(s) -
KOH Y. Y.,
KIM Y. W.,
PARK J. D.,
OH J. W.
Publication year - 1996
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1996.tb00509.x
Subject(s) - exacerbation , haptoglobin , asthma , medicine , immunology , asthma exacerbations , acute severe asthma , intensive care medicine , respiratory disease , lung
Summary Background Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haploglobin (Hp), one of the acute phase reactant proteins, has been reported to correlate with bronchial hyperresponsiveness. The extent to which bronchoconstriction or airway inflammation contributes to airflow obstruction of exacerbation is presumed to determine the responsiveness to the initial bronchodilator therapy. Objective To see whether the Hp levels vary with the disease status of asthma, and also to test whether the Hp level at an acute exacerbation(AE) is correlated with the degree of response to initial bronchodilator therapy. Methods We measured serum Hp levels in 50 children with asthma at the times of an AE and a clinical remission(CR), and analysed the data according to the response to the initial bronchodilator therapy at AE. Results The serum concentration of Hp at AE (228.5 ± 80.8mg/dl, mean ± SD) was significantly ( P < 0.01) higher than that at CR (152.3 ± 49.8mg/dl) in the total study population. The difference of Hp levels between AE and CR was more marked (101.7 ± 82.2 mg/dl) in the subjects ( n = 19) who responded poorly (post‐bronchodi‐lator FEV 1 < 75% predicted) to the initial bronehodilator therapy at AE than that (61.0 ± 56.5mg/dl) of those ( n = 31) who responded well (post‐bronchodilator FEV 1 ± 75% predicted). The Hp level at AE eorrelated with the degree of response to initial bronchodilator therapy ( r =−0.36, P < 0.05), whereas it had no relationship with the severity of exacerbation ( r = 0.04. P = 0.79). Conclusion Our results showed that Hp levels may be increased al ihe time of exacerbation in a given asthma patient. The finding that the elevation of Hp level at AE is more marked in the cases with poor response to initial bronchodilaior therapy at AE suggests that the increased Hp level at AE in asthma might relied the degree of airway inflammation.