A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma

Y. Y. Koh, Y. W. Kim, J. D. Park, Jae-Won Oh

Research output: Contribution to journalArticle

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Abstract

Background: Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haptoglobin (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 ± 80.8 mg/dl, mean ± SD) was significantly (P < 0.01) higher than that at CR (152.3 ± 49.8 mg/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-bronchodilator FEV1 <75% predicted) to the initial bronchodilator therapy at AE than that (61.0 ± 56.5 mg/dl) of those (n = 31) who responded well (post-bronchodilator FEV1 ≤75% predicted). The Hp level at AE correlated 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 at the 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 bronchodilator therapy at AE suggests that the increased Hp level at AE in asthma might reflect the degree of airway inflammation.

Original languageEnglish
Pages (from-to)1202-1209
Number of pages8
JournalClinical and Experimental Allergy
Volume26
Issue number10
DOIs
StatePublished - 1996 Nov 2

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Haptoglobins
Bronchodilator Agents
Asthma
Serum
Acute-Phase Proteins
Inflammation
Therapeutics
Bronchoconstriction

Keywords

  • Acute exacerbation
  • Airway inflammation
  • Bronchial asthma
  • Clinical remission
  • Haptoglobin

Cite this

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title = "A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma",
abstract = "Background: Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haptoglobin (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 ± 80.8 mg/dl, mean ± SD) was significantly (P < 0.01) higher than that at CR (152.3 ± 49.8 mg/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-bronchodilator FEV1 <75{\%} predicted) to the initial bronchodilator therapy at AE than that (61.0 ± 56.5 mg/dl) of those (n = 31) who responded well (post-bronchodilator FEV1 ≤75{\%} predicted). The Hp level at AE correlated 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 at the 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 bronchodilator therapy at AE suggests that the increased Hp level at AE in asthma might reflect the degree of airway inflammation.",
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A comparison of serum haptoglobin levels between acute exacerbation and clinical remission in asthma. / Koh, Y. Y.; Kim, Y. W.; Park, J. D.; Oh, Jae-Won.

In: Clinical and Experimental Allergy, Vol. 26, No. 10, 02.11.1996, p. 1202-1209.

Research output: Contribution to journalArticle

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N2 - Background: Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haptoglobin (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 ± 80.8 mg/dl, mean ± SD) was significantly (P < 0.01) higher than that at CR (152.3 ± 49.8 mg/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-bronchodilator FEV1 <75% predicted) to the initial bronchodilator therapy at AE than that (61.0 ± 56.5 mg/dl) of those (n = 31) who responded well (post-bronchodilator FEV1 ≤75% predicted). The Hp level at AE correlated 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 at the 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 bronchodilator therapy at AE suggests that the increased Hp level at AE in asthma might reflect the degree of airway inflammation.

AB - Background: Bronchial asthma is characterized by airway inflammation, which underlies the phenomenon of bronchial hyperresponsiveness. The concentration of serum haptoglobin (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 ± 80.8 mg/dl, mean ± SD) was significantly (P < 0.01) higher than that at CR (152.3 ± 49.8 mg/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-bronchodilator FEV1 <75% predicted) to the initial bronchodilator therapy at AE than that (61.0 ± 56.5 mg/dl) of those (n = 31) who responded well (post-bronchodilator FEV1 ≤75% predicted). The Hp level at AE correlated 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 at the 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 bronchodilator therapy at AE suggests that the increased Hp level at AE in asthma might reflect the degree of airway inflammation.

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KW - Airway inflammation

KW - Bronchial asthma

KW - Clinical remission

KW - Haptoglobin

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