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Effects of cysteinyl-leukotriene receptor antagonist, thromboxane A2 receptor antagonist, and thromboxane A2 synthetase inhibitor on antigen-induced bronchoconstriction in patients with asthma.
Chest 1998; 114(4):1028-32Chest

Abstract

BACKGROUND

Leukotriene (LT) and thromboxane A2 (TXA2) receptor antagonists have been used in the treatment of asthma.

OBJECTIVES

We examined the effects of an LT receptor antagonist, TXA2 receptor antagonist, and TXA2 synthetase inhibitor on bronchoprovocation test (BPT) in patients with mild-to-moderate atopic asthma.

METHODS

BPT was performed four times in each of six asthmatics. Development of the immediate asthmatic reaction (IAR) and late asthmatic reaction (LAR) was confirmed on the first BPT (BPT1). After a 7-day washout period, an LT receptor antagonist (pranlukast, 450 mg/d), TXA2 receptor antagonist (seratrodast, 80 mg/d), or TXA2 synthetase inhibitor (ozagrel, 800 mg/d) was administered orally over 7 days at random using a cross-over method (BPT2-4). Blood levels of LTB4, LTC4, LTD4, 11-dehydrothromboxane B2, eosinophil cationic protein, and histamine were measured at reaction phases of pre-BPT, IAR, and LAR.

RESULTS

Administration of pranlukast suppressed IAR by 80.5% (p < 0.0001) and LAR by 54.6% (p = 0.0391). Ozagrel significantly suppressed IAR by 39.5% (p = 0.0413), but the fall in FEV1 was >20% (21.56+/-4.173%). Seratrodast did not suppress IAR or LAR. Blood levels of chemical mediators did not correlate with the suppressive effects of the tested drugs.

CONCLUSIONS

The LT receptor antagonist was considered to be the most effective. LT might play a more important role in the pathogenesis of asthma than TXA2. Our data showed that measurement of blood levels of chemical mediators is not useful in identifying the pathogenic mechanisms of asthma.

Authors+Show Affiliations

Second Department of Internal Medicine, Nagasaki University School of Medicine, Japan. obadann-ngs@umin.u-tokyo.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Comparative Study
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

9792572

Citation

Obase, Y, et al. "Effects of Cysteinyl-leukotriene Receptor Antagonist, Thromboxane A2 Receptor Antagonist, and Thromboxane A2 Synthetase Inhibitor On Antigen-induced Bronchoconstriction in Patients With Asthma." Chest, vol. 114, no. 4, 1998, pp. 1028-32.
Obase Y, Shimoda T, Matsuo N, et al. Effects of cysteinyl-leukotriene receptor antagonist, thromboxane A2 receptor antagonist, and thromboxane A2 synthetase inhibitor on antigen-induced bronchoconstriction in patients with asthma. Chest. 1998;114(4):1028-32.
Obase, Y., Shimoda, T., Matsuo, N., Matsuse, H., Asai, S., & Kohno, S. (1998). Effects of cysteinyl-leukotriene receptor antagonist, thromboxane A2 receptor antagonist, and thromboxane A2 synthetase inhibitor on antigen-induced bronchoconstriction in patients with asthma. Chest, 114(4), pp. 1028-32.
Obase Y, et al. Effects of Cysteinyl-leukotriene Receptor Antagonist, Thromboxane A2 Receptor Antagonist, and Thromboxane A2 Synthetase Inhibitor On Antigen-induced Bronchoconstriction in Patients With Asthma. Chest. 1998;114(4):1028-32. PubMed PMID: 9792572.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of cysteinyl-leukotriene receptor antagonist, thromboxane A2 receptor antagonist, and thromboxane A2 synthetase inhibitor on antigen-induced bronchoconstriction in patients with asthma. AU - Obase,Y, AU - Shimoda,T, AU - Matsuo,N, AU - Matsuse,H, AU - Asai,S, AU - Kohno,S, PY - 1998/10/29/pubmed PY - 1998/10/29/medline PY - 1998/10/29/entrez SP - 1028 EP - 32 JF - Chest JO - Chest VL - 114 IS - 4 N2 - BACKGROUND: Leukotriene (LT) and thromboxane A2 (TXA2) receptor antagonists have been used in the treatment of asthma. OBJECTIVES: We examined the effects of an LT receptor antagonist, TXA2 receptor antagonist, and TXA2 synthetase inhibitor on bronchoprovocation test (BPT) in patients with mild-to-moderate atopic asthma. METHODS: BPT was performed four times in each of six asthmatics. Development of the immediate asthmatic reaction (IAR) and late asthmatic reaction (LAR) was confirmed on the first BPT (BPT1). After a 7-day washout period, an LT receptor antagonist (pranlukast, 450 mg/d), TXA2 receptor antagonist (seratrodast, 80 mg/d), or TXA2 synthetase inhibitor (ozagrel, 800 mg/d) was administered orally over 7 days at random using a cross-over method (BPT2-4). Blood levels of LTB4, LTC4, LTD4, 11-dehydrothromboxane B2, eosinophil cationic protein, and histamine were measured at reaction phases of pre-BPT, IAR, and LAR. RESULTS: Administration of pranlukast suppressed IAR by 80.5% (p < 0.0001) and LAR by 54.6% (p = 0.0391). Ozagrel significantly suppressed IAR by 39.5% (p = 0.0413), but the fall in FEV1 was >20% (21.56+/-4.173%). Seratrodast did not suppress IAR or LAR. Blood levels of chemical mediators did not correlate with the suppressive effects of the tested drugs. CONCLUSIONS: The LT receptor antagonist was considered to be the most effective. LT might play a more important role in the pathogenesis of asthma than TXA2. Our data showed that measurement of blood levels of chemical mediators is not useful in identifying the pathogenic mechanisms of asthma. SN - 0012-3692 UR - https://www.unboundmedicine.com/medline/citation/9792572/Effects_of_cysteinyl_leukotriene_receptor_antagonist_thromboxane_A2_receptor_antagonist_and_thromboxane_A2_synthetase_inhibitor_on_antigen_induced_bronchoconstriction_in_patients_with_asthma_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0012-3692(16)33001-X DB - PRIME DP - Unbound Medicine ER -