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Eur J Clin Pharmacol. 2002 Jun;58(3):171-6. Epub 2002 May 18.

Effect of suplatast tosilate, a Th2 cytokine inhibitor, on cough variant asthma.

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1
Department of Physical Therapy, Akita University College of Allied Medical Science, 1-1-1 Hondo, Akita, 010-8543, Japan. shioya@hos.akita-u.ac.jp

Abstract

STUDY OBJECTIVE:

Th2 cytokines play an important role in the pathogenesis of asthma. Our study objective was to determine the effect of suplatast tosilate, a Th2 cytokine inhibitor, on patients with cough-variant asthma.

METHODS:

Twenty patients with cough-variant asthma (CVA) were assigned to a suplatast tosilate (100 mg three times daily) group or a placebo group for 6 weeks in a double-blind randomized study. The cough scores, medication scores, pulmonary function, bronchial hyperresponsiveness to methacholine, cough threshold for capsaicin, percentage of eosinophils and concentrations of eosinophilic cationic protein (ECP) in hypertonic saline-induced (induced) sputum were evaluated. The main outcome measures were capsaicin cough threshold and concentrations of ECP in induced sputum.

RESULTS:

In the suplatast group, the cough scores and the medication scores decreased significantly over time. The percentage of eosinophils in induced sputum significantly decreased from 53.5+/-5.6% to 13.6+/-2.6%. The cough threshold for capsaicin improved significantly from 2.72+/-3.41 microM to 39.7+/-22.7 microM in the suplatast group. The concentrations of ECP in induced sputum decreased significantly from 435+/-123 microg/l to 56+/-34 microg/l in the suplatast group. The bronchial responsiveness to methacholine changed from 8.45+/-3.43 units to 11.4+/-3.76 units in the suplatast group.

CONCLUSIONS:

Suplatast improved the cough scores and the cough threshold for capsaicin in patients with CVA without significant side effects, suggesting the effectiveness of suplatast in the treatment of CVA. Suplatast also decreased the percentage of eosinophils and concentrations of ECP in induced sputum, suggesting improvement in eosinophilic inflammation in patients with CVA. Further pharmacodynamic research is needed to explain the precise mechanism.

PMID:
12107601
DOI:
10.1007/s00228-002-0468-z
[Indexed for MEDLINE]
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