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a Second Department
of Internal Medicine, Toho University School of Medicine, 6- 11- 1 Ohmorinishi, Ohta-ku, Tokyo 143, Japan, b Department of Trauma and Critical Care Medicine, Kurume
University School of Medicine, 67 Asahi-machi, Kurume-shi, Fukuoka
830, Japan
Correspondence to: Dr Y Nakamura, Meakins-Christie Laboratories, McGill University, 3626 St Urbain Street, Montreal, Canada H2X 2P2.
Received 6 October 1997; Returned to authors 9 December 1997; Revised version received 12 February 1998; Accepted for publication 20 May 1998
BACKGROUND
It has been reported that
pranlukast reduces the antigen induced immediate and late phase
asthmatic responses, airway hyperreactivity to acetylcholine, and
pulmonary eosinophil accumulation in guinea pigs. A study was
undertaken to test the hypothesis that pranlukast may reduce the number
of inflammatory cells in the bronchial mucosa of patients with asthma.
METHODSA double blind, placebo controlled
study was performed in 17 mild to moderate asthmatic subjects to
examine changes in inflammatory cell infiltration in response to
pranlukast (225 mg orally twice per day for four weeks). Comparisons
of the mean daily 
2 agonist use, symptom score,
FEV1 percentage predicted, and airway methacholine responsiveness were made before and after treatment. Using fibreoptic bronchoscopy, bronchial biopsy specimens were obtained before and
after treatment with either pranlukast (n = 10) or placebo (n = 7).
Immunohistology was performed using monoclonal antibodies for CD3, CD4,
CD8, CD68, NP57, AA1, EG1, EG2, 
GTP and CD19.
RESULTSWhen the pranlukast and placebo
treated groups were compared there were decreases in 2
agonist use, symptom score, and airway methacholine responsiveness
after pranlukast but no increase in FEV1 was seen. The
clinical response in patients treated with pranlukast was accompanied
by a reduction in CD3 (median difference -37, 95% confidence interval
(CI) -69 to -1; p<0.05), CD4 (median difference -28, 95% CI -49
to -8; p<0.01), AA1 (median difference -15, 95% CI -26 to 0;
p<0.05) and EG2 positive cells (95% CI -35 to 0;
p<0.05), but not in EG1 positive eosinophils, GTP positive cells,
and CD19 positive plasma cells.
CONCLUSIONSThese results support the view
that pranlukast may act by inhibition of bronchial inflammation in
patients with asthma.
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