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Effects of Pranlukast on Chemical Mediators in Induced Sputum on Provocation Tests in Atopic and Aspirin-Intolerant Asthmatic Patients^*

^* From The Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.

Correspondence to: Yasushi Obase, MD, Skin and Allergy Hospital, Helsinki University Central Hospital, PO Box 160, HUS, Helsinki, Finland; e-mail: yasushi.obase{at}hus.fi

Background: Leukotrienes (LTs) are important in asthma, and LT modifiers modulate antigen-induced asthma. Overproduction of LT by suppression of cyclooxygenase activity is involved in patients with aspirin-intolerant asthma (AIA).

Methods: House dust mite (HDM) inhalation provocation tests were performed in HDM-sensitive asthmatic inpatients without AIA (HDM group; n = 6), and aspirin oral provocation tests were performed in AIA patients (ASA group; n = 7). Tests were repeated using the same regimen after 7 days of treatment with pranlukast, an LT receptor antagonist (LTRA). The effects of pranlukast on changes in sputum LTC₄-LTD₄, eosinophil cationic protein (ECP), eosinophil count, urinary LTE₄/creatinine, 11-dehydrothromboxane B₂ (11-dhTXB₂)/creatinine, serum LTC₄-LTD₄, ECP, and peripheral blood eosinophil count, during immediate asthmatic reaction (IAR) and late asthmatic reaction (LAR) in the HDM group and during IAR in the ASA group for each test, were compared in each group.

Results: In the HDM group, IAR and LAR were observed. Sputum LTC₄-LTD₄ and urinary LTE₄/creatinine increased significantly both during IAR and LAR. Sputum ECP increased during IAR and further increased during LAR. Eosinophil count in the sputum did not increase during IAR but significantly increased during LAR. Pranlukast suppressed the fall in FEV₁ both during IAR and LAR (73.8% and 51.9%, respectively) and inhibited the increase in sputum eosinophil count during LAR and sputum ECP during IAR and LAR. In the ASA group, aspirin-induced IAR was associated with a fall in urinary 11-dhTXB₂/creatinine, increased the levels of sputum LTC₄-LTD₄ and ECP and urinary LTE₄/creatinine. Pranlukast suppressed IAR and inhibited the increase of the level of sputum ECP, but failed to change aspirin-induced LT production in the sputum and urine. The levels of sputum LTC₄-LTD₄ and urinary LTE₄/creatinine in the stable phase in the ASA group were significantly greater than those in the HDM group.

Conclusion: Our results indicated that HDM-provoked asthma is associated with overproduction of LT with an antigen-antibody reaction, while AIA is associated with overproduction of LT with a shift to the 5-lipoxygenase series of the arachidonate cascade. LTRA may be useful against both types of asthma through inhibition of LT activity and eosinophilic inflammation of the airways.

Key Words: allergen provocation • aspirin-intolerant asthma • aspirin oral challenge • asthma • chemical mediators • induced sputum • leukotriene receptor antagonist

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