Prevention of severe premenstrual asthma attacks by leukotriene receptor antagonist

Background: The etiology and treatment of premenstrual exacerbations of asthma (PMA) remain uncertain. Objective: We investigated the role of cellular mediators released from inflammatory cells in the airflow limitation during PMA. Methods: Serum levels of leukotriene (LT) B 4 , LTC 4 , platelet- ac...

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Veröffentlicht in:Journal of allergy and clinical immunology 1999-09, Vol.104 (3), p.585-588
Hauptverfasser: Nakasato, Hiroko, Ohrui, Takashi, Sekizawa, Kiyohisa, Matsui, Toshifumi, Yamaya, Mutsuo, Tamura, Gen, Sasaki, Hidetada
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container_end_page 588
container_issue 3
container_start_page 585
container_title Journal of allergy and clinical immunology
container_volume 104
creator Nakasato, Hiroko
Ohrui, Takashi
Sekizawa, Kiyohisa
Matsui, Toshifumi
Yamaya, Mutsuo
Tamura, Gen
Sasaki, Hidetada
description Background: The etiology and treatment of premenstrual exacerbations of asthma (PMA) remain uncertain. Objective: We investigated the role of cellular mediators released from inflammatory cells in the airflow limitation during PMA. Methods: Serum levels of leukotriene (LT) B 4 , LTC 4 , platelet- activating factor, histamine, IL-1β, IL-4, IL-5, IL-6, and GM-CSF were measured at different time points, first just before or during menstruation when the peak expiratory flow rate (PEFR) began to decrease precipitously and second during the menstrual midcycle week (days 10-16) when the PEFR returned to baseline values in patients with PMA and in age-matched asthma patients without PMA at the same intervals. Results: Serum levels of LTC 4 were significantly higher during exacerbations of asthma than after recovery (69.0 ± 16.0 pg/mL vs 24.0 ± 9.5 pg/mL, P < .05), whereas those of IL-1β, IL-4, IL-5, IL-6, GM-CSF, histamine, LTB 4 , and platelet-activating factor did not differ between 2 periods in 5 patients with PMA. In contrast, in 5 asthmatic patients without PMA serum levels of cellular mediators did not differ between corresponding periods. Oral administration of pranlukast, an LT receptor antagonist (225 mg twice daily), significantly reduced decreases in PEFR from the baseline values (110 ± 21 L/min with pranlukast vs 233 ± 20 L/min without pranlukast, P < .01) in association with an improvement of asthma symptom scores (6.5 ± 1.1 with pranlukast vs 9.8 ± 0.7 without pranlukast, P
doi_str_mv 10.1016/S0091-6749(99)70327-1
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Objective: We investigated the role of cellular mediators released from inflammatory cells in the airflow limitation during PMA. Methods: Serum levels of leukotriene (LT) B 4 , LTC 4 , platelet- activating factor, histamine, IL-1β, IL-4, IL-5, IL-6, and GM-CSF were measured at different time points, first just before or during menstruation when the peak expiratory flow rate (PEFR) began to decrease precipitously and second during the menstrual midcycle week (days 10-16) when the PEFR returned to baseline values in patients with PMA and in age-matched asthma patients without PMA at the same intervals. Results: Serum levels of LTC 4 were significantly higher during exacerbations of asthma than after recovery (69.0 ± 16.0 pg/mL vs 24.0 ± 9.5 pg/mL, P &lt; .05), whereas those of IL-1β, IL-4, IL-5, IL-6, GM-CSF, histamine, LTB 4 , and platelet-activating factor did not differ between 2 periods in 5 patients with PMA. In contrast, in 5 asthmatic patients without PMA serum levels of cellular mediators did not differ between corresponding periods. Oral administration of pranlukast, an LT receptor antagonist (225 mg twice daily), significantly reduced decreases in PEFR from the baseline values (110 ± 21 L/min with pranlukast vs 233 ± 20 L/min without pranlukast, P &lt; .01) in association with an improvement of asthma symptom scores (6.5 ± 1.1 with pranlukast vs 9.8 ± 0.7 without pranlukast, P &lt;0.05) in 5 patients with PMA. Conclusion: LTs are partly involved in the pathogenesis of PMA, and LT receptor antagonists may be useful for preventing airflow obstruction in patients with PMA. 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Objective: We investigated the role of cellular mediators released from inflammatory cells in the airflow limitation during PMA. Methods: Serum levels of leukotriene (LT) B 4 , LTC 4 , platelet- activating factor, histamine, IL-1β, IL-4, IL-5, IL-6, and GM-CSF were measured at different time points, first just before or during menstruation when the peak expiratory flow rate (PEFR) began to decrease precipitously and second during the menstrual midcycle week (days 10-16) when the PEFR returned to baseline values in patients with PMA and in age-matched asthma patients without PMA at the same intervals. Results: Serum levels of LTC 4 were significantly higher during exacerbations of asthma than after recovery (69.0 ± 16.0 pg/mL vs 24.0 ± 9.5 pg/mL, P &lt; .05), whereas those of IL-1β, IL-4, IL-5, IL-6, GM-CSF, histamine, LTB 4 , and platelet-activating factor did not differ between 2 periods in 5 patients with PMA. In contrast, in 5 asthmatic patients without PMA serum levels of cellular mediators did not differ between corresponding periods. Oral administration of pranlukast, an LT receptor antagonist (225 mg twice daily), significantly reduced decreases in PEFR from the baseline values (110 ± 21 L/min with pranlukast vs 233 ± 20 L/min without pranlukast, P &lt; .01) in association with an improvement of asthma symptom scores (6.5 ± 1.1 with pranlukast vs 9.8 ± 0.7 without pranlukast, P &lt;0.05) in 5 patients with PMA. Conclusion: LTs are partly involved in the pathogenesis of PMA, and LT receptor antagonists may be useful for preventing airflow obstruction in patients with PMA. (J Allergy Clin Immunol 1999;104:585-8.)</description><subject>Adolescent</subject><subject>Adult</subject><subject>Anti-Asthmatic Agents - therapeutic use</subject><subject>asthma</subject><subject>Asthma - blood</subject><subject>Asthma - drug therapy</subject><subject>Asthma - physiopathology</subject><subject>Asthma - prevention &amp; control</subject><subject>Biological and medical sciences</subject><subject>Chromones - therapeutic use</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>Cytokines - blood</subject><subject>Female</subject><subject>female sex steroids</subject><subject>glucocorticoids</subject><subject>Histamine - blood</subject><subject>Humans</subject><subject>inflammatory cells</subject><subject>Leukotriene Antagonists - therapeutic use</subject><subject>Leukotriene B4 - blood</subject><subject>Leukotriene C4 - blood</subject><subject>leukotrienes</subject><subject>Mast Cells - metabolism</subject><subject>Medical sciences</subject><subject>Menstruation</subject><subject>Peak Expiratory Flow Rate - physiology</subject><subject>Pharmacology. 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Drug treatments</topic><topic>Pneumology</topic><topic>Respiratory system</topic><topic>T-Lymphocytes - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakasato, Hiroko</creatorcontrib><creatorcontrib>Ohrui, Takashi</creatorcontrib><creatorcontrib>Sekizawa, Kiyohisa</creatorcontrib><creatorcontrib>Matsui, Toshifumi</creatorcontrib><creatorcontrib>Yamaya, Mutsuo</creatorcontrib><creatorcontrib>Tamura, Gen</creatorcontrib><creatorcontrib>Sasaki, Hidetada</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakasato, Hiroko</au><au>Ohrui, Takashi</au><au>Sekizawa, Kiyohisa</au><au>Matsui, Toshifumi</au><au>Yamaya, Mutsuo</au><au>Tamura, Gen</au><au>Sasaki, Hidetada</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prevention of severe premenstrual asthma attacks by leukotriene receptor antagonist</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>1999-09-01</date><risdate>1999</risdate><volume>104</volume><issue>3</issue><spage>585</spage><epage>588</epage><pages>585-588</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><coden>JACIBY</coden><abstract>Background: The etiology and treatment of premenstrual exacerbations of asthma (PMA) remain uncertain. Objective: We investigated the role of cellular mediators released from inflammatory cells in the airflow limitation during PMA. Methods: Serum levels of leukotriene (LT) B 4 , LTC 4 , platelet- activating factor, histamine, IL-1β, IL-4, IL-5, IL-6, and GM-CSF were measured at different time points, first just before or during menstruation when the peak expiratory flow rate (PEFR) began to decrease precipitously and second during the menstrual midcycle week (days 10-16) when the PEFR returned to baseline values in patients with PMA and in age-matched asthma patients without PMA at the same intervals. Results: Serum levels of LTC 4 were significantly higher during exacerbations of asthma than after recovery (69.0 ± 16.0 pg/mL vs 24.0 ± 9.5 pg/mL, P &lt; .05), whereas those of IL-1β, IL-4, IL-5, IL-6, GM-CSF, histamine, LTB 4 , and platelet-activating factor did not differ between 2 periods in 5 patients with PMA. In contrast, in 5 asthmatic patients without PMA serum levels of cellular mediators did not differ between corresponding periods. Oral administration of pranlukast, an LT receptor antagonist (225 mg twice daily), significantly reduced decreases in PEFR from the baseline values (110 ± 21 L/min with pranlukast vs 233 ± 20 L/min without pranlukast, P &lt; .01) in association with an improvement of asthma symptom scores (6.5 ± 1.1 with pranlukast vs 9.8 ± 0.7 without pranlukast, P &lt;0.05) in 5 patients with PMA. Conclusion: LTs are partly involved in the pathogenesis of PMA, and LT receptor antagonists may be useful for preventing airflow obstruction in patients with PMA. (J Allergy Clin Immunol 1999;104:585-8.)</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>10482831</pmid><doi>10.1016/S0091-6749(99)70327-1</doi><tpages>4</tpages></addata></record>
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source MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects Adolescent
Adult
Anti-Asthmatic Agents - therapeutic use
asthma
Asthma - blood
Asthma - drug therapy
Asthma - physiopathology
Asthma - prevention & control
Biological and medical sciences
Chromones - therapeutic use
Chronic obstructive pulmonary disease, asthma
Cytokines - blood
Female
female sex steroids
glucocorticoids
Histamine - blood
Humans
inflammatory cells
Leukotriene Antagonists - therapeutic use
Leukotriene B4 - blood
Leukotriene C4 - blood
leukotrienes
Mast Cells - metabolism
Medical sciences
Menstruation
Peak Expiratory Flow Rate - physiology
Pharmacology. Drug treatments
Pneumology
Respiratory system
T-Lymphocytes - metabolism
title Prevention of severe premenstrual asthma attacks by leukotriene receptor antagonist
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