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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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 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70041833</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0091674999703271</els_id><sourcerecordid>70041833</sourcerecordid><originalsourceid>FETCH-LOGICAL-c390t-730e65df9c5dd0e11e4f48d871cb3089717a2daddacb81be918595fc9a594dcb3</originalsourceid><addsrcrecordid>eNqF0EFLHDEUwPEgLbrafgQlh1Law9hkZ2aTd5IitRaEFmzP4U3yRlNnJtskI_jtzbqLeuspPPi9JPwZO5biVAq5-nItBMhqpRr4BPBZiXqpKrnHFlKAqlZ62b5hi2dywA5T-ivKXGvYZwdSNHqpa7lg178i3dOUfZh46HkqQyS-jjTSlHKcceCY8u2IHHNGe5d498AHmu9Cjp4m4pEsrXOIHKeMN2HyKb9jb3scEr3fnUfsz8W33-eX1dXP7z_Ov15VtgaRK1ULWrWuB9s6J0hKavpGO62k7WqhQUmFS4fOoe207AikbqHtLWALjSvmiH3c3ruO4d9MKZvRJ0vDgBOFORklRCN1XRfYbqGNIaVIvVlHP2J8MFKYTU3zVNNsUhkA81TTyLJ3sntg7kZyr7a2-Qr4sAOYLA59xMn69OKgASU27GzLqNS49xRNsiWeJedLvmxc8P_5ySORepM9</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>70041833</pqid></control><display><type>article</type><title>Prevention of severe premenstrual asthma attacks by leukotriene receptor antagonist</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Nakasato, Hiroko ; Ohrui, Takashi ; Sekizawa, Kiyohisa ; Matsui, Toshifumi ; Yamaya, Mutsuo ; Tamura, Gen ; Sasaki, Hidetada</creator><creatorcontrib>Nakasato, Hiroko ; Ohrui, Takashi ; Sekizawa, Kiyohisa ; Matsui, Toshifumi ; Yamaya, Mutsuo ; Tamura, Gen ; Sasaki, Hidetada</creatorcontrib><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 <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><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/S0091-6749(99)70327-1</identifier><identifier>PMID: 10482831</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>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</subject><ispartof>Journal of allergy and clinical immunology, 1999-09, Vol.104 (3), p.585-588</ispartof><rights>1999 Mosby, Inc.</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-730e65df9c5dd0e11e4f48d871cb3089717a2daddacb81be918595fc9a594dcb3</citedby><cites>FETCH-LOGICAL-c390t-730e65df9c5dd0e11e4f48d871cb3089717a2daddacb81be918595fc9a594dcb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0091674999703271$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1949701$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10482831$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><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><title>Prevention of severe premenstrual asthma attacks by leukotriene receptor antagonist</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><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 <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 & 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. Drug treatments</subject><subject>Pneumology</subject><subject>Respiratory system</subject><subject>T-Lymphocytes - metabolism</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0EFLHDEUwPEgLbrafgQlh1Law9hkZ2aTd5IitRaEFmzP4U3yRlNnJtskI_jtzbqLeuspPPi9JPwZO5biVAq5-nItBMhqpRr4BPBZiXqpKrnHFlKAqlZ62b5hi2dywA5T-ivKXGvYZwdSNHqpa7lg178i3dOUfZh46HkqQyS-jjTSlHKcceCY8u2IHHNGe5d498AHmu9Cjp4m4pEsrXOIHKeMN2HyKb9jb3scEr3fnUfsz8W33-eX1dXP7z_Ov15VtgaRK1ULWrWuB9s6J0hKavpGO62k7WqhQUmFS4fOoe207AikbqHtLWALjSvmiH3c3ruO4d9MKZvRJ0vDgBOFORklRCN1XRfYbqGNIaVIvVlHP2J8MFKYTU3zVNNsUhkA81TTyLJ3sntg7kZyr7a2-Qr4sAOYLA59xMn69OKgASU27GzLqNS49xRNsiWeJedLvmxc8P_5ySORepM9</recordid><startdate>19990901</startdate><enddate>19990901</enddate><creator>Nakasato, Hiroko</creator><creator>Ohrui, Takashi</creator><creator>Sekizawa, Kiyohisa</creator><creator>Matsui, Toshifumi</creator><creator>Yamaya, Mutsuo</creator><creator>Tamura, Gen</creator><creator>Sasaki, Hidetada</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19990901</creationdate><title>Prevention of severe premenstrual asthma attacks by leukotriene receptor antagonist</title><author>Nakasato, Hiroko ; Ohrui, Takashi ; Sekizawa, Kiyohisa ; Matsui, Toshifumi ; Yamaya, Mutsuo ; Tamura, Gen ; Sasaki, Hidetada</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-730e65df9c5dd0e11e4f48d871cb3089717a2daddacb81be918595fc9a594dcb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Anti-Asthmatic Agents - therapeutic use</topic><topic>asthma</topic><topic>Asthma - blood</topic><topic>Asthma - drug therapy</topic><topic>Asthma - physiopathology</topic><topic>Asthma - prevention & control</topic><topic>Biological and medical sciences</topic><topic>Chromones - therapeutic use</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>Cytokines - blood</topic><topic>Female</topic><topic>female sex steroids</topic><topic>glucocorticoids</topic><topic>Histamine - blood</topic><topic>Humans</topic><topic>inflammatory cells</topic><topic>Leukotriene Antagonists - therapeutic use</topic><topic>Leukotriene B4 - blood</topic><topic>Leukotriene C4 - blood</topic><topic>leukotrienes</topic><topic>Mast Cells - metabolism</topic><topic>Medical sciences</topic><topic>Menstruation</topic><topic>Peak Expiratory Flow Rate - physiology</topic><topic>Pharmacology. 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 < .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 <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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