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Der Einfluss Von Montelukast Und Ramatroban Auf Die Allergische Frühreaktion Bei Leicht

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Der Einfluss Von Montelukast Und Ramatroban Auf Die Allergische Frühreaktion Bei Leicht Aus der Medizinischen Klinik des Forschungszentrums Borstel Leibnizzentrum für Medizin und Biowissenschaften Ärztlicher Direktor: Prof. Dr. P. Zabel Der Einfluss von Montelukast und Ramatroban auf die allergische Frühreaktion bei leicht- bis mittelgradigem allergischen Asthma bronchiale mit Sensibilisierung gegenüber Hausstaubmilben Inauguraldissertation zur Erlangung der Doktorwürde der Universität zu Lübeck -Aus der Medizinischen Fakultät- Vorgelegt von Stefanie Heinemann aus Kassel Lübeck 2007 1. Berichterstatter: Prof. Dr. med. Peter Zabel 2. Berichterstatter: Priv.-Doz. Dr. rer. nat. Dr. med. Jürgen Kreusch Tag der mündlichen Prüfung: 10.06.2008 Zum Druck genehmigt. Lübeck, den 10.06.2008 gez. Prof. Dr. med. Werner Solbach - Dekan der Medizinischen Fakultät - 1 Einleitung und Fragestellung ________________________________5 1.1 Asthmaformen________________________________________________________ 6 1.2 Pathogenese des allergischen Asthmas ____________________________________ 7 1.3 Diagnostik ___________________________________________________________ 9 1.3.1 Spezifische inhalative Provokation ____________________________________________ 10 1.4 Schweregradeinteilung ________________________________________________ 11 1.5 Therapie des Asthma bronchiale________________________________________ 13 1.5.1 Entwicklung der Asthmatherapie und Ausblick __________________________________ 14 1.6 Asthmamodelle ______________________________________________________ 15 1.6.1 Ovalbuminmodell _________________________________________________________ 15 1.6.2 Lungenschnitte Ratte _______________________________________________________ 15 1.6.3 Humane Lungenschnitte ____________________________________________________ 16 1.7 Lipidmediatoren _____________________________________________________ 17 1.7.1 Leukotriene ______________________________________________________________ 17 1.7.1.1 Synthese ____________________________________________________________ 17 1.7.1.2 Effekte _____________________________________________________________ 18 1.7.1.3 Rezeptoren __________________________________________________________ 19 1.7.2 Thromboxan A 2 ___________________________________________________________ 19 1.7.2.1 Synthese ____________________________________________________________ 20 1.7.2.2 Effekte _____________________________________________________________ 20 1.7.2.3 Rezeptoren __________________________________________________________ 20 1.7.3 Prostaglandin D 2 __________________________________________________________ 21 1.7.3.1 Synthese ____________________________________________________________ 22 1.7.3.2 Effekte _____________________________________________________________ 22 1.7.3.3 Rezeptoren __________________________________________________________ 22 1.8 Prüfsubstanzen ______________________________________________________ 23 1.8.1 CysLT1-Rezeptor Antagonist Montelukast/ Singulair® ____________________________ 23 1.8.1.1 Pharmakodynamische Eigenschaften______________________________________ 23 1.8.1.2 Klinische Effekte _____________________________________________________ 23 1.8.1.3 Pharmakokinetische Eigenschaften _______________________________________ 25 1.8.1.4 Nebenwirkungsprofil __________________________________________________ 25 ® 1.8.2 TXA 2 /CRTH2-Rezeptor Antagonist Ramatroban/ Baynas _________________________ 26 1.8.2.1 Anwendungsgebiete und Art der Anwendung _______________________________ 26 1.8.2.2 Tierexperimentelle und klinische Effekte __________________________________ 26 1.8.2.3 Pharmakokinetische Eigenschaften _______________________________________ 27 1.8.2.4 Nebenwirkungsprofil __________________________________________________ 27 1.9 Fragestellung________________________________________________________ 28 2 Material, Methoden und Probanden__________________________29 2.1 Studiendesign _______________________________________________________ 29 2.2 Studienplanung und Durchführung _____________________________________ 29 2.3 Einschlusskriterien ___________________________________________________ 30 2.4 Ausschlusskriterien___________________________________________________ 30 2.5 Abbruchkriterien ____________________________________________________ 31 2.6 Probanden __________________________________________________________ 31 2.6.1 Monotherapiegruppe _______________________________________________________ 31 2.6.2 Kombinationstherapiegruppe_________________________________________________ 32 2.7 Zielparameter _______________________________________________________ 33 2.7.1 PD 20 FEV 1________________________________________________________________ 33 2.7.2 FEV 1 (forced expiratory volume in one second) __________________________________ 33 2.7.3 RAW (Resistance) _________________________________________________________ 33 1 2.8 Randomisierung _____________________________________________________ 34 2.9 Allergologische Diagnostik_____________________________________________ 34 2.10 Prüfsubstanzen ______________________________________________________ 34 2.10.1 Montelukast ___________________________________________________________ 34 2.10.2 Ramatroban____________________________________________________________ 35 2.10.3 Placebo _______________________________________________________________ 35 2.11 Zeitlicher Ablauf_____________________________________________________ 36 2.12 Lungenfunktionelle Messungen_________________________________________ 38 2.12.1 Bodyplethysmographie ___________________________________________________ 38 2.12.2 Peak-Flow-Messungen ___________________________________________________ 38 2.12.3 Spezifische bronchiale Provokation _________________________________________ 39 2.13 Serologische Untersuchungen __________________________________________ 39 2.13.1 Blutentnahme __________________________________________________________ 39 2.13.2 Thromboxan B 2 - Spiegel Bestimmung im Serum ______________________________ 40 2.13.3 Leukotrien C 4 und Leukotrien E 4- Spiegel Bestimmung im Serum _________________ 40 2.14 Statistische Auswertung _______________________________________________ 40 3 Ergebnisse _______________________________________________42 3.1 Vergleichbarkeit der Kollektive ________________________________________ 42 3.1.1 PD 20 FEV 1 native Provokation ________________________________________________ 42 3.1.2 FEV 1 native Provokation ____________________________________________________ 42 3.1.3 RAW native Provokation____________________________________________________ 43 3.1.4 Peak-Flow-Protokoll _______________________________________________________ 44 3.1.5 Sensibilisierung ___________________________________________________________ 45 3.2 Vergleichbarkeit der Provokationen_____________________________________ 46 3.2.1 FEV 1 ___________________________________________________________________ 46 3.2.2 RAW ___________________________________________________________________ 47 3.2.3 Peakflow ________________________________________________________________ 48 3.3 Einfluss der Therapie auf die PD 20 FEV 1__________________________________ 49 3.3.1 Monotherapiegruppe _______________________________________________________ 49 3.3.2 Kombinationstherapiegruppe_________________________________________________ 49 3.3.3 Vergleich der beiden Therapiegruppen _________________________________________ 50 3.4 Thromboxan B 2-Serum-Spiegel_________________________________________ 53 3.5 Leukotrien C 4-Serum-Spiegel __________________________________________ 54 3.6 Leukotrien E 4-Serum-Spiegel __________________________________________ 55 4 Ergebnisdiskussion________________________________________56 4.1 Methodenkritik ______________________________________________________ 56 4.1.1 Vergleichbarkeit der Kollektive ______________________________________________ 57 4.1.2 Vergleichbarkeit der beiden Provokationen______________________________________ 58 4.2 Medikamente________________________________________________________ 58 4.3 Der Effekt von Montelukast auf die allergische Frühreaktion________________ 59 4.4 Der Einfluss von Montelukast auf die basale FEV 1 _________________________ 60 4.5 Der Effekt von Montelukast und Ramatroban auf die allergische Frühreaktion 61 4.6 Hat Ramatroban einen additiven Effekt zu Montelukast?___________________ 63 4.7 Lipidmediatoren- Spiegel im Serum _____________________________________ 64 4.8 Ausblick ____________________________________________________________ 66 5 Zusammenfassung ________________________________________68 2 6 Literaturverzeichnis_______________________________________69 7 Anhang _________________________________________________86 7.1.1 Monotherapiegruppe _______________________________________________________ 86 7.1.2 Kombinationstherapiegruppe_________________________________________________ 88 7.1.3 Ethikkommission__________________________________________________________ 88 8 Danksagung______________________________________________89 9 Lebenslauf_______________________________________________90 3 Abkürzungsverzeichnis BIB belastungsinduzierte Bronchokonstriktion BAL bronchoalveoläre Lavage CRTH2 chemoattractant receptor expressed on T-helpercells CVA cough variant asthma CysLT1/2 Cysteinylleukotrien 1/2 ECP eosinophile kationische Proteine eNO exhaliertes NO FEV 1 forcierte expiratorische Einsekundenkapazität FLAP 5-Lipoxygenase aktivierendes Protein GINA Global Initiative for Asthma HWZ Halbwertszeit IAR immediate allergic reaction ICS inhalative corticosteroid IgE Immunglobulin E IL Interleukin LABA long-acting β2-agonist LAR late allergic
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