6メチルプレドニソロンによるアスピリン無感性イコサノイド生物合成の調節は,不安定なアンギナで行われる
Francesco Cipollone1, Antonina Ganci, Anita Greco
1Department of Medicine and Aging, University of Chieti G. D'Annunzio School of Medicine, Chieti, Italy. fcipollone@unich.it
Circulation
|January 8, 2003
まとめ
グルココルチコイド治療は,不安定な胸痛患者の白血球C4 (LT C4) 産生を低下させ,炎症を示唆した.
科学分野:
- 心臓病学 心臓病学
- 炎症の研究 炎症の研究
- 薬理学 薬理学とは
背景:
- 炎症は,急性冠動脈症候群に関連しています.
- 不安定性 angina の炎症メディエーターを調査した.
研究 の 目的:
- 不安定性アンギナにおけるルオコトリエンC4 (LT C4) とトロンボキサンA2 (TX A2) のバイオシンセシスに対するグルココルチコイド効果を調査する.
- 不安定性アンギナの病理生理学における炎症の役割を調査する.
主な方法:
- 尿路LTE4と11-デヒドロ-TXB2を不安定性アンギナ,安定性アンギナ,非血症性胸痛患者で比較した.
- 静脈内投与の6メチルプレドニソロン (6-MP) またはプラセボを不安定な心筋梗塞の患者に投与.
- 治療前のおよび治療中の尿サンプルを採取し,イコサノイドの排泄量を測定します.
主要な成果:
- 尿中のLTE4および11-デヒドロ-TXB2は,不安定な胸痛患者で上昇した.
- 6-MPは,不安定なアンギナ患者のLTE4排出を著しく低下させた.
- 11-デヒドロ-TXB2レベルは,6-MP治療で有意に変化しませんでした.
結論:
- 静脈活性型白血球トリエン (LT) とトロンボキサン (TX) は,不安定な胸痛で過剰に生成される可能性があります.
- グルココルチコイドは,短期的にLT C4バイオシンセシスを抑制することができます.
- グルココルチコイドは,不安定性胸痛における炎症性細胞活性化の役割を明らかにするのに役立ちます.
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