アトルバスタチンによる短期治療は,高コレステロール血症患者の血小板CD40リンガンドとトロンビン生成を減少させます
Valerio Sanguigni1, Pasquale Pignatelli, Luisa Lenti
1Department of Experimental Medicine and Pathology, University of Rome La Sapienza, Rome, Italy.
Circulation
|February 3, 2005
まとめ
高コレステロール血症では,溶性CD40L (sCD40L) と血小板CD40Lの上昇は,血栓生成の増加と関連しています. アトルバスタチン治療はこれらのマーカーを減少させ,コレステロールの減少とは関係のない直接的な抗血栓効果を示した.
科学分野:
- 心血管生物学 心血管生物学
- 血液学 ヘマトロジ
- 薬理学 薬理学とは
背景:
- 血小板活性化のマーカーである溶性CD40L (sCD40L) は,高コレステロール血症では上昇しています.
- 血小板CD40Lおよび血sCD40Lレベルは,体内の血小板活性化を反映しています.
研究 の 目的:
- 高コレステロール血症患者のsCD40Lと血小板CD40Lの関係を調査する.
- これらのマーカーに対する短期アトルバスタチン治療の効果を評価する.
主な方法:
- コラーゲン誘発血小板CD40L,プラズマsCD40L,プロトロンビン断片F1+2を30人の高コレステロール患者と20人の対照群で研究した.
- 患者は,ベースラインおよび治療後の測定値で3日間,ダイエットまたはアトルバスタチン (10 mg/d) を受けました.
主要な成果:
- 高コレステロール血症の患者は,対照群と比較して,血小板CD40L,sCD40L,F1+2が高かった.
- 血小板CD40LはsCD40Lと有意に相関しており,sCD40LはF1+2.2と相関していた.
- アトルバスタチン治療は血小板CD40L,sCD40L,F1+2を著しく減少させ,食事だけでは効果がなかった.
結論:
- 高コレステロール血症における血小板CD40L過剰発現は,sCD40Lとトロンビン生成の上昇に寄与する.
- アトルバスタチンは,脂質を下げる性質に関係なく,血小板CD40Lおよびその後のトロンビン生成を阻害することによって,直接の抗血栓効果を示しています.
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