阻害性睡眠時無呼吸症と学校に通う年齢の非肥満児の内皮機能:アデノトンシルエクトミーの効果
David Gozal1, Leila Kheirandish-Gozal, Laura D Serpero
1Kosair Children's Hospital Research Institute, University of Louisville School of Medicine, 570 S Preston St, Suite 204, Louisville, KY 40202, USA. david.gozal@louisville.edu
Circulation
|October 31, 2007
まとめ
小児阻害性睡眠無呼吸症 (OSA) は,内皮機能不全を引き起こし,治療後に改善します. この改善は,心臓血管疾患の家族歴のない子供に特に効果的です.
科学分野:
- ペディアトリック・カルディオロジー
- スリープ・メディシン (睡眠医学)
- 血管生物学 血管生物学
背景:
- 子どもにおける阻害性睡眠時無呼吸症 (OSA) は,高血圧などの心血管疾患に関連しています.
- 小児性OSAにおける内皮機能障害の存在と可逆性は十分に理解されていません.
研究 の 目的:
- OSAの小児における内皮機能を調査する.
- アデノトンジレクトミーが小児OSAにおける内皮機能不全を逆転させるかどうかを判断する.
主な方法:
- OSAと対照群の小児におけるカフオクラッション試験を用いて,内皮機能の評価.
- 溶解性CD40リガンド,ADMA,およびニトロチロシンの血濃度が測定されました.
- アデノトンジレクトミー後の4~6ヶ月間,再評価を繰り返す.
主要な成果:
- OSAの小児は,閉塞後の鈍化性高血症を示し,内皮機能の障害を示した.
- Adenotonsillectomyは,ほとんどのOSA患者の内皮機能を正常化しました.
- OSAの子供における溶解性CD40リガンド濃度の上昇は,治療後の減少で,高血圧の改善と相関しています.
- ADMAまたはニトロチロシン濃度の有意な差異は,グループ間で観察されなかった.
結論:
- 内皮機能不全は小児性OSAに存在し,治療で回復する.
- 心血管疾患の家族歴のない子供では,治療効果がより高い.
- 溶性CD40リガンドレベルは,小児OSAにおける内皮機能不全と治療反応のバイオマーカーとして機能する可能性があります.
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