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Kokyu to Junkan Volume 44, Issue 6 （June 1996）

呼吸と循環 44巻6号（1996年6月発行）

Japanese English

研究

急性心筋梗塞症における抑制サイトカイン測定の意義 Elevated Plasma Interleukin-1 Receptor Antagonist and Interleukin-10 in Patients with Acute Myocardial Infarction 柴田雅士 ¹ , 遠藤重厚 ¹ , 佐藤紀夫 ¹ , 荒川直志 ¹ , 鈴木知己 ¹ , 青木英彦 ¹ , 鈴木智之 ¹ , 栗城聡 ² , 原田雅子 ² , 瀬川郁夫 ² , 平盛勝彦 ² , 稲田捷也 ³ Masashi Shibata ¹ , Shigeatsu Endo ¹ , Norio Sato ¹ , Naoshi Arakawa ¹ , Tomomi Suzuki ¹ , Hidehiko Aoki ¹ , Tomoyuki Suzuki ¹ , Satoshi Kuriki ² , Masako Harada ² , Ikuo Segawa ² , Katsuhiko Hiramori ² , Katsuya Inada ³ ¹岩手医科大学高次救急センター ²岩手医科大学第二内科 ³岩手医科大学細菌学 ¹Critical Care and Emergency Center, Iwate Medical University ²2nd Department of Internal Medicine, Iwate Medical University ³Department of Bacteriology, Iwate Medical University キーワード：インターロイキン−1受容体拮抗物質 , インターロイキン−10 , 急性心筋梗塞症 , interleukin-1 recepter antagonist , interleukin-10 , acute myocardial infarction Keyword: インターロイキン−1受容体拮抗物質 , インターロイキン−10 , 急性心筋梗塞症 , interleukin-1 recepter antagonist , interleukin-10 , acute myocardial infarction pp.635-640

発行日 1996年6月15日 Published Date 1996/6/15

DOI https://doi.org/10.11477/mf.1404901273

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Abstract 文献概要
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　急性心筋梗塞症（AMI）の心不全および急性期予後と，抑制サイトカインの血中インターロイキン1受容体拮抗物質（IL−1ra）およびIL−10との関係をみた．AMI 27例を心不全合併［CHF（＋）］17例と，非合併［CHF（−）］10例とに分け，IL−1raとIL−10をAMI発症後72時間まで経時的にELISA法で測定した．CHF（＋）群のIL−1raピーク値（pIL−1ra）は白血球数ピーク値，肺動脈入楔入圧，心係数とにr＝0.63^＊，0.78^＊＊，−0.51^＊の相関を，IL−10ピーク値（pIL−10）と，それぞれにr＝0.60^＊，0.73^＊＊，−0.50^＊の相関を，さらに，pIL−1raとpIL−10との間にr＝0.91^＊＊＊の正相関を認めた（^＊p＜0.05，^＊＊p＜0.01，^＊＊＊p＜0.001）．CHF（＋）群と早期死亡群のpIL−1raとpIL−10はCHF（−）群に比して有意に高く，特に，IL−1raは早期に高値を示した．AMI急性期のIL−1raおよびIL−10の測定は，AMIの重症度および入院中の予後推定に有用であると考えられた．

The main pathogenetic factor causing shock and organ dysfunction in critically ill patients is the variety of host responses to severe clinical insults. Cytokines are known to play a central role in these pathogenic mechanisms. In the present study, we attempted to define the kinetics of plasma interleukin-1 receptor antagonist (IL-1ra) and plasma interleukin-10 (IL-10) in patients with acute myocardial infarction (AMI) (n=27, age 42.91yr, mean 66yr). Plasma IL-1ra levels and plasma IL-10 levels were measured by enzyme-linked immunosorbent assay. Patients in Group 1 (n= 17) had severe AMI (Killip class 2, 3 or 4). Patients in Group 2 (n=10) had uncomplicated AMI (Killip class 1). Peak IL-lra levels and peak IL-10 levels in Group I were significantly higher (p＜0.05) than those of Group 2. In Group 1, the peak IL-1ra levels were significantly correlated with white blood cell counts (r=0.63, p=0.006), pulmonary wedge pressure (r=0.78, p= 0.0002) and cardiac index (r=-0.51, p=0.04). Peak IL-10 levels were significantly correlated with white blood cell counts (r=0.60, p=0.01), the pulmonary wedge pressure (r =0.73, p =0.0008) and cardiac index (r=-0.50, p=0.04). Moreover, a significant correlation was found between the peak IL-1ra levels and peak IL-10 levels (r=0.91, p＜0.0001). The peak IL-1ra levels in non-survivors (n=6) were significantly higher (p＜ 0.01) than those in survivors (n=21).

The plasma IL-1ra levels and plasma IL-10 levels were closely correlated with the severity of hemodynamics in AMI and with the clinical status of patients with severe AMI. Results suggest that IL-1ra and IL-10 can serve as prognostic indicators in cases of severe AMI.