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Histopathological study on developmental mechanism of the coronary, artery destruction in acute stage Kawasaki Disease patients

Histopathological study on developmental mechanism of the coronary, artery destruction in acute stage Kawasaki Disease patients
川崎病急性期冠状动脉破坏发育机制的组织病理学研究
批准号:
14570168
负责人:
TAKAHASHI Kei
金额:
$1.54万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2002
资助国家:
日本
项目状态:
已结题
起止时间:
2002 至 2003

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中文摘要
翻译
急性川崎患者冠状动脉病变中有中性粒细胞浸润,但临床资料显示外周血中有中性粒细胞活化,但尚无形态学证据。因此,我们对中性粒细胞在川崎病急性期冠状动脉损害中的作用进行了组织学研究。材料包括8例尸检的KD急性期死亡的患者。将组织固定并包埋在石蜡中。常规组织学检查采用苏木精-伊红染色、弹性货车Gieson染色和azan-Mallory染色。此外,CD 3、CD 20、CD 68、中性粒细胞弹性蛋白酶和免疫球蛋白的抗体用于免疫组织化学以鉴定动脉病变中的浸润细胞。所有患者冠状动脉病变中出现的炎性细胞均以巨噬细胞为主。此外,在KD发病后10天死亡的患者的冠状动脉病变中也发现了大量中性粒细胞。中性粒细胞浸润的高峰早于CD 68+巨噬细胞、CD 3+淋巴细胞和CD 20+淋巴细胞的高峰。提示中性粒细胞参与了川崎病早期冠状动脉的损害。中性粒细胞和巨噬细胞对血管壁的损伤可能导致血管扩张。我们比较了IVGG给药患者和未使用IVGG患者的冠状动脉病变组织学。结果表明,CD 20 ~+淋巴细胞浸润程度在后一种患者中有增高的趋势。而浆细胞、CD 68+细胞和中性粒细胞在两组间无差异。
英文摘要
There has been no morphological evidence that neutrophils infiltrate the coronary arterialn lesions of acute Kawasaki Disease(KD) patients, although clinical data indicate the activation of neutrophils in the peripheral blood. Therefore, we carried out histological examination about the role of neutrophils in the damage to coronary arteries in acute stage of KD. The materials consisted of eight autopsy patients who died during the acute phase of KD. The tissues were fixed and embedded in paraffin. Hematoxylin and eosin, elastica van Gieson and azan-Mallory stainings were performed for routine histological examination. In addition, antibodies to CD3, CD20, CD68, neutrophil elastase and immunoglobulins were used for immunohistochemistry to identify infiltrating cells in the arterial lesions. The inflammatory cells which appeared in the coronary arterial lesions were mainly composed of macrophages in all patients. In addition, numerous neutrophils were also identified in the coronary arterial lesions of the patients who died 10 days after the onset of KD. Neutrophilic infiltration reached a peak earlier than the peaks of CD68+ macrophages, CD3+ lymphocytes and CD20+ lymphocytes. These results suggest that neutrophils are involved in the damage occurring to coronary arteries in the early stage of KD. Vascular dilatation might occur as a result of damage to vascular walls caused by neutrophils, as well as macrophages. We compared histology of coronary arterial lesions between a patient with IVGG administration and a patient without IVGG. It showed the tendency that the degree of CD20+ lymphocytic infiltration was higher in the latter patient. However, there was not difference in plasma cells, CD68+ cells and neutrophils between two patients.
期刊论文(42)
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会议论文
高橋 啓, 大原関利章, 他: "川崎病既往は粥状動脈硬化症の危険因子となりえるか(病理の立場より)"小児内科. 35. 1435-1346 (2003)
Kei Takahashi、Toshiaki Oharaseki 等人:“川崎病病史是否是动脉粥样硬化的危险因素(从病理学角度来看)” 35. 1435-1346 (2003)
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K.Takahashi, et al.: "Histopathological features of murine systemic vasculitis caused by Candida albicans extract-an animal model of Kawasaki Disease"Inflammation Research. 53. 72-77 (2004)
K.Takahashi等:“白色念珠菌提取物引起的小鼠系统性血管炎的组织病理学特征——川崎病动物模型”炎症研究。
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通讯作者:
Takahashi Kei, et al.: "Histopathological features of murine systemic vasculitis caused by Candida albicans extract -an animal model of Kawasaki Disease."Inflammation Research. 53. 72-77 (2004)
Takahashi Kei 等人:“白色念珠菌提取物引起的小鼠系统性血管炎的组织病理学特征 - 川崎病的动物模型。”炎症研究。
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高橋 啓: "瘤を確認できなかつた冠状動脈の狭窄性病変への進展の可能性について"Prog.Med.. 22. 1676-1678 (2002)
Kei Takahashi:“无法确认动脉瘤的冠状动脉狭窄病变的可能性”Prog.Med.. 22. 1676-1678 (2002)
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