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
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
中文摘要
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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.
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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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高橋 啓: "小児血管炎の病理"病理と臨床. 21. 926-927 (2003)
Kei Takahashi:“小儿血管炎的病理学”病理学和临床实践 21. 926-927 (2003)。
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