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川崎病・冠動脈・血管⑧

[III-P-118] 川崎病心嚢液貯例の心血管後遺症に関する検討

^○岡田 清吾¹, 長谷川 俊史¹, 鈴木 康夫¹, 松原 知代², 下村 麻衣子¹, 奥田 昌之³, 市山 高志^1,4, 大賀 正一¹ (1.山口大学大学院医学系研究科　小児科学分野,　2.獨協医科大学越谷病院　小児科,　3.山口大学大学院理工学研究科　安全環境学分野,　4.鼓ヶ浦こども医療福祉センター　小児科)

Keywords:Kawasaki disease, pericardial effusion, coronary artery lesions

Objective: To search the appropriate inflammation control of Kawasaki disease (KD), the pathophysiological basis of acute pericardial effusion (PE) in KD patients were investigated. Methods: Clinical and laboratory features of Japanese KD children with PE (PE group: n = 9) and without PE (non-PE group: n = 89) were retrospectively studied based on the medical records. Serum levels of soluble tumor necrosis factor receptor 1 (sTNFR1), interleukin (IL)-6 and vascular endothelial growth factor (VEGF) were measured by the enzyme-linked immunosorbent assays. Results: PE group patients had coronary artery lesions (CAL) more frequently than non-PE group patients during the acute phase of KD (33% vs 5.6%, p = 0.024). The PE patients showed lower levels of hemoglobin (p＜0.01) and serum albumin (p＜0.01), and higher platelet counts (p = 0.013) than non-PE patients. The proportion of neurological symptoms, but not other manifestations, in the PE group was higher than that in the non-PE group (p = 0.022). All patients survived with no coronary artery aneurisms. Serum levels of sTNFR1, but not the other cytokines, in the PE group were higher than those in the non-PE group (p＜0.001). The sTNFR1 levels correlated positively with CRP (r = 0.30, p = 0.019) or total bilirubin (r = 0.40, p＜0.01) levels. Conclusions: Acute PE in KD patients indicated the severity of TNF-mediated vascular inflammation and concurrent CAL. According to the progression, they might need more targeted therapy of anti-inflammation for the better coronary outcome.