Qing-Mei Zou1, Xiao-Hui Li1, Rui-Xia Song1, Nan-Ping Xu2, Ting Zhang3, Ming-Ming Zhang1, Yao Lin1, Lin Shi1, Jin Fu4, Xiao-Dai Cui4. 1. Department of Cardiovascular Diseases, Children's Hospital Affiliated to Capital Institute of Pediatrics, Beijing, China. 2. Department of Emergency, Children's Hospital of Jiangxi Province, Nanchang, Jiangxi, China. 3. Central Laboratory of Infection and Immunity, Capital Institute of Pediatrics, Beijing, China. 4. Clinical Center Laboratory, Capital Institute of Pediatrics, Beijing, China.
Abstract
BACKGROUND: The mechanisms underpinning Kawasaki disease (KD) are incompletely understood. There is an unmet need for specific biomarkers for the early diagnosis of KD. METHODS: Eighty-five KD patients suffering from acute-phase and subacute-phase KD, 40 healthy children, and 40 febrile children comprised the study cohort. An enzyme-linked immunosorbent assay was used to measure plasma levels of C1q, C1q-circulating immune complex (C1q-CIC), mannan-binding lectin-associated serine protease (MASP)-1, factor B, C4d, C3d, C5a, C5b-9 and CD59. RESULTS: Plasma concentrations of factor B and C5a in the acute phase were lower than those in healthy and febrile control groups (all P < 0.05). Compared with acute-phase KD patients, plasma concentrations of C1q, factor B, and C3d in KD patients were increased significantly (P < 0.05), but those of C4d, MASP-1 and CD59 decreased significantly (P < 0.05), in patients with sub-acute KD. CONCLUSION: These data suggest that more than one pathway in the complement system is activated in KD. Importantly, decreased plasma concentrations of factor B and C5a in the acute phase (6-10 d) could be employed as biomarkers for the early diagnosis of KD.
BACKGROUND: The mechanisms underpinning Kawasaki disease (KD) are incompletely understood. There is an unmet need for specific biomarkers for the early diagnosis of KD. METHODS: Eighty-five KDpatients suffering from acute-phase and subacute-phase KD, 40 healthy children, and 40 febrile children comprised the study cohort. An enzyme-linked immunosorbent assay was used to measure plasma levels of C1q, C1q-circulating immune complex (C1q-CIC), mannan-binding lectin-associated serine protease (MASP)-1, factor B, C4d, C3d, C5a, C5b-9 and CD59. RESULTS: Plasma concentrations of factor B and C5a in the acute phase were lower than those in healthy and febrile control groups (all P < 0.05). Compared with acute-phase KDpatients, plasma concentrations of C1q, factor B, and C3d in KDpatients were increased significantly (P < 0.05), but those of C4d, MASP-1 and CD59 decreased significantly (P < 0.05), in patients with sub-acute KD. CONCLUSION: These data suggest that more than one pathway in the complement system is activated in KD. Importantly, decreased plasma concentrations of factor B and C5a in the acute phase (6-10 d) could be employed as biomarkers for the early diagnosis of KD.
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