Interleukin-18 and coronary artery lesions in patients with Kawasaki disease

Weng, Ken‐Pen; Hsieh, Kai‐Sheng; Huang, Shih-Hui; Ou, Shan-F.; Lai, Tsung-Jen; Tang, Chia-Wan; Lin, Chu-Chuan; Ho, Tsyr-Yuh; Liou, Horng-Huei; Ger, Luo‐Ping

doi:10.1016/j.jcma.2013.04.005

Cited by 21 publications

(15 citation statements)

References 41 publications

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“…This provides some support to one hypothesis about the pathogenesis of Kawasaki disease, which states that Kawasaki disease is an immune reaction caused by some kinds of infectious agents. 1,15,24 Our results using IVIG as the indicator are similar to those found in reports from Hong Kong and Beijing and somewhat different from those found in reports from Japan and Korea. 2,8e10 We believe that our results are more reasonable from both a geographic and a genetic perspective, as we mentioned above.…”

Section: Discussionsupporting

confidence: 51%

Epidemiologic features of Kawasaki disease in acute stages in Taiwan, 1997–2010: Effect of different case definitions in claims data analysis

Lin

Lai

Jan

et al. 2015

Journal of the Chinese Medical Association

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Section: Discussionsupporting

confidence: 51%

Epidemiologic features of Kawasaki disease in acute stages in Taiwan, 1997–2010: Effect of different case definitions in claims data analysis

Lin

Lai

Jan

et al. 2015

Journal of the Chinese Medical Association

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“…In humans, the ITPKC CC genotype, which is implicated as a determinant of KD susceptibility and outcome (4,17), is associated with highest basal and stimulated [Ca 2+ ] i levels, increased mitochondrial superoxide production, highest levels of NLRP3 protein, greatest production of IL-1b and IL-18 from their PBMCs and EBV-transformed cell lines, and highest circulating levels of IL-1b and IL-18 during acute KD. Associations of IL-18 levels and genetic polymorphisms with risks and outcomes in KD have been reported in KD patients (29,30). The ITPKC CC genotype is associated with failure of IVIG therapy.…”

Section: Discussionmentioning

confidence: 99%

Inositol-Triphosphate 3-Kinase C Mediates Inflammasome Activation and Treatment Response in Kawasaki Disease

Alphonse

Duong

Shumitzu

et al. 2016

The Journal of Immunology

113

114

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Kawasaki disease (KD) is a multisystem vasculitis that predominantly targets the coronary arteries in children. Phenotypic similarities between KD and recurrent fever syndromes point to the potential role of inflammasome activation in KD. Mutations in NLRP3 are associated with recurrent fever/autoinflammatory syndromes. We show that the KD-associated genetic polymorphism in Inositoltriphosphate 3-kinase C (ITPKC) (rs28493229) has important functional consequences, governing ITPKC protein levels and thereby intracellular calcium, which in turn regulates NLRP3 expression and production of IL-1β and IL-18. Analysis of transcript abundance, protein levels, and cellular response profiles from matched, serial biospecimens from a cohort of genotyped KD subjects points to the critical role of ITPKC in mediating NLRP3 inflammasome activation. Treatment failure in those with the 'high-risk' ITPKC-genotype was associated with the highest basal and stimulated intracellular calcium levels and with increased cellular production of IL-1β and IL-18 and higher circulating levels of both cytokines. Mechanistic studies using Itpkc-deficient mice in a disease model support the genomic, cellular and clinical findings in affected children. Our findings provide the mechanism behind the observed efficacy of rescue therapy with IL-1 blockade in recalcitrant KD, and identify that regulation of calcium mobilization is fundamental to the underlying immunobiology in KD.

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“…In addition, serum NT pro-B-type natriuretic peptide above 1,000 pg/ml [ 6 ] or serum sodium less than 135 mEq/l [ 13 ] has been used to diagnose CALs secondary to KD. More recently, serum interleukin-18 was also used to identify CALs in children with KD[ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Prediction of the risk of coronary arterial lesions in Kawasaki disease by serum 25-hydroxyvitamin D3

Chen

Wang

2014

Eur J Pediatr

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Kawasaki disease (KD) is associated with the development of coronary arterial lesions (CALs) in children. We aimed to test the hypothesis that circulating 25-hydroxyvitamin D3 [25-(OH)D3] could be identified as a clinical parameter for predicting CALs secondary to KD in children. We enrolled 35 children with KD in the acute phase and measured serum 25-(OH)D3 levels in all of them, then followed up by echocardiography for CALs. Additionally, serum 25-(OH)D3 levels were obtained in 23 febrile children with respiratory tract infections and 30 healthy children. Of the 35 KD children, nine had CALs according to echocardiography and 26 did not (NCALs). Serum 25-(OH)D3 levels were not significantly different between NCALs and healthy children (49.2 ± 23.8 versus 44.1 ± 30.2 ng/ml; P = 0.49). Serum 25-(OH)D3 levels were significantly higher in children with CALs than those without CALs (83.9 ± 26.3 versus 49.2 ± 23.8 ng/ml; P = 0.001). The cutoff value of 65 ng/ml to predict subsequent CALs had a specificity of 0.73, sensitivity of 0.78, and diagnostic accuracy of 0.74. Conclusion: Serum 25-(OH)D3 levels were elevated dur-ing the acute phase in KD children who had subsequent CALs. Serum 25-(OH)D3 levels in the acute phase of KD may be used to predict subsequent CALs.

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Interleukin-18 and coronary artery lesions in patients with Kawasaki disease

Abstract: Our data show that IL-18 levels were elevated in the acute phase of KD and might be related to the formation of CALs.

Cited by 21 publications

References 41 publications

Epidemiologic features of Kawasaki disease in acute stages in Taiwan, 1997–2010: Effect of different case definitions in claims data analysis

Epidemiologic features of Kawasaki disease in acute stages in Taiwan, 1997–2010: Effect of different case definitions in claims data analysis

Inositol-Triphosphate 3-Kinase C Mediates Inflammasome Activation and Treatment Response in Kawasaki Disease

Prediction of the risk of coronary arterial lesions in Kawasaki disease by serum 25-hydroxyvitamin D3

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