TNF-α blockers for the treatment of Kawasaki disease in children

Yamaji, Noyuri; Lopes, Katharina da Silva; Shoda, Tetsuo; Ishitsuka, Kazue; Kobayashi, Toshimitsu; Ota, Erika; Mori, Rintaro

doi:10.1002/14651858.cd012448.pub2

Cited by 39 publications

(44 citation statements)

References 60 publications

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“…Recent advances have increased the accuracy of diagnoses and resulted in the development of therapeutic strategies for better acute as well as long-term outcomes. [6][7][8][9][10] We and others reported that Candida albicans-derived substances (CADS) and the C. albicans water-soluble fraction (CAWS) induced coronary vasculitis similar to KD in mice. Previous studies demonstrated the contribution of various factors to the induction of CAWS-vasculitis, including the induction of Th17 cells, activation of the IL-1β pathway, changes in the microbiome, CCL2 production, CCR2-, CXCL9-, and CXCL10-dependent signaling, LPA-LPA1 signaling, the MBL-dependent complement pathway, and the cytoplasmic domain, but associates with the Fc-receptor gamma (FcRγ) chain.…”

Section: Introductionmentioning

confidence: 99%

Coronary Vasculitis Induced in Mice by the Cell Wall Mannoprotein of <i>Candida krusei</i>

Yanai

Tanaka

Miura

et al. 2020

Biological & Pharmaceutical Bulletin

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Kawasaki disease (KD) is an inflammatory disease that was identified by Professor Tomisaku Kawasaki in 1961. Candida albicans-derived substances, such as the hot water extract of C. albicans (CADS) and Candida water-soluble fraction (CAWS), induced coronary vasculitis similar to KD in mice. An increasing proportion of deep-seated candidiasis cases are caused by non-albicans Candida and are often resistant to antifungal drugs. We herein investigated whether the hot water extract of C. krusei, inherently resistant to fluconazole, induces vasculitis in mice. Three strains of C. krusei, NBRC1395, NBRC1162, and NBRC10737, were cultured in natural (Y) and chemically defined (C) media and cell wall mannoprotein (MN) fractions were prepared by autoclaving cells (CKY1395MN, CKC1395MN, CKY1162MN, CKC1162MN, CKY10737MN, and CKC10737MN). All MN fractions reacted strongly with Con A and dectin-2 and induced anaphylactoid shock in ICR mice. MNs induced severe coronary vasculitis in DBA/2 mice, resulting in cardiac hypertrophy. MNs also induced coronary vasculitis in C57Bl/6 mice. These results suggest that the MNs of non-albicans Candida, such as C. krusei, induce similar toxicity to those of C. albicans.

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Section: Introductionmentioning

confidence: 99%

Coronary Vasculitis Induced in Mice by the Cell Wall Mannoprotein of <i>Candida krusei</i>

Yanai

Tanaka

Miura

et al. 2020

Biological & Pharmaceutical Bulletin

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“…Concentrations of these 2, as well as some other pro-inflammatory cytokines, do diminish after IVIG treatment, even in the refractory patients [4]. The role of the pro-inflammatory cytokines TNFα and IL-1β, as well as the Nod-like receptor protein3 inflammasome in association with this disease has been shown by many other studies [5][6][7].…”

Section: Contents Lists Available At Sciencedirectmentioning

confidence: 74%

Insights into pediatric multi-system inflammatory syndrome and COVID-19

Bar‐Or

Rael

Brody

2020

Clinica Chimica Acta

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“…However, further large-scaled high-quality trials including the timing and type of TNF-α blockers are needed to determine the effects of TNF-α blockers for KD. In the study of Yamaji et al (42), TNF-α blockers reduced the incidence of treatment resistance and infusion reaction, but no clear difference was observed between groups in the incidence of CAAs, rash or contact dermatitis. The conclusions about CAA is consistent with the present analysis.…”

Section: P-value ---------------------------------mentioning

confidence: 92%

“…Specific blocking of TNF-α has been demonstrated to prevent coronary inflammation and the formation of CAA in mouse KD models induced by Lactobacillus casei cell wall extracts. In a previous study of a KD model in mice, it was indicated that a TNF-α anticoagulant can reduce the adhesion of neutrophils to vascular endothelial cells and the inflammation of arterial vascular endothelial cells (24,(39)(40)(41)(42). In the present meta-analysis, no significant differences in CAL, CAA, non-response rate, length of hospital stay, conjunctival injection or polymorphous exanthema between the two groups were observed; however, IFX or IFX plus IVIG significantly reduced the incidence of adverse events, the Table III.…”

Section: P-value N (Case/ ---------------------------------mentioning

confidence: 99%

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Efficacy of infliximab in the treatment of Kawasaki disease: A systematic review and meta‑analysis

Lu¹,

Wang

2020

Exp Ther Med

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The present study aimed to review the relevant studies in order to determine the efficacy of infliximab (IFX) in the treatment of Kawasaki disease (KD). The relevant studies were retrieved using the PubMed, Cochrane and Embase databases. Key sources in the literature were reviewed; all articles published by July 2019 were considered for inclusion. For each study, odds ratios, mean difference and 95% confidence interval (95% CI) were assessed to evaluate study outcomes. A total of 16 studies involving 429 patients were relevant to the questions of interest of the current meta-analysis. Compared with intravenous immunoglobulin (IVIG), IFX or IFX plus IVIG significantly reduced the incidence of adverse events, including the number of patients with fever, changes in lip and oral cavity and/or cervical lymphadenopathy. The white blood cell (WBC), neutrophil and C-reactive protein (CRP) levels were also reduced in the IFX or IFX plus IVIG group compared with those in the IVIG or polyethylene glycol-treated human immunoglobulin (VGIH) groups. The platelet counts, alanine aminotransferase (ALT) levels and Z-scores were increased in the IFX or IFX plus IVIG groups compared with those in the IVIG or VGIH groups. In the single-arm studies, the incidence of coronary artery aneurysm was 0.150 (95% CI: 0.024, 0.277), the non-response rate was 0.097 (95% CI: 0.056, 0.138), and the incidence of adverse events was 0.156 (95% CI: 0.122, 0.190). IFX not only effectively reduced the incidence of fever, conjunctival injection, changes in lip and oral cavity and cervical lymphadenopathy polymorphous exanthema, but also the WBC, neutrophil, ALT and CRP levels. The platelet levels were increased in patients after the IFX therapy compared with patients in the IVIG or VGIH groups. IFX or IFX plus IVIG exhibited improved clinical efficacy in the treatment of KD compared with that of IVIG or VGIH. However, as a limited number of studies was included in the current study, the findings should be verified further.

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TNF-α blockers for the treatment of Kawasaki disease in children

Cited by 39 publications

References 60 publications

Coronary Vasculitis Induced in Mice by the Cell Wall Mannoprotein of <i>Candida krusei</i>

Coronary Vasculitis Induced in Mice by the Cell Wall Mannoprotein of <i>Candida krusei</i>

Insights into pediatric multi-system inflammatory syndrome and COVID-19

Efficacy of infliximab in the treatment of Kawasaki disease: A systematic review and meta‑analysis

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