ArticlePloS one2016
Unique Molecular Patterns Uncovered in Kawasaki Disease Patients with Elevated Serum Gamma Glutamyl Transferase Levels: Implications for Intravenous Immunoglobulin Responsiveness.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Validation of a 2-Gene Blood Test for Kawasaki Disease in Febrile Children.JAMA network open · 2026Article
- Decoding clinical heterogeneity and age-related coronary risk in incomplete Kawasaki disease: a multicenter cluster analysis and structural equation modeling study.Frontiers in immunology · 2026Article
- Nutrition-Associated Biomarkers in Predicting Intravenous Immunoglobulin Resistance and Coronary Artery Lesions in Kawasaki Disease: A Systematic Review and Meta-Analysis.Food science & nutrition · 2025Review
- Subgroups of children with Kawasaki disease: a data-driven cluster analysis.The Lancet. Child & adolescent health · 2023Article
- Development of a nomogram prediction model for early identification of persistent coronary artery aneurysms in kawasaki disease.BMC pediatrics · 2023Article
- Comparison of IVIG resistance predictive models in Kawasaki disease.Pediatric research · 2022Article
- Gamma-Glutamyltransferase Activity (GGT) Is a Long-Sought Biomarker of Redox Status in Blood Circulation: A Retrospective Clinical Study of 44 Types of Human Diseases.Oxidative medicine and cellular longevity · 2022Article
- The factors affecting the disease course in Kawasaki disease.Rheumatology international · 2019Article
- Whole blood transcriptional profiles as a prognostic tool in complete and incomplete Kawasaki Disease.PloS one · 2018Article
- The Efficacy and Safety of High-Dose Intravenous Immunoglobulin in the Treatment of Kawasaki Disease: How Can We Predict Resistance to Intravenous Immunoglobulin Treatment of Kawasaki Disease?Korean circulation journal · 2017Article
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Authors and funding
23 authors at 8 institutions in 3 countries.
Funding
Abstract
backgroundResistance to intravenous immunoglobulin (IVIG) occurs in 10-20% of patients with Kawasaki disease (KD). The risk of resistance is about two-fold higher in patients with elevated gamma glutamyl transferase (GGT) levels. We sought to understand the biological mechanisms underlying IVIG resistance in patients with elevated GGT levels.
methodWe explored the association between elevated GGT levels and IVIG-resistance with a cohort of 686 KD patients (Cohort I). Gene expression data from 130 children with acute KD (Cohort II) were analyzed using the R square statistic and false discovery analysis to identify genes that were differentially represented in patients with elevated GGT levels with regard to IVIG responsiveness. Two additional KD cohorts (Cohort III and IV) were used to test the hypothesis that sialylation and GGT may be involved in IVIG resistance through neutrophil apoptosis.
resultsThirty-six genes were identified that significantly explained the variations of both GGT levels and IVIG responsiveness in KD patients. After Bonferroni correction, significant associations with IVIG resistance persisted for 12 out of 36 genes among patients with elevated GGT levels and none among patients with normal GGT levels. With the discovery of ST6GALNAC3, a sialyltransferase, as the most differentially expressed gene, we hypothesized that sialylation and GGT are involved in IVIG resistance through neutrophil apoptosis. We then confirmed that in Cohort III and IV there was significantly less reduction in neutrophil count in IVIG non-responders.
conclusionsGene expression analyses combining molecular and clinical datasets support the hypotheses that: (1) neutrophil apoptosis induced by IVIG may be a mechanism of action of IVIG in KD; (2) changes in sialylation and GGT level in KD patients may contribute synergistically to IVIG resistance through blocking IVIG-induced neutrophil apoptosis. These findings have implications for understanding the mechanism of action in IVIG resistance, and possibly for development of novel therapeutics.
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