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Metabolomic Profiling for Predicting Coronary Artery Aneurysms and IVIG Resistance in Kawasaki Disease- An
Zahra Amirsardari1,2,3, Ehsan Aghaei Moghadam4,3, Ali Mohebbi5,3
1School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Insights
This study reveals key metabolic differences in Kawasaki disease (KD) patients, identifying specific metabolites linked to coronary artery aneurysms (CAA) and resistance to intravenous immunoglobulin (IVIG) therapy.
Area of Science:
- Biochemistry
- Pediatric Medicine
- Metabolomics
Background:
- Kawasaki disease (KD) is a critical pediatric illness.
- Coronary artery aneurysms (CAA) are a major complication of KD.
- Resistance to intravenous immunoglobulin (IVIG) therapy impacts KD patient outcomes.
Purpose of the Study:
- To investigate the metabolomic profile of KD patients.
- To identify metabolic biomarkers associated with CAA development.
- To explore metabolic differences in IVIG-resistant versus IVIG-responsive KD patients.
Main Methods:
- Metabolomic profiling of 26 KD patients using liquid chromatography-tandem mass spectrometry (LC-MS/MS).
- Analysis of 44 metabolites, including amino acids and acylcarnitines.
- Pathway analysis utilizing the KEGG database.
Main Results:
- Methylglutarylcarnitine identified as a differentially expressed metabolite in KD patients with CAA.
- Specific acylcarnitines (C2, C3, C14, C16, C16OH, C18:2, C18:2OH) differed between IVIG-resistant and responsive groups.
- Arginine biosynthesis and alanine, aspartate, and glutamate metabolism were significantly affected in KD patients with CAA.
Conclusions:
- This study identified distinct metabolomic profiles in KD patients with CAA and IVIG resistance.
- Findings offer novel insights into the metabolic pathways contributing to KD complications.
- Metabolomic analysis may aid in predicting KD prognosis and treatment response.
Abstract:
We investigated the metabolomic profile of Kawasaki disease(KD) and its association with the development of coronary artery aneurysms (CAA) and resistance to intravenous immunoglobulin(IVIG) therapy. Metabolomic profiling was performed on 26 patients with KD. A total of 44 metabolites-including 12 amino acids, L-carnitine, and 31 acylcarnitines-were analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS) after IVIG administration. Methylglutarylcarnitine, a medium-chain acylcarnitine, was identified as a differentially expressed metabolite in KD patients with CAA. Additionally, C2, C3, C14, C16, C16OH, C18:2, and C18:2OH were differentially expressed between IVIG-resistant and IVIG-responsive patients. Pathway analysis using the KEGG database revealed that arginine biosynthesis and alanine, aspartate, and glutamate metabolism were among the most affected pathways in KD patients with CAA. This study demonstrated several differentially expressed metabolites in KD patients with CAA and IVIG resistance. These findings provide new insights into the metabolic pathways underlying KD complications.
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