Ischemia-modified albumin in children with clinically suspected acute myocarditis: diagnostic performance and incremental value beyond conventional biomarkers.

内容摘要

Pediatric acute myocarditis is challenging because presentations range from chest pain to cardiogenic shock, and no single biomarker reflects its inflammatory, ischemic, and hemodynamic components. Ischemia-modified albumin (IMA), a marker of oxidative stress-related alteration in albumin measured by the albumin cobalt-binding assay, has been investigated in ischemic and inflammatory conditions, but its role in pediatric myocarditis remains unclear. In this prospective, single-center case-control study, 47 children with clinically suspected acute myocarditis and 47 age- and sex-matched healthy controls were evaluated between 1 July 2023 and 1 July 2025. Clinically suspected acute myocarditis was defined according to pediatric guidance as at least one compatible clinical feature together with at least one supportive biomarker, electrocardiographic, or echocardiographic finding after exclusion of alternative diagnoses. IMA levels were measured using the albumin cobalt-binding method and expressed as absorbance units (ABSU). The statistical analysis included between-group comparisons, receiver operating characteristic (ROC) analyses, incremental discrimination analyses, and exploratory clinical severity analyses. IMA concentrations were significantly higher in the myocarditis group than in controls [0.57 (0.55-0.63) vs. 0.55 (0.49-0.59) ABSU, p = 0.021], with a Hodges-Lehmann median difference of 0.04 ABSU (95% CI, 0.01-0.07). However, the diagnostic performance of IMA alone was modest (AUC, 0.64; 95% CI, 0.52-0.75). At the optimal cutoff of 0.53 ABSU, sensitivity was 89.36% and specificity was 38.30%. Conventional biomarkers showed stronger discrimination, including troponin I (AUC, 0.96), troponin T (AUC, 0.93), NT-proBNP (AUC, 0.88), CRP (AUC, 0.85), and CK-MB (AUC, 0.83). A base model including CK-MB, NT-proBNP, and CRP yielded an AUC of 0.92; adding IMA increased the AUC marginally to 0.93 (delta AUC, 0.01; p = 0.153). All children in the clinically suspected myocarditis group were symptomatic at presentation, and exploratory analyses showed no significant association between IMA and selected electrocardiographic or echocardiographic abnormalities or length of hospital stay. IMA is elevated in children with clinically suspected acute myocarditis, but its standalone diagnostic performance is limited and its added value beyond conventional biomarkers appears small. IMA may be considered an adjunctive rather than a primary diagnostic biomarker, and any putative triage role in ultra-early presentations remains hypothesis-generating.