Life · 7 authors, 2 centres
This summary was generated by AI from a single paper. It has not been reviewed by a clinician and is not clinical advice. Verify against the source before acting on it.
This cross-sectional study of 21 children with MIS-C found that 95% had hypovitaminosis D, with 71% being vitamin D deficient. Lower vitamin D levels were significantly associated with more severe MIS-C and worse cardiac function, including lower left ventricular ejection fraction and diastolic dysfunction. The findings suggest vitamin D may serve as a biomarker for MIS-C severity and that vitamin D replacement therapy should be considered early in treatment.
**Background:** Multisystem inflammatory syndrome in children (MIS-C) is a rare post-infectious complication of COVID-19 characterized by hyperinflammation resembling Kawasaki disease. Vitamin D (VD) has known immunomodulatory effects via vitamin D receptors on immune cells, and hypovitaminosis D has been linked to increased risk of immune-related disorders. This study aimed to determine the incidence of hypovitaminosis D in MIS-C patients and evaluate correlations between 25(OH)D levels and clinical severity, laboratory markers, and echocardiographic findings.
**Methods:** This single-center cross-sectional study included patients hospitalized at the University Hospital of Split with MIS-C from 1 June 2020 to 31 May 2022. MIS-C diagnosis was confirmed per guidelines. Serum 25(OH)D was measured using an Elecsys Vitamin D total assay. Sufficiency was defined as >75 nmol/L, insufficiency as 50–75 nmol/L, and deficiency as <50 nmol/L. Patients underwent full cardiac evaluation including ECG and transthoracic echocardiogram. MIS-C severity was classified as mild, moderate, or severe based on clinical and hemodynamic status. Statistical analysis used linear/nonlinear regression and t-tests.
**Key Results:** Of 25 eligible patients, 21 were included (4 excluded for missing 25(OH)D data). Median age was 8.08 years (range 1.25–16.58); 67% were male. COVID-19 rapid antigen tests were negative in all patients; 76% had documented/suspected prior COVID-19 (mean 41 days before MIS-C onset); 86% had positive SARS-CoV-2 serology. Five patients (24%) had mild, 8 (38%) moderate, and 8 (38%) severe MIS-C. Systolic dysfunction and symptomatic myocarditis occurred in 33%. No coronary artery dilatation or aneurysms were observed. VD insufficiency was found in 5 patients (24%), deficiency in 15 (71%), and only 1 patient (5%) had sufficient 25(OH)D. Median 25(OH)D was 35.3 nmol/L (range 22.5–80). MIS-C severity was inversely and linearly related to 25(OH)D levels (β = −10.26 nM/severity category, 95% CI −18.38 to −2.13, p = 0.0162, R² = 27.62%). Children with LV diastolic dysfunction had significantly lower 25(OH)D levels (Δ = 15.85 nM, 95% CI 3.3 to 28.37, p = 0.0158, R² = 26.99%). LVEF was associated with 25(OH)D levels by a power law (p = 0.0018, R² = 40.9%). No conclusive relationships were found between 25(OH)D and individual inflammatory markers (CRP, PCT, IL-6, ferritin, D-dimer, troponin T, NT-pro-BNP, etc.).
**Clinical Implications:** Hypovitaminosis D is highly prevalent (95%) in children with MIS-C and is significantly associated with disease severity and cardiac dysfunction. Lower 25(OH)D levels correlated with worse LV systolic and diastolic function. While the study cannot establish causality—hypovitaminosis D may be either a predisposing factor or a consequence of the inflammatory process—the authors recommend VD replacement therapy early in MIS-C treatment. The findings align with prior research linking VD deficiency to worse COVID-19 outcomes and Kawasaki disease severity. Larger randomized controlled trials are needed to confirm these associations and evaluate the therapeutic benefit of VD supplementation in MIS-C.