ReviewFrontiers in pharmacology2026
Vitamin D and Kawasaki disease.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Vitamin D deficiency has been widely reported worldwide. Vitamin D is essential for mineral homeostasis and skeletal health, and is also associated with numerous extra-skeletal diseases, including cancer, autoimmune diseases, psychosis, allergies and cardiovascular disease. Recent evidence suggests that vitamin D deficiency might be a risk factor for immunoglobulin resistance in Kawasaki disease (KD), and that levels of 25-hydroxyvitamin D Mechanisms and evidence reviewed: Previous studies found that proinflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, are elevated during the acute phase of KD and are associated with activation of vascular endothelial cells, which can lead to varying degrees of vascular wall inflammation. Vitamin D, a multifunctional prohormone with well-documented anti-inflammatory properties, may exert protective effects in KD by enhancing endothelial function, reducing coronary artery damage risk, and inhibiting platelet activity to alleviate fibrinolysis, thrombosis, and inflammation. Conclusions: This study updates the current understanding of the association between serum vitamin D levels and KD, explores potential regulatory mechanisms underlying this relationship, and identifies critical knowledge gaps to guide future cohort studies and clinical trials in KD research. Early clinical data indicate that adjunctive vitamin D may modulate inflammatory responses in acute KD, but whether supplementation reduces intravenous immunoglobulin (IVIG) resistance or prevents coronary artery lesions remains unproven and requires prospective investigation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.