Burns : journal of the International Society for Burn Injuries · 2026
Characteristics of burn-associated liver injury and its association with admission vitamin D levels.
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Gao Xingxin, Tang Qiuyan, Huang Jing, Li Dehui, Liang Sen, Huang Xiaoce, Zhang Liming, Zhang Min
Аннотация
BACKGROUND: Severe burns can induce burn-associated liver injury (BALI). The relationship between vitamin D and BALI remains unclear. This study aimed to characterise BALI in the context of burn severity and to explore its association with vitamin D.
METHODS: A retrospective analysis was conducted on 163 adult patients with thermal burns. Statistical analyses included correlation tests, multiple linear regression, and multivariable logistic regression.
RESULTS: BALI (30.2%) occurred only in severe burn patients. Multivariable analysis identified the Burn Index (BI) as a significant independent predictor of BALI (odds ratio [OR] = 1.069, 95% CI: 1.042-1.096, P < 0.001) and of elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBil) (all P < 0.05). Compared to patients with non-severe burns, severe burn patients without BALI had higher ALT and AST levels (all P < 0.01). Among severe burn patients, those who developed BALI had significantly further elevated levels of TBil, ALT, and AST compared to those without BALI (all P < 0.05). Admission vitamin D levels were inversely correlated with ALT and AST (all P < 0.05). However, after adjusting for the BI, vitamin D deficiency was not an independent risk factor for BALI.
CONCLUSIONS: BALI exhibits a dose-response trend with burn severity, with the BI as a reliable predictor. Post-burn hepatic injury manifests across a spectrum from subclinical to overt. In an exploratory analysis with limited sample size, admission vitamin D deficiency was not independently associated with BALI. Future studies are needed to validate this dose-response trend and to further clarify the potential role of vitamin D in BALI.
METHODS: A retrospective analysis was conducted on 163 adult patients with thermal burns. Statistical analyses included correlation tests, multiple linear regression, and multivariable logistic regression.
RESULTS: BALI (30.2%) occurred only in severe burn patients. Multivariable analysis identified the Burn Index (BI) as a significant independent predictor of BALI (odds ratio [OR] = 1.069, 95% CI: 1.042-1.096, P < 0.001) and of elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBil) (all P < 0.05). Compared to patients with non-severe burns, severe burn patients without BALI had higher ALT and AST levels (all P < 0.01). Among severe burn patients, those who developed BALI had significantly further elevated levels of TBil, ALT, and AST compared to those without BALI (all P < 0.05). Admission vitamin D levels were inversely correlated with ALT and AST (all P < 0.05). However, after adjusting for the BI, vitamin D deficiency was not an independent risk factor for BALI.
CONCLUSIONS: BALI exhibits a dose-response trend with burn severity, with the BI as a reliable predictor. Post-burn hepatic injury manifests across a spectrum from subclinical to overt. In an exploratory analysis with limited sample size, admission vitamin D deficiency was not independently associated with BALI. Future studies are needed to validate this dose-response trend and to further clarify the potential role of vitamin D in BALI.