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水溶性维生素的个体化补充:炎症和肾功能对危重症消化系统疾病患者循环浓度的影响

Individualized supplement of water-soluble vitamins: the influence of inflammation and renal function on circulating concentrations in critically digestive disease patients.

作者信息

Wang Jingjing, Yan Jing, Chen Qi, Shi Linlin, Wang Ying, Tian Xiaoxiao, Qi Yumei, Li Guoxun, Cao Hailong

机构信息

Department of Nutrition, the Third Central Hospital of Tianjin, National Medical Quality Control Center of Clinical Nutrition, Tianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin, China.

Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, National Key Clinical Specialty, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, Tianjin, China.

出版信息

Front Immunol. 2025 Jul 25;16:1583568. doi: 10.3389/fimmu.2025.1583568. eCollection 2025.

DOI:10.3389/fimmu.2025.1583568
PMID:40787467
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12331502/
Abstract

BACKGROUND

Existing studies have shown the association of circulating vitamin and disease outcome. The study aimed to elucidate individual response of plasma water-soluble vitamins after supplement by PN in critically digestive disorder patients.

METHODS

We measured the plasma levels of nine water-soluble vitamins (i.e., C, B1, B2, B3, B5, B6, B7, B9, and B12) in consecutive 478 hospitalized critically digestive disease patients receiving identical vitamin-supplemented by PN. Univariate and multifactorial logistic regression analysis were used to evaluated vitamins deficiency and accumulation. The receiver operating characteristic (ROC) curves were used to predict vitamin abnormalities. Furthermore, restricted cubic spline (RCS) was used to analyze the National Health and Nutrition Examination Survey (NHANES) database (2003-2020). Additionally, plasma vitamins levels were contrastive analyzed after PN.

RESULTS

There were high prevalence of vitamin C and B9 deficiency (79.71% and 78.45%) but vitamin B2, B5, and B6 accumulation (34.52%, 12.13%, and 11.09%). Multivariate logistic regression analysis revealed that inflammation is an independent risk factor for vitamin C and B9 deficiency, whereas renal dysfunction is an independent risk factor for vitamin B2, B5, and B6 accumulation. The areas under the ROC curves predicting vitamin C, B9 deficiency and vitamin B2, B5, B6 accumulation were 0.80, 0.75, 0.69, 0.79, and 0.89, respectively. The NHANES database further confirms our conclusion. Conventional vitamin supplementation may not efficiently alleviate vitamin C and B9 deficiency in patients with high inflammation, however, it may accelerate plasma vitamin B2, B5, and B6 accumulation with renal dysfunction.

CONCLUSION

Water-soluble vitamin levels were associated with inflammation and renal function. For high inflammation, vitamin C and B9 doses may need to exceed standard levels. In renal impairment, avoid indiscriminate B2, B5, and B6 use; if needed, use alternate-day dosing or lower doses.

摘要

背景

现有研究表明循环维生素与疾病转归之间存在关联。本研究旨在阐明严重消化系统疾病患者经肠外营养(PN)补充后血浆水溶性维生素的个体反应。

方法

我们对连续478例接受相同PN维生素补充的住院严重消化系统疾病患者的血浆9种水溶性维生素(即维生素C、B1、B2、B3、B5、B6、B7、B9和B12)水平进行了测定。采用单因素和多因素逻辑回归分析评估维生素缺乏和蓄积情况。采用受试者工作特征(ROC)曲线预测维生素异常情况。此外,使用受限立方样条(RCS)分析美国国家健康与营养检查调查(NHANES)数据库(2003 - 2020年)。另外,对PN后血浆维生素水平进行对比分析。

结果

维生素C和B9缺乏的患病率较高(分别为79.71%和78.45%),但维生素B2、B5和B6有蓄积(分别为34.52%、12.13%和11.09%)。多因素逻辑回归分析显示,炎症是维生素C和B9缺乏的独立危险因素,而肾功能不全是维生素B2、B5和B6蓄积的独立危险因素。预测维生素C、B9缺乏以及维生素B2、B5、B6蓄积的ROC曲线下面积分别为0.80、0.75、0.69、0.79和0.89。NHANES数据库进一步证实了我们的结论。常规维生素补充可能无法有效缓解炎症程度高的患者的维生素C和B9缺乏,然而,对于肾功能不全的患者,可能会加速血浆维生素B2、B5和B6的蓄积。

结论

水溶性维生素水平与炎症和肾功能相关。对于炎症程度高的患者,维生素C和B9的剂量可能需要超过标准水平。在肾功能损害时,避免盲目使用维生素B2、B5和B6;如有需要,采用隔日给药或较低剂量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/180dc8aad0e5/fimmu-16-1583568-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/5d8b1b6c063a/fimmu-16-1583568-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/dc9db995959b/fimmu-16-1583568-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/405f9762bb2e/fimmu-16-1583568-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/180dc8aad0e5/fimmu-16-1583568-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/5d8b1b6c063a/fimmu-16-1583568-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/6c7b0be82328/fimmu-16-1583568-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/dc9db995959b/fimmu-16-1583568-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/405f9762bb2e/fimmu-16-1583568-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65a/12331502/180dc8aad0e5/fimmu-16-1583568-g005.jpg

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