Vitamin K and vascular calcification

Lees, Jennifer S; Mark, Patrick B.; Witham, Miles

doi:10.1097/mnh.0000000000000712

Cited by 5 publications

(2 citation statements)

References 66 publications

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“…Conversely, vitamin K supplementation may boost antithrombotic activity, frequently diminished in those with vitamin K deficiency [ 55 ]. Since vitamin K exhibits procoagulant and anticoagulant properties, the balance between these effects can be influenced by the subtype-specific vitamin K administered [ 113 ]. Vitamin K1 may show a particularly pro-coagulative response, with the pro-coagulative proteins increasing more than proteins C and S [ 24 ].…”

Section: Resultsmentioning

confidence: 99%

Vitamin K: a potential missing link in critical illness–a scoping review

Paulus,

Drent,

Kouw

et al. 2024

Crit Care

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Background Vitamin K is essential for numerous physiological processes, including coagulation, bone metabolism, tissue calcification, and antioxidant activity. Deficiency, prevalent in critically ill ICU patients, impacts coagulation and increases the risk of bleeding and other complications. This review aims to elucidate the metabolism of vitamin K in the context of critical illness and identify a potential therapeutic approach. Methods In December 2023, a scoping review was conducted using the PRISMA Extension for Scoping Reviews. Literature was searched in PubMed, Embase, and Cochrane databases without restrictions. Inclusion criteria were studies on adult ICU patients discussing vitamin K deficiency and/or supplementation. Results A total of 1712 articles were screened, and 13 met the inclusion criteria. Vitamin K deficiency in ICU patients is linked to malnutrition, impaired absorption, antibiotic use, increased turnover, and genetic factors. Observational studies show higher PIVKA-II levels in ICU patients, indicating reduced vitamin K status. Risk factors include inadequate intake, disrupted absorption, and increased physiological demands. Supplementation studies suggest vitamin K can improve status but not normalize it completely. Vitamin K deficiency may correlate with prolonged ICU stays, mechanical ventilation, and increased mortality. Factors such as genetic polymorphisms and disrupted microbiomes also contribute to deficiency, underscoring the need for individualized nutritional strategies and further research on optimal supplementation dosages and administration routes. Conclusions Addressing vitamin K deficiency in ICU patients is crucial for mitigating risks associated with critical illness, yet optimal management strategies require further investigation. Impact research To the best of our knowledge, this review is the first to address the prevalence and progression of vitamin K deficiency in critically ill patients. It guides clinicians in diagnosing and managing vitamin K deficiency in intensive care and suggests practical strategies for supplementing vitamin K in critically ill patients. This review provides a comprehensive overview of the existing literature, and serves as a valuable resource for clinicians, researchers, and policymakers in critical care medicine.

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Section: Resultsmentioning

confidence: 99%

Vitamin K: a potential missing link in critical illness–a scoping review

Paulus,

Drent,

Kouw

et al. 2024

Crit Care

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“…Vitamin K, as a health-promoting supplement, plays an important regulatory role in inflammation [ 20 ]. It has been shown that some vitamin K family members have the potential to reduce COVID-19 mortality and play an important role in SARS-CoV-2-induced lung injury and thromboembolism formation [ 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Protective Role of Vitamin K3 on SARS-CoV-2 Structural Protein-Induced Inflammation and Cell Death

et al. 2023

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The structure proteins of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), such as nucleocapsid protein (N protein) and envelop protein (E protein), are considered to be the critical pro-inflammatory factors in coronavirus disease 2019 (COVID-19). Vitamin K3 has been reported to exert an anti-inflammatory effect. In this study, we investigated the protective effects of vitamin K3 on SARS-CoV-2 N protein induced-endothelial activation and SARS-CoV-2 E protein induced-cell death in THP-1 cells. The results showed that vitamin K3 reduced N protein-induced monocyte adhesion, suppressed the expression of adhesion molecules, and decreased the mRNA levels of pro-inflammatory cytokines in HLMECs. We confirmed that the effects of vitamin K3 on endothelial activation may be related to the inhibition of the NF-κB signal pathway. In addition, vitamin K3 reversed E protein-induced pyroptosis, inhibited NLRP3/GSDMD signal pathway and reduced the mRNA expression of pro-inflammatory cytokines in THP-1 cells. Our results also showed the protective effects of vitamin K3 on the SARS-CoV-2 structural protein-induced THP-1 cells pyroptosis and endothelial activation via NF-κB signaling pathway. These findings suggested that vitamin K3 potently suppressed the inflammatory response to prevent endothelial activation and monocyte pyroptosis induced by SARS-CoV-2 proteins. This may provide a new strategy for the treatment of COVID-19.

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