Vitamin DNEW2026-09

Vitamin D Receptor Polymorphisms Are Associated with 25(OH)D Concentrations and Systemic Inflammation in Decompensated Cirrhosis.

Bauschen Alina, Langer Mona-May, Stadler Helena, Zeuzem Nicholas et al. — Nutrients

Summary

This study explored how genetic differences in the vitamin D receptor might affect vitamin D levels and inflammation in individuals with advanced liver disease. Researchers found that certain genetic variations were linked to lower vitamin D concentrations and higher markers of inflammation in these patients. This suggests that a person's genetics could play a role in their vitamin D status and inflammatory response, particularly in the context of severe liver conditions.

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Key points

Severe vitamin D deficiency is frequently observed in patients with advanced liver disease.
Genetic variations in the vitamin D receptor may influence an individual's vitamin D levels.
These specific genetic variations might also be linked to increased markers of systemic inflammation.
Further research is needed to confirm these exploratory findings in larger, independent groups.

What the study looked at

This research investigated whether variations in the gene for the vitamin D receptor (VDR) influence vitamin D levels and systemic inflammation in patients suffering from decompensated liver cirrhosis. The study enrolled 355 patients with various stages of liver cirrhosis, including those with acute-on-chronic liver failure, from a single medical center. Researchers analyzed specific genetic differences (polymorphisms) in their VDR genes and measured their circulating vitamin D levels and markers of inflammation. They observed that severe vitamin D deficiency was common in those with advanced liver disease. Interestingly, certain VDR gene variations were associated with lower circulating vitamin D levels. Furthermore, a specific VDR gene variant was linked to higher levels of an inflammatory marker called IL-6, even after accounting for other factors. While vitamin D supplementation generally increased vitamin D levels in most patients, this benefit was not as clear in those with the most severe acute-on-chronic liver failure. These findings suggest a complex interplay between genetics, vitamin D, and inflammation in severe liver disease.

Dietary takeaway

While this study focuses on specific genetic factors in severe liver disease, it broadly reinforces the importance of adequate vitamin D. For the general public, ensuring sufficient vitamin D intake through diet, such as fatty fish and fortified foods, and safe sun exposure remains a key part of a healthy lifestyle. However, it's crucial to remember that this is just one study, and its findings, particularly regarding genetics, require further confirmation before definitive conclusions can be drawn for the broader population.

Abstract

: Vitamin D regulates both the adaptive and the innate immune system, while having anti-inflammatory, immunomodulatory and anti-fibrotic properties. In clinical studies, 25(OH)D deficiency was associated with systemic inflammation, but it is unclear whether these associations are causal. In this study, we aimed to investigate the impact of Vitamin D receptor (VDR) polymorphisms (SNPs)-as surrogates for functional relationships-on 25(OH)D status and systemic inflammation in decompensated liver cirrhosis. : Patients with compensated and decompensated cirrhosis with or without ACLF were enrolled prospectively from a monocentric cohort study (N = 355). Pyrosequencing was performed for genotyping SNPs (, , , and ). VDR-SNPs were analysed for their association with 25(OH)D concentrations and markers of systemic inflammation. : Severe 25(OH)D deficiency was frequent in decompensated cirrhosis. 25(OH)D supplementation was associated with significantly higher circulating 25(OH)D in compensated and decompensated liver cirrhosis, whereas in ACLF, 25(OH)D levels did not differ significantly between supplemented and unsupplemented patients. An inverse correlation of 25(OH)D and IL-6 levels was identified (R = -0.2286, 95% CI -0.328 to -0.124, < 0.0001). In exploratory analyses among the analyzed VDR-SNPs, the GG-variant of was associated with lower 25(OH)D levels (β = 0.705, 95% CI 0.498-0.998, = 0.049). Moreover, the functionally important VDR-SNP -variant showed a nominal independent association with higher IL-6 levels (ß = 1.685, 95% CI 1.102-2.576, = 0.016) after adjustment. : These exploratory findings suggest that VDR genetics may partially contribute to 25(OH)D status and systemic inflammation in liver cirrhosis and ACLF and warrant further replication in independent cohorts.

View on PubMed →DOI: 10.3390/nu18193234