Low serum vitamin D level associated with incident advanced liver disease in the general population – a prospective study

Abstract

Background

Vitamin D deficiency is a common finding in chronic liver disease. It has also been linked to the pathogenesis of non-alcoholic fatty liver disease, hepatic fibrogenesis, decompensation and hepatocellular carcinoma.

Aims

We analyzed whether serum vitamin D is associated with incident advanced liver disease in the general population.

Methods

Serum 25-hydroxyvitamin D was measured in 13807 individuals participating in the Finnish population-based health examination surveys FINRISK 1997 and Health 2000. Data were linked with incident advanced liver disease (hospitalization, cancer or death related to liver disease). During a follow-up of 201444 person-years 148 severe liver events occurred. Analyses were performed using multivariable Cox regression analyses.

Results

Vitamin D level associated with incident advanced liver disease with the hazard ratio of 0.972 (95% confidence interval 0.943-0.976, p < .001), when adjusted for age, sex, blood sampling season and stratified by cohort.The association remained robust and significant in multiple different adjustment models adjusting sequentially for 22 potential confounders.

Conclusion

Low vitamin D level is linked to incident advanced liver disease at population level.

Keywords:

• Advanced liver disease
• vitamin D
• S-25(OH)D
• cirrhosis

Correction Statement

This article has been corrected with minor changes. These changes do not impact the academic content of the article.

Acknowledgement

The data used for the research were from THL (obtained from THL Biobank). We thank all study participants for their generous participation in the FINRISK 1997 and Health 2000 studies.

Disclosure statement

VS has received honoraria for consulting from Novo Nordisk and Sanofi. He also has ongoing research collaboration with Bayer (all unrelated with the present study). SB reports grants and personal fees from Abbott Laboratories, Bayer, Siemens, and Thermo Fisher Scientific, grants from Singulex, and personal fees from Astra Zeneca, Amgen, Medtronic, Pfizer, and Roche, outside the submitted work.

Additional information

Funding

VM has received grant from Sigrid Jusélius Foundation, VS was supported by the Finnish Foundation for Cardiovascular Research, FÅ received research grants from Mary and Georg Ehrnrooth Foundation, Medicinska Understödsföreningen Liv och Hälsa and Finska Läkaresällskapet. TZ is supported by the German Center for Cardiovascular Research (grant number 81Z0710102). Part of this research was funded by the European Union Seventh Framework Program (FP7/2007–2013) for the BiomarCaRE project under grant agreement no. HEALTH-F2-2011-278913.