Vitamin D deficiency is associated with hepatic decompensation and inflammation in patients with liver cirrhosis: A prospective cohort study

PLoS One. 2018 Nov 8;13(11):e0207162. doi: 10.1371/journal.pone.0207162. eCollection 2018.


Background: Vitamin D is required to maintain the integrity of the intestinal barrier and inhibits inflammatory signaling pathways.

Objective: Vitamin D deficiency might be involved in cirrhosis-associated systemic inflammation and risk of hepatic decompensation in patients with liver cirrhosis.

Methods: Outpatients of the Hepatology Unit of the University Hospital Frankfurt with advanced liver fibrosis and cirrhosis were prospectively enrolled. 25-hydroxyvitamin D (25(OH)D3) serum concentrations were quantified and associated with markers of systemic inflammation / intestinal bacterial translocation and hepatic decompensation.

Results: A total of 338 patients with advanced liver fibrosis or cirrhosis were included. Of those, 51 patients (15%) were hospitalized due to hepatic decompensation during follow-up. Overall, 72 patients (21%) had severe vitamin D deficiency. However, patients receiving vitamin D supplements had significantly higher 25(OH)D3 serum levels compared to patients without supplements (37 ng/mL vs. 16 ng/ml, P<0.0001). Uni- and multivariate analyses revealed an independent association of severe vitamin D deficiency with the risk of hepatic decompensation during follow-up (multivariate P = 0.012; OR = 3.25, 95% CI = 1.30-8.2), together with MELD score, low hemoglobin concentration, low coffee consumption, and presence of diabetes. Of note, serum levels of C-reactive protein, IL-6 and soluble CD14 were significantly higher in patients with versus without severe vitamin D deficiency, and serum levels of soluble CD14 levels declined in patients with de novo supplementation of vitamin D (median 2.15 vs. 1.87 ng/mL, P = 0.002).

Conclusions: In this prospective cohort study, baseline vitamin D levels were inversely associated with liver-cirrhosis related systemic inflammation and the risk of hepatic decompensation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Bacterial Translocation
  • Biomarkers / blood
  • Calcifediol / blood
  • Cohort Studies
  • Female
  • Humans
  • Inflammation / blood
  • Inflammation / etiology*
  • Inflammation / microbiology
  • Lipopolysaccharide Receptors / blood
  • Liver Cirrhosis / blood
  • Liver Cirrhosis / complications*
  • Liver Cirrhosis / microbiology
  • Liver Failure / blood
  • Liver Failure / etiology*
  • Liver Failure / microbiology
  • Male
  • Middle Aged
  • Prospective Studies
  • Risk Factors
  • Vitamin D Deficiency / blood
  • Vitamin D Deficiency / complications*
  • Vitamin D Deficiency / microbiology


  • Biomarkers
  • Lipopolysaccharide Receptors
  • Calcifediol

Grant support

This study was supported by the Deutsche Forschungsgemeinschaft (LA 2806/2-1 and LA 2806/5-1 to CML). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.