Specifically, the study aimed to identify the prevalence of severe vitamin D deficiency in patients with PSC and investigate its relationship with cirrhosis progression, hepatobiliary malignancies, liver-related mortality, and the need to undergo liver transplantation.

This chronic cholestatic liver disease, Primary sclerosing cholangitis (PSC), is characterized by progressive inflammation of the biliary tracts and fibrosis of the extra- and intra-hepatic ducts. 

For this patient population, the long-term prognosis is poor due to the absence of medical treatments and the risks associated with hepatobiliary malignancies, cholangitis, and decompensated cirrhosis.

Many PSC patients also have concurrent inflammatory bowel disease (IBD), usually ulcerative colitis or Crohn’s disease. PSC patients generally have a median survival time of 10 to 22 years.

Besides its anti-inflammatory, anti-proliferative, and anti-fibrotic properties, vitamin D is also a secosteroid. Due to the liver’s significant role in converting cholecalciferol into 25-hydroxyvitamin D, chronic liver disease may interfere with vitamin D production.

It is also pertinent to note that vitamin D has a critical role in the natural history and development of liver disease. Therefore vitamin D deficiency in patients with chronic liver disease may be linked to liver damage and impaired vitamin D3 hydroxylation.

There is no clear etiology for PSC; however, impaired regulatory T-cells may contribute to its pathogenesis and progression. Vitamin D modulates the number and phenotype of circulating T regulatory cells. 

Vitamin D’s role in modulating inflammatory and immune-mediated pathways may impact PSC; however, only a few studies have examined this link.

Methodology & Results of the Study

In the study, 354 patients with PSC were followed by the University of Alberta’s autoimmune liver disease clinic. A severely deficient vitamin D level is defined as 25 nmol/L, and Cox proportional hazards regression models were used to conduct univariate and multivariate analyses.

Sixty-three patients (18%) had severe vitamin D deficiency, and the mean vitamin D level was 59 ± 2 nmol/L. Patients with severe vitamin D deficiency had 2.5 times the risk of developing hepatobiliary cancer. 

In addition, poor clinical liver outcomes were independently associated with severe vitamin D deficiency at diagnosis and persistent deficiencies over time.

18% of PSC patients were severely vitamin D deficient at diagnosis, associated with hepatobiliary cancer. Low serum vitamin D levels at diagnosis also appeared to be independent predictors of cirrhosis; however, these findings were only based on univariate analysis. 

Liver-related mortality or the need for transplantation was significantly associated with severe vitamin D deficiency at diagnosis and persistent deficiency at longitudinal assessments.

Vitamin D levels should be routinely assessed in patients with PSC, as this could be a prognostic biomarker.

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