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Low 25-OH-vitamin D levels reflect hepatic dysfunction and are associated with mortality in patients with liver cirrhosis

BACKGROUND AND AIMS: Vitamin D deficiency is frequent in patients with cirrhosis. The aims of this study were to evaluate the relation of vitamin D status to portal hypertension, degree of liver dysfunction and survival. METHODS: Patients with cirrhosis who have been tested for 25-OH-vitamin D level...

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Detalles Bibliográficos
Autores principales: Paternostro, Rafael, Wagner, Doris, Reiberger, Thomas, Mandorfer, Mattias, Schwarzer, Remy, Ferlitsch, Monika, Trauner, Michael, Peck-Radosavljevic, Markus, Ferlitsch, Arnulf
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Vienna 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5247538/
https://www.ncbi.nlm.nih.gov/pubmed/27888359
http://dx.doi.org/10.1007/s00508-016-1127-1
Descripción
Sumario:BACKGROUND AND AIMS: Vitamin D deficiency is frequent in patients with cirrhosis. The aims of this study were to evaluate the relation of vitamin D status to portal hypertension, degree of liver dysfunction and survival. METHODS: Patients with cirrhosis who have been tested for 25-OH-vitamin D levels were retrospectively included. Vitamin D deficiency was defined as 25-OH-vitamin D levels <10 ng/ml. Child–Pugh score, model for end-stage liver disease (MELD) and available hepatic venous pressure gradient (HVPG) were recorded. Mortality was documented during follow-up. RESULTS: A total of 199 patients were included. Prevalence of vitamin D deficiency (<10 ng/ml) was 40% (79/199), with 14% in Child–Pugh stage A, 39% in Child–Pugh stage B and 47% in Child–Pugh stage C (p = 0.001). Vitamin D deficiency was more common in patients with clinically significant portal hypertension (CSPH, HVPG ≥ 10 mm Hg) than in patients without (43.5% vs. 24.4%, p = 0.025). Significantly more deaths were observed in patients with vitamin D deficiency (32.9%, 26/79 vs. 13.3%, 16/120; p = 0.001). COX regression found presence of hepatocellular carcinoma (p < 0.001; HR: 5.763 95%CI:2.183–15.213), presence of CSPH (p = 0.026; HR: 5.487 95%CI: 1.226–24.55) and Child–Pugh stage C (p = 0.003; HR:5.429 95%CI: 1.771–16.638) as independent risk factors for mortality. Furthermore we could show a tendency towards group vitamin D deficiency being an independent risk factor (p = 0.060; HR: 1.86 95%CI:0.974–3.552). CONCLUSIONS: Vitamin D levels progressively decrease in more advanced Child stages and in patients with increasing HVPG. Vitamin D deficiency might be a valuable predictor of mortality in cirrhosis.