Factors associated with 25-hydroxyvitamin D levels in patients with liver cirrhosis
Date
2015
Authors
Silva, M.
Silva, T.
de Alentar, M.
Coelho, M.
Wildner, L.
Bazzo, M.
González-Chica, D.
Dantas-Corrêa, E.
Narciso-Schiavon, J.
Schiavon, L.
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Journal article
Citation
Annals of Hepatology, 2015; 14(1):99-107
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Mariana Costa Silva, Telma Erotides Silva, Maria Luiza Aires de Alentar, Mara Sergia Pacheco Honorio Coelho, Leticia Muraro Wildner … David Alejandro Gonzalez-Chica … et al.
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Abstract
Lower 25-hydroxyvitamin D [25(OH)D] levels have been observed in cirrhotic patients and have been related to disease severity. However, most previous studies included patients with very advanced disease, lacking an adequate control for other variables that could interfere with vitamin D levels. We sought to investigate the prevalence of hypovitaminosis D and the factors related to its occurrence. MATERIAL AND METHODS: This cross-sectional study included 133 cirrhotic patients and 30 healthy controls. Bivariate and multivariate analyses were performed to determine factors associated with 25(OH)D levels below the lower tertile. Thirty patients who had been recently hospitalized were compared in two time points. RESULTS: Mean 25(OH)D levels were 32.34 ± 11.38 in controls and 27.03 ± 6.22 ng/mL in patients (P = 0.018). 25(OH)D levels were < 30 ng/mL in 69.9% and < 20 ng/mL in 14.3% of the sample. Levels of 25(OH)D below the lower tertile (< 24 ng/mL) were independently associated with higher triceps skinfold and non-Caucasian race. Parathyroid hormone above the reference value (65 pg/mL) was found in 24.6% of patients without association with 25(OH)D or severity of liver disease. Significantly lower levels of 25(OH)D were found at the time of acute decompensation of cirrhosis. CONCLUSIONS: In conclusion, hypovitaminosis D was prevalent in cirrhotics and it was associated with adiposity and non-Caucasian race in stable patients with relatively well preserved liver function. However, significantly lower levels were observed during admission for acute decompensation suggesting an impact of systemic inflammation or liver dysfunction on 25(OH)D levels.
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