Relationship between 25-Hydroxyvitamin D Levels and Liver Fibrosis as Assessed by Transient Elastography in Patients with Chronic Liver Disease

Abstract

Background/AimsDeficiencies of 25-hydroxyvitamin D (25(OH)D) are prevalent in patients with chronic liver disease (CLD). Liver fibrosis is the main determinant of CLD prognosis. The present study was performed to evaluate the correlation between 25(OH)D levels and liver fibrosis as assessed by transient elastography (TE) in patients with compensated CLD.MethodsSerum 25(OH)D levels and liver stiffness were determined in a total of 207 patients who were subjected to the following exclusion criteria: patients with decompensated CLD; patients who had malignancies; patients who were taking medications; and patients who were pregnant.ResultsThe most common etiology was chronic hepatitis B (53.1%). Advanced liver fibrosis (defined by TE [≥9.5 kPa]) was present in 75 patients (36.2%). There was a significant correlation between 25(OH)D deficiency and liver stiffness. Based on the multivariate analysis, the following factors were independently associated with advanced liver fibrosis: 25(OH)D deficiency (odds ratio [OR], 3.46; p=0.004), diabetes mellitus (OR, 3.04; p=0.041), and fibrosis-4 index (OR, 2.01; p<0.001).ConclusionsPatients with compensated CLD exhibit a close correlation between vitamin D level and liver stiffness as assessed by TE. Vitamin D deficiency was independently associated with advanced liver fibrosis.

The GC2 haplotype of the vitamin D binding protein is a risk factor for a low plasma 25-hydroxyvitamin D concentration in a Han Chinese population

“…In the blood stream, the majority of 25OHD and other VD sterols are bound to the VD binding protein (VDBP, encoded by the GC gene) [15–18], which was initially named as group-specific protein [16]. In healthy people, the circulating VDBP concentration seems to be independent of genetic or racial differences [19], age, adiposity [20], sunshine exposure [21], concentrations of VD sterols, and other hormones [22]; however, both 25OHD and VDBP are predominantly synthesized and secreted by the liver, and their circulating concentrations are impaired by hepatic disease [23, 24]. Moreover, sunshine exposure (including season, latitude, exposure time of the day, and so on), skin colour, VD-rich food, and others affect the circulating concentration of 25OHD.…”

Vitamin D supplementation improves serum markers associated with hepatic fibrogenesis in chronic hepatitis C patients: A randomized, double-blind, placebo-controlled study

“…CHC genotype 1 patients with VD deficiency show lower responses to standard pegylated interferon/ribavirin treatment, while the response rate in difficult-to-treat patients increases after the restoration of VD levels 7 , 8 . Clinical data also suggest that CHC patients with VD deficiency have more severe progressive liver fibrosis and liver stiffness, leading to the hypothesis that VD might be involved in liver fibrogenesis 9 , 10 .…”

The fibrolytic potentials of vitamin D and thymoquinone remedial therapies: insights from liver fibrosis established by CCl4 in rats

“…Indeed, VitD regulates hundreds of different genes together with its well-established immunomodulatory and anti-inflammatory effects [ 21 – 23 ]. Additionally, pathological alterations in VitD concentrations have been observed with a variety of chronic liver diseases and there was a significant correlation between the levels of the hormone with the degree of liver fibrosis [ 24 – 26 ]. TQ is another natural product that has been shown to exhibit immunomodulatory and hepatoprotective actions and is the most abundant constituent of the Nigella sativa seeds, which are popularly known as black seeds or the seeds of blessing [ 27 – 29 ].…”

“…TQ is another natural product that has been shown to exhibit immunomodulatory and hepatoprotective actions and is the most abundant constituent of the Nigella sativa seeds, which are popularly known as black seeds or the seeds of blessing [ 27 – 29 ]. Despite the previous reports on the anti-fibrotic properties of VitD and TQ [ 21 , 23 , 24 , 27 – 29 ], none of the previous studies explored whether dual therapy with both agents could have potential fibrolytic activities and/or boosted interactions for the treatment of liver fibrosis.…”