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      Effect of vitamin D therapy on interleukin-6, visfatin, and hyaluronic acid levels in chronic hepatitis C Egyptian patients

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          Abstract

          Objectives

          We aimed to compare serum levels of interleukin-6, visfatin, and hyaluronic acid in chronic hepatitis C Egyptian patients who received standard of care (SOC) therapy for chronic hepatitis C virus (HCV) consisting of pegylated interferon (PEG-IFN) and ribavirin (RBV) and in those who received SOC with vitamin D (vit D) for 48 weeks in HCV genotype 4a subjects.

          Design and methods

          One hundred chronic HCV patients were classified into two groups: study 50 patients received SOC therapy PEG-IFN/RBV + vit D and control 50 patients received SOC PEG-IFN/RBV without vit D. Both groups were followed up at 12 weeks, 24 weeks, and 48 weeks of treatment.

          Results

          Results showed a significant elevation in vit D levels in the group treated with SOC and vit D compared to SOC group and a reduction in HCV RNA from the 12th week to reach zero level in the 24th week. Interleukin-6, visfatin, and hyaluronic acid levels were also reduced significantly. Alanine transaminase and aspartate transaminase biomarkers were significantly reduced, indicating decreased liver injury.

          Conclusion

          SOC PEG-IFN/RBV + vit D therapy for chronic HCV led to reduced interleukin-6, visfatin, and hyaluronic acid levels and follow up liver biochemical biomarkers as aspartate transaminase and alanine transaminase indicates proper liver healing and monitoring.

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          Most cited references 20

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          Diagnosis, management, and treatment of hepatitis C: an update.

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            Visfatin, an adipocytokine with proinflammatory and immunomodulating properties.

            Adipocytokines are mainly adipocyte-derived cytokines regulating metabolism and as such are key regulators of insulin resistance. Some adipocytokines such as adiponectin and leptin affect immune and inflammatory functions. Visfatin (pre-B cell colony-enhancing factor) has recently been identified as a new adipocytokine affecting insulin resistance by binding to the insulin receptor. In this study, we show that recombinant visfatin activates human leukocytes and induces cytokine production. In CD14(+) monocytes, visfatin induces the production of IL-1beta, TNF-alpha, and especially IL-6. Moreover, it increases the surface expression of costimulatory molecules CD54, CD40, and CD80. Visfatin-stimulated monocytes show augmented FITC-dextran uptake and an enhanced capacity to induce alloproliferative responses in human lymphocytes. Visfatin-induced effects involve p38 as well as MEK1 pathways as determined by inhibition with MAPK inhibitors and we observed activation of NF-kappaB. In vivo, visfatin induces circulating IL-6 in BALB/c mice. In patients with inflammatory bowel disease, plasma levels of visfatin are elevated and its mRNA expression is significantly increased in colonic tissue of Crohn's and ulcerative colitis patients compared with healthy controls. Macrophages, dendritic cells, and colonic epithelial cells might be additional sources of visfatin as determined by confocal microscopy. Visfatin can be considered a new proinflammatory adipocytokine.
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              Vitamin D controls T cell antigen receptor signaling and activation of human T cells.

              Phospholipase C (PLC) isozymes are key signaling proteins downstream of many extracellular stimuli. Here we show that naive human T cells had very low expression of PLC-gamma1 and that this correlated with low T cell antigen receptor (TCR) responsiveness in naive T cells. However, TCR triggering led to an upregulation of approximately 75-fold in PLC-gamma1 expression, which correlated with greater TCR responsiveness. Induction of PLC-gamma1 was dependent on vitamin D and expression of the vitamin D receptor (VDR). Naive T cells did not express VDR, but VDR expression was induced by TCR signaling via the alternative mitogen-activated protein kinase p38 pathway. Thus, initial TCR signaling via p38 leads to successive induction of VDR and PLC-gamma1, which are required for subsequent classical TCR signaling and T cell activation.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2015
                19 February 2015
                : 11
                : 279-288
                Affiliations
                [1 ]Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Cairo University, Giza, Egypt
                [2 ]Biochemistry Department, Faculty of Pharmacy, Al-Azhar University, Gaza, State of Palestine, Egypt
                [3 ]Internal Medicine Department, Cairo University, Giza, Egypt
                [4 ]Tropical Medicine Department, Faculty of Medicine, Cairo University, Giza, Egypt
                [5 ]Biochemistry Department, Faculty of Pharmacy, Cairo University, Giza, Egypt
                [6 ]Medical Biochemistry Department, Faculty of Medicine, Suez Canal University, Ismaileya, Egypt
                [7 ]Medical Biochemistry Department, Faculty of Medicine, October 6 University, Giza, Egypt
                [8 ]Tropical Medicine Department, Faculty of Medicine, Cairo University, Giza, Egypt
                [9 ]Tropical Medicine Department, Bny Swif University, Bny Swif, Egypt
                Author notes
                Correspondence: Dina Sabry, Biochemistry Department, Faculty of Medicine, Cairo University, Cairo University Road, Oula, Giza, Egypt, Tel +20 11 1120 0200, Email dinnasabry69@ 123456yahoo.com ; dinasabry@ 123456kasralainy.edu.eg
                Mohamed AS Al Ghussein, Biochemistry Department, Faculty of Pharmacy, Al-Azhar University, PO box 1277, Gaza, Gaza strip, Palestine, Email mohamedghussein@ 123456yahoo.com
                Article
                tcrm-11-279
                10.2147/TCRM.S66763
                4344182
                © 2015 Sabry et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Medicine

                hepatitis c virus, hcv 4a rna, pegylated interferon, ribavirin, ast, alt

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