Marked 25-hydroxyvitamin D deficiency is associated with poor prognosis in patients with alcoholic liver disease

Trépo, Eric; Ouziel, Romy; Pradat, Pierre; Momozawa, Yukihide; Quertinmont, Eric; Gervy, Christine; Gustot, Thierry; Degré, Delphine; Vercruysse, Vincent; Deltenre, Pierre; Verset, Laurine; Gulbis, Béatrice; Franchimont, Denis; Devière, Jacques; Lemmers, Arnaud; Moreno, Christophe

doi:10.1016/j.jhep.2013.03.024

Cited by 113 publications

(104 citation statements)

References 29 publications

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“…We have previously demonstrated that vitamin D deficiency increases mortality in those with advanced cirrhosis, and this association was also found in patients with alcoholic-related liver disease [35,36]. Thus, there are many justifications for correcting vitamin D concentrations in CLD and, coupled with the fact that these patients often suffer from co-morbid depression, vitamin D substitution could play a more prominent part in future clinical care of patients presenting with CLD and inadequate vitamin D levels.…”

Section: Discussionmentioning

confidence: 94%

Vitamin D supplementation reduces depressive symptoms in patients with chronic liver disease

et al. 2016

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Section: Discussionmentioning

confidence: 94%

Vitamin D supplementation reduces depressive symptoms in patients with chronic liver disease

et al. 2016

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“…Low serum levels of 25-hydroxyvitamin D have been reported in diverse chronic liver diseases [314][315][316][317][318], including autoimmune hepatitis [319,320], and this deficiency has been associated with disease severity and hepatic fibrosis. Hepatic fibrosis scores and interface hepatitis are independently associated with vitamin D deficiency in autoimmune hepatitis, and the serum level of 25-hydroxyvitamin D may be a biomarker of the histological response to severe or protracted tissue damage [319].…”

Section: Insights Into the Cytopathic Mechanisms Of Autoimmune Hepatitismentioning

confidence: 99%

Transitioning from Idiopathic to Explainable Autoimmune Hepatitis

Czaja

2015

Dig Dis Sci

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Autoimmune hepatitis lacks an identifiable cause, and its diagnosis requires the exclusion of etiologically defined diseases that resemble it. Insights into its pathogenesis are moving autoimmune hepatitis from an idiopathic to explainable disease, and the goal of this review is to describe the insights that are hastening this transition. Two types of autoimmune hepatitis are justified by serological markers, but they also have distinctive genetic associations (DRB1 and DQB1 genes) and autoantigens. DRB1 alleles are the principal susceptibility factors in white adults, and a six amino acid sequence encoded in the antigen-binding groove of class II molecules of the major histocompatibility complex can influence the selection of autoantigens. Polymorphisms, including variants of SH2B3 and CARD10 genes, may affect immune reactivity and disease severity. The cytochrome mono-oxygenase, CYP2D6, is the autoantigen associated with type 2 autoimmune hepatitis, and it shares homologies with multiple viruses that might promote self-intolerance by molecular mimicry. Chemokines, especially CXCL9 and CXCL10, orchestrate the migration of effector cells to sites of injury and are associated with disease severity. Cells of the innate and adaptive immune responses promote tissue damage, and possible deficiencies in the number and function of regulatory T cells may facilitate the injurious process. Receptor-mediated apoptosis is the principal mechanism of hepatocyte loss, and cell-mediated and antibody-dependent mechanisms of cytotoxicity also contribute. Insights that explain autoimmune hepatitis will allow triggering exogenous antigens to be characterized, risk management to be improved, prognostic indices to be refined, and site-specific therapeutic interventions to emerge.

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“…Fascinating functions of vitamin D in hepatic biology and fibrosis are emerging. Patients with alcoholic liver disease and low 25(OH) D levels have more severe hepatic damage and worse outcomes [88], and patients with the highest baseline 25(OH)D levels have a 50% reduction in HCC risk irrespective of underlying liver disease [89]. It is feasible that some of this effect may be due to the anti-proliferative effect of the activated form of vitamin D, 1,25(OH) 2 D 3 , which when added to primary rat HSCs suppresses HSC proliferation, increases MMP-9, and decreases TIMP-1 expression [90].…”

Section: Proliferationmentioning

confidence: 99%