Daily Cannabis Use: A Novel Risk Factor of Steatosis Severity in Patients With Chronic Hepatitis C

Hézode, Christophe; Zafrani, Élie Serge; Roudot‐Thoraval, Françoise; Costentin, Charlotte; Hessami, Ali; Bouvier‐Alias, Magali; Medkour, Fatiha; Pawlostky, Jean–Michel; Lotersztajn, Sophie; Mallat, Ariane

doi:10.1053/j.gastro.2007.11.039

Cited by 175 publications

(111 citation statements)

References 39 publications

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“…197,198 As noted earlier, cannabinoids also mediate steatosis, and daily cannabis use is a risk factor for steatosis and fibrosis in HCV. 199,200 Interestingly, a recent study directly links CB1 receptor signaling to alcoholic steatosis in rodents fed a liquid ethanol diet. 201 Moreover, in these animals, activated stellate cells are a key source of the endogenous cannabinoid, 2-AG, which drives increased CB1 signaling.…”

Section: Nash and Ashmentioning

confidence: 99%

Mechanisms of Hepatic Fibrogenesis

2008

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Substantial improvements in the treatment of chronic liver disease have accelerated interest in uncovering the mechanisms underlying hepatic fibrosis and its resolution. Activation of resident hepatic stellate cells into proliferative, contractile, and fibrogenic cells in liver injury remains a dominant theme driving the field. However, several new areas of rapid progress in the past 5-10 years also have taken root, including: (1) identification of different fibrogenic populations apart from resident stellate cells, for example, portal fibroblasts, fibrocytes, and bone-marrow-derived cells, as well as cells derived from epithelial mesenchymal transition; (2) emergence of stellate cells as finely regulated determinants of hepatic inflammation and immunity; (3) elucidation of multiple pathways controlling gene expression during stellate cell activation including transcriptional, posttranscriptional, and epigenetic mechanisms; (4) recognition of disease-specific pathways of fibrogenesis; (5) re-emergence of hepatic macrophages as determinants of matrix degradation in fibrosis resolution and the importance of matrix cross-linking and scar maturation in determining reversibility; and (6) hints that hepatic stellate cells may contribute to hepatic stem cell behavior, cancer, and regeneration. Clinical and translational implications of these advances have become clear, and have begun to impact significantly on the management and outlook of patients with chronic liver disease.The field of hepatic fibrosis is flourishing thanks to continued experimental advances complemented by exciting progress in the treatment of chronic liver disease. 1 Control of chronic hepatitis B and C by antiviral therapies has established that advanced fibrosis can regress in association with improved clinical outcomes, 2-4 thereby intensifying enthusiasm to uncover the mechanistic basis for hepatic fibrogenesis and its attenuation. At the same time, simple paradigms defining the cellular sources of extracellular matrix (ECM), and the roles of cytokines and paracrine interactions among resident liver cells and inflammatory cells have yielded a more nuanced understanding of how the liver responds to injury. These advances have had a collateral benefit towards understanding fibrosis in other organs, particularly the pancreas. 5 Thus, a review of the mechanisms underlying hepatic fibrosis is not only timely, but is more clinically relevant than ever. This article focuses on recent advances in the field, building on established principles from earlier reviews 6,7 while weaving in their clinical relevance, but also emphasizing the molecular subtleties that have emerged through continued progress in the field. General PrinciplesFibrosis, or scarring of the liver, is a wound-healing response that engages a range of cell types and mediators to encapsulate injury. Although even acute injury will activate mechanisms of fibrogenesis, the sustained signals associated with chronic liver disease caused by infection, Cirrhosis, the most advanced stage ...

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Section: Nash and Ashmentioning

confidence: 99%

Mechanisms of Hepatic Fibrogenesis

2008

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“…In addition, pharmacological inhibition of CB1 with rimonabant, a CB1 antagonist, reduced expression of transforming growth factor β1 (TGFβ1) and α-smooth muscle actin (αSMA), and improved histology of BDL-, TAA-or CCl 4 treated mice (8,9). Clinically, patients with chronic hepatitis C and daily canna-bis consumption displayed more severe fibrosis progression than non-or occasional consumers (11)(12)(13). Endocannabinoid expression is faint in patients with healthy livers, whereas in cirrhosis, fatty liver, acute hepatitis or bile duct obstruction, hepatic and serum levels of AEA and 2-AG were found increased (14)(15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Cannabinoid Receptor Type I Modulates Alcohol-Induced Liver Fibrosis

Patsenker

Stoll

Millonig

et al. 2011

Mol Med

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“…28,29,32 However, the World Health Organization, (WHO) has been more cautious noting 'paucity of data' and 'conflicting reports on any association with liver disease'. 30 Clearly, further research is required to explore the role of cannabis use among people in drug treatment, especially OST.…”

Section: Discussionmentioning

confidence: 99%