Background: Uric acid is a natural antioxidant. Previous studies have suggested a protective role of hyperuricemia against liver fibrosis among patients with nonalcoholic fatty liver disease (NAFLD). However, the results were conflicting.
Methods: MEDLINE and EMBASE databases were searched through August 2016 for studies that investigated the association between hyperuricemia and fibrosis stage among patients with biopsy-proven NAFLD. Pooled odds ratio and 95% confidence interval were calculated using a random-effects model, generic inverse variance method of DerSimonian and Laird. The between-study heterogeneity of effect size was quantified using the Q statistic and I.
Results: A total of five observational studies with 749 NAFLD patients were identified. Patients with NAFLD who had hyperuricemia were not significantly more likely or less likely to have advanced liver fibrosis (defined as fibrosis stage of ≥3) compared with patients with NAFLD who had normal serum uric with the pooled odds ratio of 0.72 (95% confidence interval: 0.34-1.53). The statistical heterogeneity was low with an I of 22% (Pheterogeneity=0.27).
Conclusion: Significant protective role of hyperuricemia against the development of advanced liver fibrosis in patients with NAFLD was not observed in this meta-analysis.
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http://dx.doi.org/10.1097/MEG.0000000000000865 | DOI Listing |
Background And Aim: There is paucity of data about the prevalence of cirrhosis and portal hypertension in the US general population.
Methods: We used National Health and Nutrition Examination Surveys (NHANES 2017-2020) to estimate the prevalence of cirrhosis and clinically significant (CS)-portal hypertension in alcoholic liver disease (ALD), MetALD, viral hepatitis (VH) to include chronic hepatitis B (CHB) and chronic hepatitis C (CHC), and metabolic dysfunction-associated steatotic liver disease (MASLD). Cirrhosis was evaluated using liver stiffness measurement (LSM) by transient elastography or FIB-4 score; CS-portal hypertension was defined via LSM and platelet count or the use of non-selective beta-blockers in the presence of cirrhosis.
Hepatology
January 2025
Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA.
Background Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects about a third of adults worldwide and is projected soon to be the leading cause of cirrhosis. It occurs when fat accumulates in hepatocytes and can progress to metabolic dysfunction-associated steatohepatitis (MASH), liver cirrhosis, and hepatocellular carcinoma. MASLD pathogenesis is believed to involve a combination of genetic and environmental risk factors.
View Article and Find Full Text PDFHepatology
January 2025
AP-HP, Sorbonne Université, Liver Intensive Care Unit, Hepatogastroenterology Department, La Pitié-Salpêtrière Hospital, 47-83 Boulevard de l'Hôpital, Paris 75013, France.
Background And Aims: In cirrhosis, some patients display acute encephalopathy without hyperammonemia (NonHep E) which is not considered as overt hepatic encephalopathy (OHE). We aimed to assess the prevalence and characteristics of NonHep E and OHE in cirrhotic patients displaying acute encephalopathy, assess their respective prognosis and compare it to other causes of acute decompensation (AD) with/without hyperammonemia.
Approach And Results: We conducted a retrolective analysis from a prospective cohort of patients hospitalized for AD.
Hepatol Commun
February 2025
Department of Anesthesiology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Background: Cell therapy demonstrates promising potential as a substitute therapeutic approach for liver cirrhosis. We have developed a strategy to effectively expand murine and human hepatocyte-derived liver progenitor-like cells (HepLPCs) in vitro. The primary objective of the present study was to apply HepLPCs to the treatment of liver cirrhosis and to elucidate the underlying mechanisms responsible for their therapeutic efficacy.
View Article and Find Full Text PDFHepatol Commun
February 2025
Department of Surgery, University of California, San Francisco, San Francisco, California, USA.
Background: Rho-associated kinases 1 and 2 (ROCK1 and ROCK2) regulate critical cell functions, including actomyosin contractility, apoptosis, and proliferation. Some studies suggest that ROCK inhibition may serve as a treatment for liver fibrosis. More investigation is needed to understand the role of hepatocyte ROCK signaling in vivo, especially in the context of profibrotic liver injury.
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