Acute Alcoholic Hepatitis.

@article{Im2019AcuteAH,
  title={Acute Alcoholic Hepatitis.},
  author={Gene Y. Im},
  journal={Clinics in liver disease},
  year={2019},
  volume={23 1},
  pages={
          81-98
        }
}
  • G. Im
  • Published 1 February 2019
  • Medicine
  • Clinics in liver disease

Acute exacerbated severe form of nonalcoholic steatohepatitis leading to acute-on-chronic liver failure: A case series

TLDR
Three patients with uncontrolled metabolic syndrome and acute-on-chronic liver failure are presented in whom the acute event was found to be a severe and exacerbated form of nonalcoholic steatohepatitis (NASH), a novel entry in the natural history of non-alcoholic fatty liver disease.

Outcomes of Hospitalized Acute Alcoholic Hepatitis (AH) in Patients With Bipolar 1 Disorder (B1D)

TLDR
This study indicates that B1D may be an independent protective factor against acute hepatic failure in patients hospitalized with AH, and can be explained by frequent laboratory monitoring and psychiatric assessments performed by psychiatrists treating B 1D patients, as well as the impact B1d has on cortisol release induced by hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis.

Utility of platelet indices in alcoholic hepatitis: a retrospective study

TLDR
platelet indices appear to be significantly altered in alcoholic hepatitis, but they do not predict severe disease.

LncRNA 1700020I14Rik promotes AKR1B10 expression and activates Erk pathway to induce hepatocyte damage in alcoholic hepatitis

TLDR
In vitro cell experiments and in vivo animal experiments validated that 1700020I14Rik reduced ethanol-induced hepatocyte damage and inflammation in AH mice through regulation of miR-137–mediated AKR1B10/Erk axis.

Chronic stress and corticosterone exacerbate alcohol-induced tissue injury in the gut-liver-brain axis

TLDR
Data indicate that chronic stress and corticosterone exacerbate alcohol-induced mucosal barrier dysfunction, endotoxemia, and systemic alcohol responses, and Corticosterone-mediated promotion ofcohol-induced intestinal epithelial barrier dysfunction and modulation of gut microbiota may play a crucial role in the mechanism of stress-induced promotion of alcohol-associated tissue injury at the GLB axis.

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