Natural History of Alcoholic Hepatitis

Galambos, John T.

doi:10.1016/s0016-5085(19)33180-4

Cited by 201 publications

(65 citation statements)

References 12 publications

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“…31 Despite alcohol cessation, most of the patients followed for 18 months by one investigator had persistent alcoholic hepatitis and 18% had developed cirrhosis. 32 …”

Section: Alcoholic Hepatitismentioning

confidence: 99%

Spectrum of Alcoholic Liver Disease

Chacko

Reinus

2016

Clinics in Liver Disease

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“…31 Despite alcohol cessation, most of the patients followed for 18 months by one investigator had persistent alcoholic hepatitis and 18% had developed cirrhosis. 32 …”

Section: Alcoholic Hepatitismentioning

confidence: 99%

Spectrum of Alcoholic Liver Disease

Chacko

Reinus

2016

Clinics in Liver Disease

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“…Instead, patients with ASH often develop hepatic fibrosis and, with time, cirrhosis occurs in a significant fraction (almost 50%) of these individuals ( Fig. 1; Galambos 1972;MacSween and Burt 1986;Maher 2002). Clearly, steatohepatitis appears to represent an important rate-limiting transition step in the orderly progression of relatively benign alcoholic steatosis (fatty liver) to more serious liver fibrosis/cirrhosis in patients with ALD ( Fig.…”

Section: Alcoholic Liver Disease Pathologic Stagesmentioning

confidence: 99%

“…Clearly, steatohepatitis appears to represent an important rate-limiting transition step in the orderly progression of relatively benign alcoholic steatosis (fatty liver) to more serious liver fibrosis/cirrhosis in patients with ALD ( Fig. 1; Diehl 2002;Galambos 1972;Nanji 2002;Uesugi et al 2001). On the other hand, patients with alcohol-induced liver cirrhosis can develop ASH.…”

Section: Alcoholic Liver Disease Pathologic Stagesmentioning

confidence: 99%

Hepatic Neutrophil Infiltration in the Pathogenesis of Alcohol-Induced Liver Injury

Ramaiah

Jaeschke

2007

Toxicology Mechanisms and Methods

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The histopathologic evidence of the presence of neutrophils within the liver parenchyma is a prominent feature of alcoholic hepatitis in both experimental animals and chronic human alcoholics. However, the precise mechanisms by which neutrophils infiltrate the liver and cause liver injury still remain to be fully elucidated. For neutrophils to infiltrate the liver, they have to undergo systemic activation (priming) by proinflammatory cytokines, chemokines, complement factors, and other biologically active molecules (e.g., platelet-activating factor). Neutrophils accumulated in the hepatic microvasculature (sinusoids and postsinusoidal venules) can extravasate (transmigrate) into the hepatic parenchyma if they receive appropriate signals from previously sensitized or distressed cells. Transmigration can be mediated by a chemokine gradient established toward the hepatic parenchyma and generally involves the interaction between adhesion molecules on neutrophils (beta(2) integrins) and on endothelial cells (intercellular adhesion molecules [ICAM-1]). Following transmigration, neutrophils adhere to sensitized hepatocytes through their beta(2) integrins and ICAM-1 expressed on hepatocytes and mediate killing of hepatocytes mostly by oxidant stress and proteases. These neutrophilic events during chronic alcohol ingestion, based mostly on experiments with rodent models, will be emphasized in this review.

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“…31 Women are twice as sensitive to alcohol-mediated hepatotoxicity as men. They develop more severe liver disease at lower doses and shorter duration of alcohol consumption.…”

Section: Hepatobiliary Quiz-5 (2013) Answers Agrawal and Dhimanmentioning

confidence: 99%