Cholestasis and Alcoholic Liver Disease

Tung, Bruce Y.; Carithers, Robert L.

doi:10.1016/s1089-3261(05)70086-6

Cited by 46 publications

(41 citation statements)

References 75 publications

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“…Bile duct lesions with a cholestatic presentation are a nonspecific feature of NASH, as other conditions of steatosis may histologically mimic it: (a) alcoholic hepatitis of varying clinical degrees (5)(6)(7)(8)19); (b) several drug-induced injuries (20,21); (c) jejuno-ileal bypass with related "shortcircuiting" of the bowel with or without total parenteral nutrition (22)(23)(24)(25)(26)(27)(28)(29); and (d) hepatitis C (11)(12)(13). Cholestasis may be present at all stages of alcoholic liver disease (5)(6)(7)(8) where microscopic cholangitis (polymorphonuclear inflammation) and intrahepatic cholestasis are the features detected at liver biopsy (8). On the contrary, in hepatitis C more severe liver damage was found, with bile ductular proliferation and ductupenia as the most common histological features in patients (most diabetics) presenting cholestatic features (10)(11)(12)(13).…”

Section: Discussionmentioning

confidence: 99%

“…clinical jaundice may be present in all stages of alcoholic liver disease (5)(6)(7)(8), the clinical and histological picture of NASH (2,9) does not include any references to possible cholestatic course due to bile duct involvement. The histological evidence of bile duct damage also in chronic hepatitis C patients with a cholestatic presentation may account for both their pruritus and the biochemical features (10)(11)(12)(13).…”

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confidence: 99%

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A Clinical–Morphological Study on Cholestatic Presentation of Nonalcoholic Fatty Liver Disease

Sorrentino

Tarantino²,

Perrella³

et al. 2005

Dig Dis Sci

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To determine the association among the clinical, biochemical, and histological features of cholestasis, we analyzed all the relevant data of the patients recorded in our non-alcoholic fatty liver disease (NAFLD) database. We selected 20 NAFLD patients with abnormal transaminase levels, with both alkaline phosphatase >500 U/L and gamma-glutamyl transpeptidase >250 U/L. Their histological features were compared with those of a group of patients with NAFLD matched for sex, age, and body mass index and of a group of patients matched for sex, body mass index and histological NAFLD grading/staging. Cases and controls satisfied, on histology, the criteria for NASH. The presence of cholestasis in our patients was correlated with injury of the bile duct epithelium, characterized by cholangitis, swelling, variable bile duct loss, and bile stasis. Compared to NAFLD patients of similar age, sex, and body mass index, the cholestatic group had total and severe histological liver impairment. When we analyzed the group of patients histologically identified on the basis of identical stage and grade severity, we could not find any evidence of significant bile damage, compared to cases, despite the control group's significantly older age. NAFLD patients with biochemical cholestasis have a histological picture of bile damage; they have more advanced histological impairment than patients matched for age, sex and body mass index.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

A Clinical–Morphological Study on Cholestatic Presentation of Nonalcoholic Fatty Liver Disease

Sorrentino

Tarantino²,

Perrella³

et al. 2005

Dig Dis Sci

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“…Although the pathophysiology of cholestasis in ALD is not that well established, alcoholinduced cholestasis is mediated by compression of intrahepatic biliary radicles and increased permeability of the bile ductules. 6 Moreover, alcoholism leading to ALD is one of the primary causes of liver diseases in India. 19 A significant finding of the present study was the presence of NAFLD in a considerable number of CCLD patients (about one-fifth) as an underlying etiology of IHC.…”

Section: Discussionmentioning

confidence: 99%

“…5 Furthermore, in patients of alcoholic liver disease, alcohol-induced compression of intrahepatic biliary radicles and increased permeability of the bile ductules appears to predispose patients to develop cholestasis. 6 Drug-induced cholestatic liver disease is a subtype of liver injury secondary to the administration of a hepatotoxic agent, characterized by abnormal liver function test values including alkaline phosphatase (ALP) and bilirubin levels. 7 Clinically, CCLD patients present with pruritus (itching), fatigue and jaundice (reflected by elevated serum bilirubin levels).…”

Section: Introductionmentioning

confidence: 99%

A prospective, multicentre, observational study of patients with chronic cholestatic liver diseases receiving Udiliv and reg; in India: splendid study

Lawate

Rooprai²,

Choudhury

et al. 2016

Int J Basic Clin Pharmacol

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“…[69][70][71][72] We assessed the structure of the hepatocyte canaliculi, which is the apical hepatocyte surface through which bile is secreted into preductules, a structure formed by the biliary preductal epithelial cells, which are unique to the livers of fishes and analogous to the mammalian canal of Hering. 73,74 The bile salt export pump (BSEP/ABCB11) is a canalicular hepatocyte apical membrane protein that shuttles bile acids out of hepatocytes into the canalicular lumen and a widely used marker of canaliculi.…”

Section: Fig 2 Tunicamycin and Ethanol Induce Hepatic Dysfunction (A)mentioning

confidence: 99%

Defining Hepatic Dysfunction Parameters in Two Models of Fatty Liver Disease in Zebrafish Larvae

et al. 2013

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Fatty liver disease in humans can progress from steatosis to hepatocellular injury, fibrosis, cirrhosis, and liver failure. We developed a series of straightforward assays to determine whether zebrafish larvae with either tunicamycin-or ethanol-induced steatosis develop hepatic dysfunction. We found altered expression of genes involved in acute phase response and hepatic function, and impaired hepatocyte secretion and disruption of canaliculi in both models, but glycogen deficiency in hepatocytes and dilation of hepatic vasculature occurred only in ethanol-treated larvae. Hepatic stellate cells (HSCs) become activated during liver injury and HSC numbers increased in both models. Whether the excess lipids in hepatocytes are a direct cause of hepatocyte dysfunction in fatty liver disease has not been defined. We prevented ethanol-induced steatosis by blocking activation of the sterol response element binding proteins (Srebps) using gonzo mbtps1 mutants and scap morphants and found that hepatocyte dysfunction persisted even in the absence of lipid accumulation. This suggests that lipotoxicity is not the primary cause of hepatic injury in these models of fatty liver disease. This study provides a panel of parameters to assess liver disease that can be easily applied to zebrafish mutants, transgenics, and for drug screening in which liver function is an important consideration.

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Cholestasis and Alcoholic Liver Disease

Cited by 46 publications

References 75 publications

A Clinical–Morphological Study on Cholestatic Presentation of Nonalcoholic Fatty Liver Disease

A Clinical–Morphological Study on Cholestatic Presentation of Nonalcoholic Fatty Liver Disease

A prospective, multicentre, observational study of patients with chronic cholestatic liver diseases receiving Udiliv and reg; in India: splendid study

Defining Hepatic Dysfunction Parameters in Two Models of Fatty Liver Disease in Zebrafish Larvae

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