Steatonecrosis—mallory Body Type

Harinasuta, Udom; Chomet, Bernhard; Ishak, Kamal G.; Zimmerman, Hyman J.

doi:10.1097/00005792-196703000-00008

Cited by 80 publications

(15 citation statements)

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“…Very high levels of AST are characteristic of this syndrome, with values >3000 IU/ml being seen in >90% of cases. This contrasts with AST levels of 200–3000 IU/ml and <250 IU/ml in acute viral and acute alcoholic hepatitis, respectively ( Harinasuta et al , 1967 ; Rozen et al , 1970 ).…”

Section: Discussionmentioning

confidence: 95%

“…Although hepatic toxicity is normally seen in patients following deliberate overdose, toxicity has also been described in alcoholics taking paracetamol with therapeutic intent. Very high levels of AST are characteristic of this syndrome, with values >3000 IU/ml being seen in and <250 IU/ml in acute viral and acute alcoholic hepatitis, respectively (Harinasuta et al, 1967;Rozen et al, 1970).…”

Section: Discussionmentioning

confidence: 99%

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Acute liver failure induced by alcohol and paracetamol in an HCV‐infected haemophiliac

et al. 1998

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Paracetamol (acetaminophen) is frequently used by haemophiliacs in the management of acute or chronic pain, primarily due to its lack of adverse effects when taken at therapeutic doses. We describe acute hepatic and renal toxicity of paracetamol in a 36-year-old patient with haemophilia B, chronic hepatitis C and chronic alcohol abuse. Moderate doses of paracetamol (6 g/d for 4 d), taken with therapeutic intent, resulted in life-threatening organ dysfunction which gradually recovered with full supportive care.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Acute liver failure induced by alcohol and paracetamol in an HCV‐infected haemophiliac

et al. 1998

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“…Alcohol-induced hepatic injury has been called as steatonecrosis (Harinasuta et al, 1967) and steatohepatitis (Ludwig et al, 1980). The injury has characteristic histologic, clinical, and biochemical features (Christoffersen and Nielsen, 1972; French, 1981; French et al, 1993; Ishak et al, 1991; Maher and Friedman, 1995; Mendenhall, 1981; Rojkind, 1985).…”

Section: Lieber's and His Colleagues' Legacymentioning

confidence: 99%

Alcoholic and non-alcoholic steatohepatitis

Neuman

French

et al. 2014

Experimental and Molecular Pathology

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This paper is based upon the “Charles Lieber Satellite Symposia” organized by Manuela G. Neuman at the Research Society on Alcoholism (RSA) Annual Meetings, 2013 and 2014. The present review includes pre-clinical, translational and clinical research that characterize alcoholic liver disease (ALD) and non-alcoholic steatohepatitis (NASH). In addition, a literature search in the discussed area was performed. Strong clinical and experimental evidence lead to recognition of the key toxic role of alcohol in the pathogenesis of ALD. The liver biopsy can confirm the etiology of NASH or alcoholic steatohepatitis (ASH) and assess structural alterations of cells, their organelles, as well as inflammatory activity. Three histological stages of ALD are simple steatosis, ASH, and chronic hepatitis with hepatic fibrosis or cirrhosis. These latter stages may also be associated with a number of cellular and histological changes, including the presence of Mallory's hyaline, megamitochondria, or perivenular and perisinusoidal fibrosis. Genetic polymorphisms of ethanol metabolizing enzymes such as cytochrome p450 (CYP) 2E1 activation may change the severity of ASH and NASH. Alcohol mediated hepatocarcinogenesis, immune response to alcohol in ASH, as well as the role of other risk factors such as its comorbidities with chronic viral hepatitis in the presence or absence of human deficiency virus are discussed. Dysregulation of hepatic methylation, as result of ethanol exposure, in hepatocytes transfected with hepatitis C virus (HCV), illustrates an impaired interferon signaling. The hepatotoxic effects of ethanol undermine the contribution of malnutrition to the liver injury. Dietary interventions such as micro and macronutrients, as well as changes to the microbiota are suggested. The clinical aspects of NASH, as part of metabolic syndrome in the aging population, are offered. The integrative symposia investigate different aspects of alcohol-induced liver damage and possible repair. We aim to (1) determine the immuno-pathology of alcohol-induced liver damage, (2) examine the role of genetics in the development of ASH, (3) propose diagnostic markers of ASH and NASH, (4) examine age differences, (5) develop common research tools to study alcohol-induced effects in clinical and pre-clinical studies, and (6) focus on factors that aggravate severity of organ-damage. The intention of these symposia is to advance the international profile of the biological research on alcoholism. We also wish to further our mission of leading the forum to progress the science and practice of translational research in alcoholism.

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“…The earlier severe prognostic implications of the MB in ALD (130) have undergone reassessment (131)(132)(133). There now seems little doubt that MBs do not have the adverse prognostic impact previously assumed by autopsy studies.…”

Section: Prognostic Importance Of the Mb All)mentioning

confidence: 99%

“…There now seems little doubt that MBs do not have the adverse prognostic impact previously assumed by autopsy studies. Several analyses (131,133,138) have suggested that MBs are associated with relatively mild cases of AH and a 6-mo mortality rate as low as 4% to 8% (131,132,134,136,138). Furthermore, some alcoholic patients with the clinical features of AH have not shown the characteristic MB in biopsy material (133,, and histological damage persists for 3 to 6 mo regardless of MB content.…”

Section: Prognostic Importance Of the Mb All)mentioning

confidence: 99%

The Mallory body: Theories on development and pathological significance (part 2 of a literature survey)

Jensen

1994

Hepatology

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Drawing on data from a previously published literature survey on the clinical and experimental epidemiology of the Mallory body, we discuss current theories on its development in a pro et contra manner. Conclusions have been largely left open to the interpretations of the reader because many are still speculative. The main results of this study characterize Mallory bodies as stereotypical histological byproducts to diverse hepatic injuries (mostly alcohol associated) of questionable pathogenic importance. The temporal characteristics of Mallory bodies cast doubt on their role in hepatic neoplasia both as a disease marker and a causative agent, and prognosis studies suggest that they may be considered preterminal markers in some nonalcoholic liver diseases but remain prognostically unimportant in most studies on alcoholic patients. By similar line of inquiry, no consistent relationships may be found with disease severity or duration in alcoholic liver diseases. The roles of vitamin A deficiency and protein-calorie malnutrition are circumstantial. Drugs known to have calcium-antagonist properties and the physiological characteristics of the stress-response protein ubiquitin support the concept of defective protein systems in Mallory body pathogenesis. Disproportionate hepatic copper accumulation seems both epidemiologically and topographically associated with Mallory bodies, but these connections are largely unsupported by exposure studies. Many arguments still downplay the importance of uncoordinated changes in hepatic oxygen delivery and consumption, but ischemia-reperfusion studies suggest a role of oxygen-derived free radicals in the liver injuries under scrutiny. Finally, the role of Mallory bodies in the control system of hepatocyte function is addressed, and indirect evidence lends credence to a cybernetic approach in future study designs. It is reasonable to assume that different elements of a multifactorial setting operate with varying intensity over time as this may account for some of the controversies that exist. In conclusion, the biological significance of Mallory bodies is still mystery. It is not known whether Mallory bodies represent an epiphenomenon or play a role themselves in the initiation and continuation of liver damage.

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Steatonecrosis—mallory Body Type

Cited by 80 publications

References 0 publications

Acute liver failure induced by alcohol and paracetamol in an HCV‐infected haemophiliac

Acute liver failure induced by alcohol and paracetamol in an HCV‐infected haemophiliac

Alcoholic and non-alcoholic steatohepatitis

The Mallory body: Theories on development and pathological significance (part 2 of a literature survey)

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