Pathology of steatohepatitis

Brunt, Elizabeth M.; Tiniakos, Dina

doi:10.1053/bega.2002.0326

Cited by 65 publications

(37 citation statements)

References 91 publications

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“…It is notable that the areas exhibiting the most lipids were around the central veins because this region is particularly susceptible to metabolic perturbations and shows the earliest onset of lipid accumulation during steatosis. 36 The hepatic changes of excess lipid and inflammation are consistent with development of NASH, an advanced stage of NAFLD. 37 If left untreated, NASH can lead to irreversible fibrosis, cirrhosis, and, in some cases, hepatic carcinoma.…”

Section: Discussionmentioning

confidence: 93%

Spinal Cord Injury Causes Chronic Liver Pathology in Rats

Sauerbeck

Laws

Bandaru

et al. 2015

Journal of Neurotrauma

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Traumatic spinal cord injury (SCI) causes major disruption to peripheral organ innervation and regulation. Relatively little work has investigated these post-SCI systemic changes, however, despite considerable evidence that multiple organ system dysfunction contributes to chronic impairments in health. Because metabolic dysfunction is common after SCI and the liver is a pivotal site for metabolic homeostasis, we sought to determine if liver pathology occurs as a result of SCI in a rat spinal contusion model. Histologic evidence showed excess lipid accumulation in the liver for at least 21 days post-injury after cervical or midthoracic SCI. Lipidomic analysis revealed an acute increase in hepatic ceramides as well as chronically elevated lactosylceramide. Post-SCI hepatic changes also included increased proinflammatory gene expression, including interleukin (IL)-1a, IL-1b, chemokine ligand-2, and tumor necrosis factor-a mRNA. These were coincident with increased CD68 + macrophages in the liver through 21 days post-injury. Serum alanine transaminase, used clinically to detect liver damage, was significantly increased at 21 days post-injury, suggesting that early metabolic and inflammatory damage preceded overt liver pathology. Surprisingly, liver inflammation was even detected after lumbar SCI. Collectively, these results suggest that SCI produces chronic liver injury with symptoms strikingly similar to those of nonalcoholic steatohepatitis (fatty liver disease). These clinically significant hepatic changes after SCI are known to contribute to systemic inflammation, cardiovascular disease, and metabolic syndrome, all of which are more prevalent in persons with SCI. Targeting acute and prolonged hepatic pathology may improve recovery and reduce long-term complications after SCI.

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Section: Discussionmentioning

confidence: 93%

Spinal Cord Injury Causes Chronic Liver Pathology in Rats

Sauerbeck

Laws

Bandaru

et al. 2015

Journal of Neurotrauma

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“…However, this does not seem to be adequately justified (Brunt & Tiniakos, 2005;Cortez-Pinto et al, 2006). Mild steatosis affects < 33% of the parenchymal surface, moderate steatosis involves 33 -66%, and severe steatosis covers > 66% (Brunt, 2001(Brunt, , 2002(Brunt, , 2005a(Brunt, , 2005bBrunt et al, 2003Brunt et al, , 2004Brunt & Tiniakos, 2002Burt et al, 1998). The steatosis (of variable degree) is accompanied by usually slight mixed-cell inflammatory infiltrates (neutrophilic, granulocytic and lymphocytic cells) in the hepatic lobes.…”

Section: Diagnostic Criteriamentioning

confidence: 99%

“…As the disease progresses, portal fibrosis with formation of portoportal and portocentral bridging septa arises. No single one of these structures should be used as a so-called 'minimal criterion' without the simultaneous demonstration of ballooning (Brunt, 2001(Brunt, , 2002(Brunt, , 2005a(Brunt, , 2005bBrunt et al, 2003Brunt et al, , 2004Brunt & Tiniakos, 2002Burt et al, 1998Neuschwander-Tetri & Caldwell, 2003. The Cleveland group suggested classification of NAFLD (on prognostic grounds) into the following types:…”

Section: Diagnostic Criteriamentioning

confidence: 99%

“…Type 1, simple steatosis Type 2, steatosis and inflammation Type 3, steatosis and cell swelling (ballooning) Type 4, steatosis, cell swelling (ballooning), and MDB or fibrosis Progression to cirrhosis is found predominantly in types 3 and 4, both of which correspond to the typical histopathological picture of NASH (Brunt, 2001(Brunt, , 2002(Brunt, , 2005aBrunt et al, 2003Brunt et al, , 2004Brunt & Tiniakos, 2002Neuschwander-Tetri & Caldwell, 2003Falck-Ytter et al, 2001Matteoni et al, 1999). For morphological manifestations of paediatric NASH (see 5.3).…”

Section: Diagnostic Criteriamentioning

confidence: 99%

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Histopathological diagnosis of non-alcoholic and alcoholic fatty liver disease

et al. 2011

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“…Deposition of misfolded proteins as cytoplasmic aggregates is also a key feature of several chronic liver diseases, particularly alcoholic and nonalcoholic steatohepatitis (NASH) [54][55][56][57] . Alcoholic steatohepatitis (ASH) is a severe necroinflammatory liver disorder, linking the still reversible fatty liver with irreversible liver cirrhosis.…”

Section: Alcoholic and Nonalcoholic Steatohepatitis And Other Liver Dmentioning

confidence: 99%

How a Cell Deals with Abnormal Proteins

Aigelsreiter

Janig²,

Stumptner³

et al. 2007

Pathobiology

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Defective protein folding is responsible for many diseases. Although these diseases seem to be quite diverse at the first glance, there is evidence for common pathogenetic principles. The basis of the pathological changes is the cell’s inability to prevent protein misfolding, to revert misfolded proteins to normal or to eliminate misfolded proteins by degradation. This could result in deposition of potentially cytotoxic protein aggregates (protein aggregation diseases). Chronic degenerative diseases of the central nervous system (e.g. Alzheimer’s and Parkinson’s disease), the amyloidoses, but also chronic liver diseases, for example alcoholic and nonalcoholic steatohepatitis, belong to this category of disorders. This review highlights general pathogenic principles of protein aggregation diseases based on immunohistochemical and biochemical studies as well as observations in a mouse model for protein aggregation in the context of alcoholic and nonalcoholic steatohepatitis. The cellular defense mechanisms involved in protein quality control as well as the pathogenesis of protein aggregation diseases will be discussed.

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Pathology of steatohepatitis

Cited by 65 publications

References 91 publications

Spinal Cord Injury Causes Chronic Liver Pathology in Rats

Spinal Cord Injury Causes Chronic Liver Pathology in Rats

Histopathological diagnosis of non-alcoholic and alcoholic fatty liver disease

How a Cell Deals with Abnormal Proteins

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