The possible occurrence of “alcoholic hepatitis” in a patient with bulimia in the absence of diagnosable alcoholism

Cuellar, Rafael E.; Tarter, Ralph E.; Hays, Amy; Thiel, David H. Van

doi:10.1002/hep.1840070514

Cited by 13 publications

(6 citation statements)

References 44 publications

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“…Despite the fact that gradual weight loss improves liver tests among obese individuals, profound or rapid alterations in body weight can lead to NASH. [34][35][36][37] A 20-year-old woman who had been bulimic for 5 years developed severe NASH with Mallory bodies, sclerosis of the central vein, and cirrhosis. 36 Similar features have been described in a 23-year-old obese woman who developed NASH after repeated attempts at rapid weight reduction, including periods of total starvation lasting from 1 to 3 weeks.…”

Section: Gastroplasty and Other Causes Of Rapid Weight Lossmentioning

confidence: 99%

Etiopathogenesis of Nonalcoholic Steatohepatitis

Chitturi¹,

Farrell²

2001

Semin Liver Dis

607

447

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The definable causes of nonalcoholic steatohepatitis (NASH) include jejunoileal bypass surgery (JIB), other causes of rapid and profound weight loss in obese subjects, total parenteral nutrition, drugs, industrial toxins, copper toxicity, and disorders characterized by extreme insulin resistance. However, the etiopathogenesis in most cases of NASH appears multifactorial. Obesity, type 2 diabetes, and hypertriglyceridemia are often associated with hepatic steatosis, and although this does not invariably lead to NASH, the fatty liver is vulnerable to hepatocellular injury initiated by reactive oxygen species (ROS). It is critical to understand not only the triggers for hepatitis (injury and inflammation) in NASH but also how this is perpetuated as chronic liver disease. The present focus is on whether the biochemical processes that generate oxidative stress lead to hepatocyte injury and secondary recruitment of inflammation or whether inflammation is the primary mediator of liver cell injury. Insulin resistance is a reproducible pathogenic factor in NASH. It favors accumulation of free fatty acids in the liver and predisposes to oxidative stress by stimulating microsomal lipid peroxidases and by the direct effects of high insulin levels in decreasing mitochondrial beta-oxidation. CYP2E1 is normally suppressed by insulin but is invariably increased in the livers of patients with NASH. In rodent dietary models of steatohepatitis, CYP2E1 is the catalyst of microsomal lipid peroxidation, while in Cyp 2e1 nullizygous mice, CYP4A proteins are induced and function as alternative microsomal lipid peroxidases. Other studies implicate activation of peroxisome proliferator-activated receptor-alpha (PPAR alpha) as leading to NASH; PPAR alpha is a transcription factor that governs both microsomal (via CYP4A) and peroxisomal (beta-oxidation) pathways of lipid oxidation and ultimately production of ROS. Increased lipid peroxidation is a crucial difference between the livers of rodents with experimental NASH and those of ob/ob genetically obese mice that have uncomplicated steatosis. Administration of endotoxin, through the release of tumor necrosis factor-alpha (TNF-alpha), provokes liver inflammation with hepatocyte injury in the steatotic liver. This may be particularly relevant in JIB and has been suggested as a pathogenic mechanism in primary NASH. It has been proposed that inheriting one or more copies of the hemochromatosis gene, C282Y, promotes fibrotic progression in NASH because of increased hepatic iron deposition, but recent studies have failed to confirm this. The relationship between the severity of hepatitis in NASH and progression to cirrhosis implies that products of the inflammatory infiltrate play a role in fibrogenesis. In summary, NASH can be regarded as the hepatic consequence of the metabolic syndrome (or syndrome X). Attention should now shift from steatosis, a generally benign process that is less evident in the advanced stages of cirrhosis, to the mechanisms for hepatocellular injury, inflammation, and he...

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Section: Gastroplasty and Other Causes Of Rapid Weight Lossmentioning

confidence: 99%

Etiopathogenesis of Nonalcoholic Steatohepatitis

Chitturi¹,

Farrell²

2001

Semin Liver Dis

607

447

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“…Additionally, there are a number of drugs and occupational exposures that have been reported to cause steatosis or NASH (Table 1), and a number of other conditions have been described as risk factors for secondary NAFL. For example, several anecdotal reports suggest that small bowel resection and dramatic diet‐related weight loss can increase the likelihood of developing NASH 53,57–59 . In one study, 13% of adult patients maintained on total parenteral nutrition (TPN) for a mean of 29 months developed NASH, 60 and one report described the development of cirrhosis from long‐term TPN 61 .…”

Section: What Are the Risk Factors For Non‐alcoholic Fatty Liver Disementioning

confidence: 99%

“…For example, several anecdotal reports suggest that small bowel resection and dramatic diet-related weight loss can increase the likelihood of developing NASH. 53,[57][58][59] In one study, 13% of adult patients maintained on total parenteral nutrition (TPN) for a mean of 29 months developed NASH, 60 and one report described the development of cirrhosis from long-term TPN. 61 Several investigators have suggested that heterozygosity for the hemochromatosis gene C282Y may play a pathogenic role in the progression of fibrosis in NASH.…”

Section: What Are the Risk Factors For Non-alcoholic Fatty Liver Disementioning

confidence: 99%

Non‐alcoholic fatty liver disease: An overview

Mulhall

Ong

Younossi

2002

J of Gastro and Hepatol

183

138

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Non-alcoholic fatty liver disease (NAFL) includes a spectrum of clinicopathological conditions with increasing prevalence in the developed world. Although steatosis alone seems to have a benign course, those patients with the diagnosis of non-alcoholic steatohepatitis (NASH) can have a progressive course. Additionally, there is now evolving, indirect evidence that some of the patients with cryptogenic cirrhosis may be the result of 'burned-out' NASH. Although NAFL and NASH are associated with insulin-resistance syndrome, some patients with NAFL may have no obvious risk factors. Despite preliminary data from a number of pilot studies, no established therapies can be offered to patients with NASH. Over the next few years, a number of exciting research projects dealing with the epidemiology as well as the pathogenesis of NAFL are expected to be completed. It is anticipated that, through a better understanding of NAFL, more effective treatment protocols can be developed targeting only those patients with NASH that are at the highest risk for progression to cirrhosis and liver failure.

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“…It is also possible that eating disorders have a direct hepatotoxic effect independent of the additional insult from drugs or alcohol. For example, Cuellar, Tarter, Hays, and van Thiel (1987) reported a case of a 20-year-old woman with a history of anorexia nervosa and current bulimia who developed cirrhosis in the absence of any history, recent or remote, of ethanol abuse.…”

Section: Discussionmentioning

confidence: 96%