Pathogenesis of Hepatic Coma

Zieve, Leslie; Nicoloff, Demétre M.

doi:10.1146/annurev.me.26.020175.001043

Cited by 84 publications

(12 citation statements)

References 56 publications

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“…Milk proteins which generate less ammonia than do blood proteins are tolerated better than meat by cirrhotics with significant portal-systemic shunting (2). Bacterial action is not the only source of ammonia from the gut.…”

Section: Acidosismentioning

confidence: 99%

“…Further clinical evidence of the role of ammonia is that the best positive correlations between severity of hepatic encephalopathy and any biochemical parameters are with spinal fluid glutamine and a-ketoglutaramate, which reflect the brain ammonia (2).…”

Section: Acidosismentioning

confidence: 99%

“…Second, the blood ammonia concentration correlates poorly with the existence or severity of hepatic encephalopathy (2,8). This discrepancy is readily explained by the fact that only a small portion of ammonia that passes through the circulation gets to the brain.…”

Section: Acidosismentioning

confidence: 99%

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The mechanism of hepatic coma†

Zieve

1981

Hepatology

157

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Section: Acidosismentioning

confidence: 99%

Section: Acidosismentioning

confidence: 99%

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The mechanism of hepatic coma†

Zieve

1981

Hepatology

157

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“…There is evidence that short chain fatty acids, phenols, bile salts, 'middle molecules' or mercaptans may have a synergistic role, particularly in relationship to the toxicity of ammonia [5]-Metabolic abnormalities such as hypokalaemia, alkalosis, hypovolaemia, hypoglycaemia and hypoxia can precipitate encephalopathy in patients. In addition, correction of these can reverse the encephalopathic state without altering the underlying hepatic disease [2].…”

Section: Synergqstic Toxinsmentioning

confidence: 99%

Neurochemical studies of hepatic encephalopathy

Maddison

1992

Drug and Alcohol Review

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Despite intensive research, the neurochemical basis of hepatic encephalopathy (HE) has not been defined. Theories that are currently favoured to explain the cerebral dysfunction that accompanies acute or chronic hepatic failure include: (1) ammonia acting as the putative neurotoxin; (2) perturbed monoamine neutrotransmission as a result of altered plasmo amino acid metabolism; (3) an imbalance between excitatory amino acid neurotransmission, mediated by glutamate, and inhibitory amino acid neurotransmission, mediated by gamma-aminobutyric acid (GABA); and (4) increased cerebral concentrations of an endogenous benzodiazepine-like substance. Studies of amino acid neurotransmitter receptors in HE have yielded conflicting results. The majority of studies in different animal models of acute and chronic HE and in patients have reported that brain GABA receptor density and affinity are unchanged. There have been fewer studies of excitatory amino acid receptors and these have also yielded conflicting results. However, the majority suggest that components of the glutamate receptor system are perturbed in HE. Further investigation is required to determine the significance of these findings to the pathogenesis of HE.

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“…However, it is known that several agents such as phenolic compounds (1), ammonia, fatty acids, bile acids, and mercaptans (2) for example are present in dramatically increased amounts in the serum of patients in liver coma. In particular, our knowledge concerning the mechanism of necrosis in fulminant liver failure and the accompanying endogenous toxicological problems is far from complete.…”

Section: Introductionmentioning

confidence: 99%

Hepatotoxic Effects of Sera from Patients with Fulminant Hepatitis B on Isolated Rat Hepatocytes in Culture

Haas¹,

Holloway²,

Osterthun³

et al. 1981

CCLM

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The hepatotoxicity of sera from patients with terminal fulminant hepatic failure has been investigated by cell culture techniques. It could be shown that both untreated and heat-treated sera are cytotoxic in nature. Compared with the action of sera from healthy individuals on liver cells in primary monolayer culture, the pathological sera exhibited significantly different behaviour with respect to morphological and biochemical parameters such as cell adhesion, growth and proliferation, and enzyme release. Hepatotoxische Wirkung von Seren von Patienten mit fulminanter Hepatitis B auf isolierte Hepatocyten in KulturZusammenfassung: Seren von Patienten mit akutem Leberversagen nach Hepatitis B wurden mit Hilfe von Zellkulturtechniken hinsichtlich ihrer Hepatotoxizität untersucht. Es konnte gezeigt werden, daß sowohl unbehandelte als auch hitze-behandelte Seren cytotoxisch wirken. Verglichen mit Normalseren beeinflussen pathologische Seren in erheblich stärkerem Maße das morphologische und biochemische Verhalten der Leberzellen in Kultur, wie Zell-Adhäsion, Wachstum und Zellteilung und Enzymaustritt.

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Pathogenesis of Hepatic Coma

Cited by 84 publications

References 56 publications

The mechanism of hepatic coma†

The mechanism of hepatic coma†

Neurochemical studies of hepatic encephalopathy

Hepatotoxic Effects of Sera from Patients with Fulminant Hepatitis B on Isolated Rat Hepatocytes in Culture

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