Hepatic Encephalopathy

Butterworth, Roger F.; Vaquero, Javier

doi:10.1002/9780470747919.ch39

Cited by 10 publications

(14 citation statements)

References 144 publications

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“…In clinical practice, lactulose is considered the gold standard for HE treatment, but its side effects may limit its clinical use. 5,17,18 The development of safe and well-tolerated alternative treatments is therefore justified. The use of probiotics was proposed as a potential alternative treatment for HE, based on previous experimental and clinical studies.…”

Section: Discussionmentioning

confidence: 99%

“…(HEPATOLOGY 2008;48:1184-1192 H yperammonemia (HA) is a well-known complication of acute and chronic liver diseases and plays a central role in the pathogenesis of hepatic encephalopathy (HE). [1][2][3][4][5] This neurological dysfunction results, at least in part, from an increase in plasma ammonia level and the severity of the symptoms correlates with blood ammonia level. 6-9 Animal models used in studying hyperammonemic disorders are multiple: fulminant hepatic failure, 10 chronic liver failure, 11 or urea cycle deficiency.…”

mentioning

confidence: 99%

“…[1][2][3][4][5] This neurological dysfunction results, at least in part, from an increase in plasma ammonia level and the severity of the symptoms correlates with blood ammonia level. [6][7][8][9] Animal models used in studying hyperammonemic disorders are multiple: fulminant hepatic failure, 10 chronic liver failure, 11 or urea cycle deficiency.…”

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confidence: 99%

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Control of acute, chronic, and constitutive hyperammonemia by wild-type and genetically engineered Lactobacillus plantarum in rodents

et al. 2008

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Hyperammonemia is a common complication of acute and chronic liver diseases. Often accompanied with side effects, therapeutic interventions such as antibiotics or lactulose are generally targeted to decrease the intestinal production and absorption of ammonia. In this study, we aimed to modulate hyperammonemia in three rodent models by administration of wild-type Lactobacillus plantarum, a genetically engineered ammonia hyperconsuming strain, and a strain deficient for the ammonia transporter. Wild-type and metabolically engineered L. plantarum strains were administered in ornithine transcarbamoylase-deficient Sparse-fur mice, a model of constitutive hyperammonemia, in a carbon tetrachloride rat model of chronic liver insufficiency and in a thioacetamide-induced acute liver failure mice model. Constitutive hyperammonemia in Sparse-fur mice and hyperammonemia in a rat model of chronic hepatic insufficiency were efficiently decreased by Lactobacillus administration. In a murine thioacetamide-induced model of acute liver failure, administration of probiotics significantly increased survival and decreased blood and fecal ammonia. The ammonia hyperconsuming strain exhibited a beneficial effect at a lower dose than its wild-type counterpart. Improved survival in the acute liver failure mice model was associated with lower blood ammonia levels but also with a decrease of astrocyte swelling in the brain cortex. Modulation of ammonia was abolished after administration of the strain deficient in the ammonium transporter. Intestinal pH was clearly lowered for all strains and no changes in gut flora were observed. Conclusion: Hyperammonemia in constitutive model or after acute or chronic induced liver failure can be controlled by the administration of L. plantarum with a significant effect on survival. The mechanism involved in this ammonia decrease implicates direct ammonia consumption in the gut. (HEPATOLOGY 2008;48:1184-1192 H yperammonemia (HA) is a well-known complication of acute and chronic liver diseases and plays a central role in the pathogenesis of hepatic encephalopathy (HE). [1][2][3][4][5] This neurological dysfunction results, at least in part, from an increase in plasma ammonia level and the severity of the symptoms correlates with blood ammonia level. 6-9 Animal models used in studying hyperammonemic disorders are multiple: fulminant hepatic failure, 10 chronic liver failure, 11 or urea cycle deficiency. 12 Ammonia is produced by many tissues but its major external source results from deaminase and urease activities of the gut flora. Although its absorption occurs through the intestinal epithelium, ammonia is carried by the portal vein into the liver where it is metabolized into urea. 13 Classical treatments of HE, except through liver transplantation and liver replacement therapies, consist in decreasing the ammonia production of urease-positive bacteria by antibiotics or decreasing the ammonia absorption into the gut by acidifying the colon content with nonabsorbable sugars such as lactulose. 4,[13][14][1...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Control of acute, chronic, and constitutive hyperammonemia by wild-type and genetically engineered Lactobacillus plantarum in rodents

et al. 2008

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“…The brain relies on a healthy liver to detoxify circulating toxins which are capable of entering the brain and leading to functional impairment and hepatic encephalopathy (HE) (Butterworth 2003). HE is characterized with a spectrum of symptoms ranging from personality and mood changes, night-time sleep disturbances, alterations in concentration and attention, severe cognitive effects, coma and death (Hazell and Butterworth 1999).…”

Section: Introductionmentioning

confidence: 99%

Portacaval anastomosis-induced hyperammonemia does not lead to oxidative stress

et al. 2010

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Yang, X. et al., 2010. Portacaval anastomosis-induced hyperammonemia does not lead to oxidative stress. Metabolic Brain Disease, 25(1), ABSTRACTAmmonia is neurotoxic and believed to play a major role in the pathogenesis of hepatic encephalopathy (HE). It has been demonstrated, in vitro and in vivo, that acute and high ammonia treatment induces oxidative stress. Reactive oxygen species (ROS) are highly reactive and can lead to oxidization of proteins resulting in protein damage. The present study was aimed to assess oxidative status of proteins in plasma and brain (frontal cortex) of rats with 4-week portacaval anastomosis (PCA). Markers of oxidative stress, 4-hydroxy-2-nonenal (HNE) and carbonylation were evaluated by immunoblotting in plasma and frontal cortex. Western blot analysis did not demonstrate a significant difference in either HNE-linked or carbonyl derivatives on proteins between PCA and sham-operated control rats in both plasma and frontal cortex. The present study suggests PCA-induced hyperammonemia does not lead to systemic or central oxidative stress.

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“…Of the possible neurotoxins implicated in hepatic encephalopathy (HE), ammonia was the first to be incriminated (Eck, 1877)and finds itself still the leading candidate as a key factor in its pathogenesis (Butterworth et al, 1987, Butterworth, 1994Lockwood et al, 1991). Recent studies using Positron Emission Tomography (PET) and 13 NH3 confirm that, in chronic liver failure, brain utilizes ammonia at increased rates and that the blood-brain barrier becomes more permeable to ammonia (Lockwood et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Michalak

Pannunzio

et al. 1998

Metabolic Brain Disease

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Strategies aimed at the lowering of blood ammonia remain the treament of choice in portal-systemic encephalopathy (PSE). L-ornithine-L-aspartate (OA) has recently been shown to be effective in the prevention of ammonia-precipitated coma in humans with PSE. These findings prompted the study of mechanisms of the protective effect of OA in portacaval-shunted rats in which reversible coma was precipitated by ammonium acetate administration (3.85 mmol/kg i.p.). OA infusions (300 mg/kg/h, i.v) offered complete protection in 12/12 animals compared to 0/12 saline-infused controls. This protective effect was accompanied by significant reductions of blood ammonia, concomitant increases of urea production and significant increases in blood and cerebrospinal fluid (CSF) glutamate and glutamine. Increased CSF concentrations of leucine and alanine also accompanied the protective effect of OA. These findings demonstrate the therapeutic efficacy of OA in the prevention of ammonia-precipitated coma in portacaval-shuntedrats and suggest that this protective effect is both peripherally-mediated (increased urea and glutamine synthesis) and centrally-mediated (increased glutamine synthesis).

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Hepatic Encephalopathy

Cited by 10 publications

References 144 publications

Control of acute, chronic, and constitutive hyperammonemia by wild-type and genetically engineered Lactobacillus plantarum in rodents

Control of acute, chronic, and constitutive hyperammonemia by wild-type and genetically engineered Lactobacillus plantarum in rodents

Portacaval anastomosis-induced hyperammonemia does not lead to oxidative stress

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