Hepatic Encephalopathy

Muñoz, Santiago J.

doi:10.1016/j.mcna.2008.03.009

Cited by 82 publications

(84 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The malaria-induced increase in the systemic ammonia levels of taut Ϫ/Ϫ mice ultimately contributes to injuries in other organs, which also suffer from the lowered taurine levels due to the breakdown of taurine homeostasis. In particular, it is known that increased ammonia levels lead to hepatic encephalopathy, characterized by astrocyte swelling and low-grade cerebral edema (19,36,55). Our data reveal that the brains of the taut Ϫ/Ϫ mice that succumbed to malaria were massively damaged.…”

Section: Discussionmentioning

confidence: 71%

“…P. chabaudi infections caused increased levels of ammonia in the blood of taut Ϫ/Ϫ mice at peak parasitemia (Table 1), suggesting undesired adverse effects on other organs. The brain is especially sensitive to ammonia intoxication, which eventually leads to hepatic encephalopathy (8,9,18,19,36). When we examined slices of cerebrum and cerebellum from taut Ϫ/Ϫ mice, which had succumbed to P. chabaudi infections during the crisis phase, destruction of the microvasculature was widespread (Fig.…”

Section: Course Of Infectionsmentioning

confidence: 99%

See 1 more Smart Citation

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

et al. 2010

View full text Add to dashboard Cite

Deletion of the taurine transporter gene (taut) results in lowered levels of taurine, the most abundant amino acid in mammals. Here, we show that taut ؊/؊ mice have lost their ability to self-heal blood-stage infections with Plasmodium chabaudi malaria. All taut ؊/؊ mice succumb to infections during crisis, while about 90% of the control taut ؉/؉ mice survive. The latter retain unchanged taurine levels even at peak parasitemia. Deletion of taut, however, results in the lowering of circulating taurine levels from 540 to 264 mol/liter, and infections cause additional lowering to 192 mol/liter. Peak parasitemia levels in taut ؊/؊ mice are approximately 60% higher than those in taut ؉/؉ mice, an elevation that is associated with increased systemic tumor necrosis factor alpha (TNF-␣) and interleukin-1␤ (IL-1␤) levels, as well as with liver injuries. The latter manifest as increased systemic ammonia levels, a perturbed capacity to entrap injected particles, and increased expression of genes encoding TNF-␣, IL-1␤, IL-6, inducible nitric oxide synthase (iNOS), NF-B, and vitamin D receptor (VDR). Autopsy reveals multiorgan failure as the cause of death for malaria-infected taut ؊/؊ mice. Our data indicate that taut-controlled taurine homeostasis is essential for resistance to P. chabaudi malaria. Taurine deficiency due to taut deletion, however, impairs the eryptosis of P. chabaudi-parasitized erythrocytes and expedites increases in systemic TNF-␣, IL-1␤, and ammonia levels, presumably contributing to multiorgan failure in P. chabaudi-infected taut ؊/؊ mice.

show abstract

Section: Discussionmentioning

confidence: 71%

Section: Course Of Infectionsmentioning

confidence: 99%

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

et al. 2010

View full text Add to dashboard Cite

show abstract

“…It can be defined as a neuropsychiatric syndrome caused by portosystemic venous shunting, 1 ranging from minimal to overt hepatic encephalopathy or profound coma. 2 Minimal hepatic encephalopathy is the mildest form of hepatic encephalopathy, and affected patients have no recognizable clinical symptoms of the disorder, but have subtle abnormalities (elicited by psychometric tests or electrophysiological techniques) in psychomotor speed, visuomotor activity, and response inhibition, as well as slowing of the electroencephalogram and prolongation of cognitive evoked potentials.…”

Section: Definition Pathogenesis and Diagnosis Of Hepatic Encephalomentioning

confidence: 99%

Rifaximin Treatment in Hepatic Encephalopathy

Sharma

Sharma²

2010

N Engl J Med

View full text Add to dashboard Cite

Hepatic encephalopathy is a challenging complication in patients with advanced liver disease. It can be defined as a neuropsychiatric syndrome caused by portosystemic venous shunting, ranging from minimal to overt hepatic encephalopathy or coma. Its pathophysiology is still unclear, although increased levels of ammonia play a key role. Diagnosis of hepatic encephalopathy is currently based on specific tests evaluating the neuropsychiatric state of patients and their quality of life; the severity of hepatic encephalopathy is measured by the West Haven criteria. Treatment of hepatic encephalopathy consists of pharmacological and corrective measures, as well as nutritional interventions. Rifaximin received approval for the treatment of hepatic encephalopathy in 2010 because of its few side effects and pharmacological benefits. The aim of this work is to review the use and efficacy of rifaximin both in acute and long-term management of hepatic encephalopathy. Treatment of overt hepatic encephalopathy involves management of the acute episode as well as maintenance of remission in those patients who have previously experienced an episode, in order to improve their quality of life. The positive effect of rifaximin in reducing health care costs is also discussed.

show abstract

“…However, neomycin therapy may be associated with some toxic side effects (Cordoba & Blei, 1997). More recently, rifaximin, a nonabsorbable derivative of the antibiotic rifamycin, has been shown to be effective in lowering blood ammonia and has proven to be of superior efficacy compared with lactulose (Bismuth et al, 2011;Munoz, 2008). Most of an orally administered dose is eliminated unchanged in the feces.…”

Section: Portal-systemic Encephalopathy (Pse)mentioning

confidence: 99%

Portal-Systemic Encephalopathy in Emergency Treatment of Cirrhosis and Bleeding Esophageal Varices

Orloff¹

2012

Miscellanea on Encephalopathies - A Second Look

View full text Add to dashboard Cite

Hepatic Encephalopathy

Cited by 82 publications

References 69 publications

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

Rifaximin Treatment in Hepatic Encephalopathy

Portal-Systemic Encephalopathy in Emergency Treatment of Cirrhosis and Bleeding Esophageal Varices

Contact Info

Product

Resources

About