Reversibility of hepatic encephalopathy after liver transplantation

Atluri, Dileep; Asgeri, Mehrdad; Mullen, Kevin D.

doi:10.1007/s11011-010-9178-x

Cited by 31 publications

(15 citation statements)

References 12 publications

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“…Only 13% of our patients qualified for mild cognitive impairment. There are many possible causes of central nervous system deficits, such as preexisting events (eg, alcoholism, trauma, stroke), intraoperative brain injury (eg, hypotension, ischemia), persistent portosystemic shunts, and toxic effects of immunosuppression 24. Although we cannot exclude participation of these factors, our data indicate that susceptibility to persistent cognitive deficits is higher among patients with alcohol‐induced disease, diabetes mellitus, and prior episodes of HE.…”

Section: Discussionmentioning

confidence: 70%

Apolipoprotein B–dependent hepatitis C virus secretion is inhibited by the grapefruit flavonoid naringenin

et al. 2008

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Section: Discussionmentioning

confidence: 70%

Apolipoprotein B–dependent hepatitis C virus secretion is inhibited by the grapefruit flavonoid naringenin

et al. 2008

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“…Liver transplantation is currently the only remedy for patients with HE. However, enough exceptions to the rule that HE is reversible by liver transplantation have been reported4748. Given the universal shortage of donors, this is most undesirable.…”

Section: Discussionmentioning

confidence: 99%

Nitrosative Stress-Induced Disruption of Baroreflex Neural Circuits in a Rat Model of Hepatic Encephalopathy: A DTI Study

Tsai

Chan

et al. 2017

Sci Rep

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The onset of hepatic encephalopathy (HE) in liver failure is associated with high mortality; the underlying mechanism is undecided. Here we report that in an acute liver failure model employing intraperitoneal administration of thioacetamide in Sprague-Dawley rats, diffusion weighted imaging revealed a progressive reduction in apparent diffusion coefficient in the brain stem. Diffusion tensor imaging further showed that the connectivity between nucleus tractus solitarii (NTS), the terminal site of baroreceptor afferents in brain stem and rostral ventrolateral medulla (RVLM), the origin of sympathetic innervation of blood vessels, was progressively disrupted until its disappearance, coincidental with the irreversible cessation of baroreflex-mediated sympathetic vasomotor tone signifying clinically the occurrence of brain death. In addition, superoxide, nitric oxide, peroxynitrite and ammonia levels in the NTS or RVLM were elevated, alongside swelling of astroctytes. A scavenger of peroxynitrite, but not an antioxidant, delivered intracisternally reversed all these events. We conclude that nitrosative stress because of augmented peroxynitrite related to accumulation of ammonia and swelling of astrocytes in the NTS or RVLM, leading to cytotoxic edema in the brain stem and severance of the NTS-RVLM connectivity, underpins the defunct baroreflex-mediated sympathetic vasomotor tone that accounts for the high mortality associated with HE.

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“…This accumulation is shown to be reversible on magnetic resonance imaging (MRI) of the brain after liver transplantation. 25 This deposition in the basal ganglia was thought to be contributing to extra-pyramidal symptoms in some patients with HE.…”

Section: Manganesementioning

confidence: 99%

Pathogenesis, Diagnosis, and Treatment of Hepatic Encephalopathy

Atluri¹,

Prakash²,

Mullen³

2011

Journal of Clinical and Experimental Hepatology

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Hepatic encephalopathy (HE) is a neuropsychiatric disorder seen in patients with advanced liver disease or porto-systemic shunts. Based on etiology and severity of HE, the World Congress of Gastroenterology has divided HE into categories and sub-categories. Many user-friendly computer-based neuropsychiatric tests are being validated for diagnosing covert HE. Currently, emphasis is being given to view HE deficits as a continuous spectrum rather than distinct stages. Ammonia is believed to play crucial role in pathogenesis of HE via astrocyte swelling and cerebral edema. However, evidence has been building up which supports the synergistic role of oxidative stress, inflammation and neurosteroids in pathogenesis of HE. At present, treatment of HE aims at decreasing the production and intestinal absorption of ammonia. But as the role of new pathogenetic mechanisms becomes clear, many potential new treatment strategies may become available for clinician.

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Reversibility of hepatic encephalopathy after liver transplantation

Cited by 31 publications

References 12 publications

Apolipoprotein B–dependent hepatitis C virus secretion is inhibited by the grapefruit flavonoid naringenin

Apolipoprotein B–dependent hepatitis C virus secretion is inhibited by the grapefruit flavonoid naringenin

Nitrosative Stress-Induced Disruption of Baroreflex Neural Circuits in a Rat Model of Hepatic Encephalopathy: A DTI Study

Pathogenesis, Diagnosis, and Treatment of Hepatic Encephalopathy

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