Acetyl-<scp>l</scp>-carnitine reduces depression and improves quality of life in patients with minimal hepatic encephalopathy

Malaguarnera, Mariano; Bella, Rita; Vacante, Marco; Giordano, Maria; Malaguarnera, Giulia; Gargante, Maria Pia; Motta, Massimo; Mistretta, Antonio; Rampello, Liborio; Pennisi, Giovanni

doi:10.3109/00365521.2011.565067

Cited by 71 publications

(46 citation statements)

References 45 publications

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“…Studies by Malaguarnera et al [82], investigated the suggested idea that L-acetylcarnitine improves blood ammonia and cognitive functions in cirrhotic patients with minimal HE. In this study, a significant clinical improvement in the neuropsychological status of the patient was observed including cognitive function, energy levels and emotional health.…”

Section: L-carnitinementioning

confidence: 98%

Pharmacotherapy for hyperammonemia

Hadjihambi

Khetan

Jalan

2014

Expert Opinion on Pharmacotherapy

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Lactulose and rifaximin have a proven role as measures to use for secondary prophylaxis and are the mainstay of current therapy. The use of molecular adsorbent recirculating system in patients with severe HE has been proven to be efficacious, but through mechanisms that appear to be independent of ammonia. The main challenge that faces the further development of treatments for HE is finding appropriate end points, and the next step would be to provide evidence of the effectiveness of established treatments and define the role of emerging new treatments.

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Section: L-carnitinementioning

confidence: 98%

Pharmacotherapy for hyperammonemia

Hadjihambi

Khetan

Jalan

2014

Expert Opinion on Pharmacotherapy

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“…The efficacy of dopaminergic drugs on motor symptoms in these patients is uncertain. For the patient with minimal or covert HE, there is evidence that they improve with disaccharides [147] and rifaximin [148], as well as LOLA [149], pre/probiotics [150], and acetylcarnitine [151]. However, because MHE has a less severe clinical impact on patients and their caregivers than overt HE [152], a reasonable approach aiming at minimizing drug use and reducing costs is shown in Figure 11.6.…”

Section: Treatmentmentioning

confidence: 99%

Hepatic encephalopathy

Amodio¹

2015

Cirrhosis: A Practical Guide to Management

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“…Serum Gamma-Glutamyltransferase (GGT) is a commonly used marker of alcohol abuse, may be an early indicator of liver damage and averaged 576 U/L (9 – 48 U/L reference range (Staff, 2015)) in subjects with alcoholic fatty liver disease (Nishimura and Teschke, 1983). Liver function tests were disrupted in a cross-section of patients with hepatic encephalopathy, levels of serum bilirubin averaged 5.5 mg/dl (0.1 – 1.2 mg/dl reference range (Staff, 2015)), albumin levels of 29 g/L (3.5 – 5.0 g/L reference range (Staff, 2015)) blood urea nitrogen 26 mg/dl (7 – 20 mg/dl (Staff, 2013)), Alkaline phosphatase 202 U/L (reference range 45 – 115 U/L (Staff, 2015)) alanine aminotransferase (ALT) of 117 U/L (7 – 55 U/L reference range (Staff, 2015))(Bustamante et al, 1999, Malaguarnera et al, 2011, Behar et al, 1999) and cholesterol levels of 113 mg/dl (< 200 mg/dl for health subjects)(Akriviadis et al, 2000, Bustamante et al, 1999, Malaguarnera et al, 2011, Behar et al, 1999). Oxidative stress is also a common hallmark of hepatic encephalopathy and results in decreased levels of brain glutathione (Lemberg and Fernandez, 2009).…”

Section: Introductionmentioning

confidence: 99%

A neurotoxic alcohol exposure paradigm does not induce hepatic encephalopathy

Hashimoto

Wiren

Wilhelm

2016

Neurotoxicology and Teratology

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Alcohol abuse is associated with neurological dysfunction, brain morphological deficits and frank neurotoxicity. Although these disruptions may be a secondary effect due to hepatic encephalopathy, no clear evidence of causality is available. This study examined whether a 72 h period of alcohol intoxication known to induce physical dependence, followed by a single withdrawal, was sufficient to induce signs of hepatic encephalopathy in male and female mice. Animals were continuously intoxicated via alcohol vapor inhalation, a procedure previously shown to induce significant neurotoxicity in female mice. At peak synchronized withdrawal (8 hours following the end of alcohol exposure), blood samples were taken and levels of several liver-regulated markers and brain swelling were characterized. Glutathione levels were also determined in the medial frontal cortex (mFC) and hippocampus. Results revealed elevated levels of cholesterol, albumin, alkaline phosphatase (ALP), alanine aminotransferase (ALT) and decreased levels of blood urea nitrogen and total bilirubin in alcohol-exposed male and female groups compared to controls. Brain water weight was not affected by alcohol exposure, though males tended to have slightly more water weight overall. Alcohol exposure led to reductions in tissue levels of glutathione in both the hippocampus and mFC which may indicate increased oxidative stress. Combined, these results suggest that hepatic encephalopathy does not appear to play a significant role in the neurotoxicity observed following alcohol exposure in this model.

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Acetyl-l-carnitine reduces depression and improves quality of life in patients with minimal hepatic encephalopathy

Cited by 71 publications

References 45 publications

Pharmacotherapy for hyperammonemia

Pharmacotherapy for hyperammonemia

Hepatic encephalopathy

A neurotoxic alcohol exposure paradigm does not induce hepatic encephalopathy

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