<scp>l</scp>‐ornithine‐<scp>l</scp>‐aspartate for hepatic encephalopathy in patients with cirrhosis: A meta‐analysis of randomized controlled trials

Bai, Ming; Yang, Zhiping; Qi, Xingshun; Fan, Daiming; Han, Guohong

doi:10.1111/jgh.12142

Cited by 88 publications

(76 citation statements)

References 33 publications

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“…Thus, it was concluded that hyperammonaemia may cause central fatigue. Since in most experimental studies [7,35,42,44,48] the greatest effect on ammonia reduction was achieved with L-ornithine L-aspartate (OA), it seems likely that oral intake of BCAA together with OA may reduce ammonia accumulation and cerebral absorption, thereby delaying fatigue.…”

Section: Introductionmentioning

confidence: 99%

Effects of supplementation with branched chain amino acids and ornithine aspartate on plasma ammonia and central fatigue during exercise in healthy men

Mikulski¹,

Dąbrowski²,

Hilgier³

et al. 2015

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Section: Introductionmentioning

confidence: 99%

Effects of supplementation with branched chain amino acids and ornithine aspartate on plasma ammonia and central fatigue during exercise in healthy men

Mikulski¹,

Dąbrowski²,

Hilgier³

et al. 2015

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“…Treatment with LOLA demonstrated a significant improvement in MHE, diminished serum ammonia levels, and no increase in adverse reactions. 59 Analysis of individual studies revealed a reduction in abnormal neuropsychological testing and increased HRQoL. Further, Ndhara et al reported the effect of LOLA administration on the nutritional status of patients diagnosed with MHE.…”

Section: Lola (L-ornithine-l-aspartate)mentioning

confidence: 98%

“…Therefore, LOLA lowers plasma ammonia concentrations by enhancing metabolism of ammonia to glutamine. 59 In a meta-analysis, Bai et al evaluated 8 randomized controlled trials (total, N = 646 patients-46% diagnosed with MHE) assessing the efficacy of LOLA compared to placebo in patients with cirrhosis. Treatment with LOLA demonstrated a significant improvement in MHE, diminished serum ammonia levels, and no increase in adverse reactions.…”

Section: Lola (L-ornithine-l-aspartate)mentioning

confidence: 99%

Management of Covert Hepatic Encephalopathy

Waghray

Mullen

2015

Journal of Clinical and Experimental Hepatology

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Hepatic encephalopathy is a reversible progressive neuropsychiatric disorder that encompasses a wide clinical spectrum. Covert hepatic encephalopathy is defined as patients with minimal hepatic encephalopathy and Grade I encephalopathy by West-Haven Criteria. Terminology such as "sub-clinical", "latent", and "minimal" appear to trivialize the disease and have been replaced by the term covert. The lack of clinical signs means that covert hepatic encephalopathy is rarely recognized or treated outside of clinical trials with options for therapy based on patients with episodic hepatic encephalopathy. This review discusses the current available options for therapy in covert hepatic encephalopathy and focuses on non-absorbable disacharides (lactulose or lactitol), antibiotics (rifaximin), probiotics/synbiotics and L-ornithine-L-aspartate. ( J CLIN EXP HEPATOL 2015;5:S75-S81)

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“…The tolerance ratio, incidence of adverse events, and mortality were not significantly different between LOLA and the placebo/nointervention control. 43 However in most of the studies low grade HE (grade I-II) patients were included in whom LOLA was given in infusion form so efficacy of oral LOLA therapy still needs to be evaluated in patients with high grade HE.…”

Section: L-ornithine-l-aspartatementioning

confidence: 99%

Management of Overt Hepatic Encephalopathy

Sharma

2015

Journal of Clinical and Experimental Hepatology

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Hepatic encephalopathy (HE) is an important complication of cirrhosis with significant morbidity and mortality. Management of HE primarily involves avoidance of precipitating factors and administration of various ammonia-lowering therapies such as non-absorbable disaccharides, antimicrobial agents like rifaximin and L-ornithine L-aspartate. The non-absorbable disaccharides which include lactulose and lactitol are considered the first-line therapy for the treatment of HE and in primary and secondary prophylaxis of HE. Lactitol is comparable to lactulose in the treatment of HE with fewer side effects. Rifaximin is effective in treatment of HE and recent systemic reviews found it comparable to disaccharides and is effective in secondary prophylaxis of HE. H epatic encephalopathy (HE) is a complex neuropsychiatric syndrome, which may complicate acute, chronic liver failure or patients with portal-systemic shunting. It is characterized by changes in mental state including a wide range of neuropsychiatric symptoms ranging from minor signs of altered brain function to deep coma. 1,2 It is one of the commonest indications for admission in intensive care unit in patients with advanced cirrhosis. There were over 40 000 patients hospitalized in the United States alone for a primary diagnosis of HE, resulting in total charges of approximately $932 million. Data in other countries are lacking, hence it causes a huge burden financially to the patient and society. 3 The West Haven Criteria are most often used to grade HE, with scores ranging from I-IV (IV being coma). However, it is a challenge to diagnose patients with minimal hepatic encephalopathy (MHE) or grade 1 HE; so it might be practical to combine these entities and name them covert HE for clinical use and overt HE to patients with grade II to IV. 1,4,5 One of the major tenets of the pathophysiology of HE is hyperammonemia that results from an increased nitrogenous load from the gastrointestinal tract and reduced urea synthesis both due to portal-systemic shunting and decreased urea hepatic synthesis. Brain and skeletal muscle neither remove nor produce ammonium in normal conditions, but they are able to seize ammonium during hyperammonemia, releasing glutamine. Ammonia is produced both by bacterial degradation of amines, aminoacids, purines, and urea as well as enterocytic glutaminase activity that converts glutamine to glutamate and ammonia. 6,7 Astrocytes play an important role in the pathogenesis of HE with consequences for neuronal function. Astrocytes have the ability to eliminate ammonia by the synthesis of glutamine through amidation of glutamate by the enzyme glutamine synthetase Hyperammonemia leads to the accumulation of glutamine within astrocytes, which exerts an osmotic stress that causes astrocytes to take in water and swell. 8,9 This article reviewed the clinical impact, pathogenesis, and management of overt HE in patients with cirrhosis. Articles published between January 1960 and November 2013 were acquired through a MEDLINE search of different combi...

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l‐ornithine‐l‐aspartate for hepatic encephalopathy in patients with cirrhosis: A meta‐analysis of randomized controlled trials

Abstract: LOLA benefits both overt and minimal HE patients in the improvement of HE by reducing the serum ammonia concentration compared with the placebo/no-intervention control. Further, evaluations between LOLA and other effective treatments are needed.

Cited by 88 publications

References 33 publications

Effects of supplementation with branched chain amino acids and ornithine aspartate on plasma ammonia and central fatigue during exercise in healthy men

Effects of supplementation with branched chain amino acids and ornithine aspartate on plasma ammonia and central fatigue during exercise in healthy men

Management of Covert Hepatic Encephalopathy

Management of Overt Hepatic Encephalopathy

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