Long-term treatment of latent portosystemic encephalopathy with branched-chain amino acids

Plauth, Mathias; Egberts, E.‐H.; Hamster, W.; Török, M.; Müller, P; Brand, O.; Fürst, Peter; Dölle, W

doi:10.1016/s0168-8278(05)80210-7

Cited by 120 publications

(64 citation statements)

References 26 publications

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“…Studies looking at supplemental BCAA in patients with minimal and episodic HE have shown supplemental BCAAs have utility (Plauth et al 1993) but it has not yet been proven to have benefit in reducing the recurrence of overt HE. A meta-analysis of more recent trials has given some support to the use of BCAAs in reducing all manifestations of HE with the supposition that BCAAs boost ammonia uptake and metabolism within skeletal muscle.…”

Section: Therapeutic Strategies Targeting the Gut-liver-brain Axismentioning

confidence: 99%

Clinical science workshop: targeting the gut-liver-brain axis

et al. 2015

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A clinical science workshop was held at the ISHEN meeting in London on Friday 11th September 2014 with the aim of thrashing out how we might translate what we know about the central role of the gut-liver-brain axis into targets which we can use in the treatment of hepatic encephalopathy (HE). This review summarises the integral role that interorgan ammonia metabolism plays in the pathogenesis of HE with specific discussion of the roles that the small and large intestine, liver, brain, kidney and muscle assume in ammonia and glutamine metabolism. Most recently, the salivary and gut microbiome have been shown to underpin the pathophysiological changes which culminate in HE and patients with advanced cirrhosis present with enteric dysbiosis with small bowel bacterial overgrowth and translocation of bacteria and their products across a leaky gut epithelial barrier. Resident macrophages within the liver are able to sense bacterial degradation products initiating a pro-inflammatory response within the hepatic parenchyma and release of cytokines such as tumour necrosis factor alpha (TNF-α) and interleukin-8 into the systemic circulation. The endotoxemia and systemic inflammatory response that are generated predispose both to the development of infection as well as the manifestation of covert and overt HE. Co-morbidities such as diabetes and insulin resistance, which commonly accompany cirrhosis, may promote slow gut transit, promote bacterial overgrowth and increase glutaminase activity and may need to be acknowledged in HE risk stratification assessments and therapeutic regimens. Therapies are discussed which target ammonia production, utilisation or excretion at an individual organ level, or which reduce systemic inflammation and endotoxemia which are known to exacerbate the cerebral effects of ammonia in HE. The ideal therapeutic strategy would be to use an agent that can reduce hyperammonemia and reduce systemic inflammation or perhaps to adopt a combination of therapies that can address both.

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Section: Therapeutic Strategies Targeting the Gut-liver-brain Axismentioning

confidence: 99%

Clinical science workshop: targeting the gut-liver-brain axis

et al. 2015

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“…Intravenous ornithine aspartate has proven its effectivity [69,70] and the benefit of orally administered ornithine aspartate is currently evaluated. Most studies on oral branched-chain amino acids (BCAA) showed clinical improvement of latent or low-grade HE and of protein tolerance [71] , but studies on i.v. BCAA have not led yet to definite results.…”

Section: Therapy Of Hementioning

confidence: 99%

Hepatic encephalopathy as a complication of liver disease

Dahl

Kircheis²,

Häussinger³

2001

WJG

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“…114 (b) In patients with latent encephalopathy, two group 109,112 and one crossover 119 trials found no difference, but another crossover study demonstrated an improvement in psychometric testing with the use of BCAAs. 120 (c) In patients with frank encephalopathy, two crossover trials could not demonstrate that such individuals tolerated increasing amounts of BCAAs any better than other nitrogen sources. 118,119 (d) In patients with latent encephalopathy, one group 110 and one crossover 115 study showed better tolerance for the increasing amounts of BCAAs, but this ®nding could not be duplicated in one other group 113 and four crossover 117,118,121,122 experiments.…”

Section: ±107mentioning

confidence: 99%

Nutritional support

Ofman

Koretz

1997

Aliment Pharmacol Ther

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Nutritional support currently accounts for about 1% of the total health care costs in the USA. Interestingly, most of the prospective randomized controlled trials to date have not been able to demonstrate that this therapeutic intervention alters morbidity or mortality. In fact, parenteral nutritional support may predispose the recipients to developing systemic infections. There have been a few areas in which nutritional support may be of benefit. Enteral supplements given to underweight women who suffer hip fractures reduce the hospital stay and, presumably, overall cost. Preoper‐ative parenteral nutritional support may produce a small absolute reduction in post‐operative morbidity, but its cost becomes prohibitive. Preoperative enteral nutritional support, especially if carried out in the home, may be of benefit (using the most optimistic interpretation of a small number of trials); if so, it is an economically defensible intervention. Particular nutrients or diets may have specific effects on certain disease processes. Indirect comparisons have suggested that elemental diets can be used to treat flares of Crohn's disease (perhaps because putative food antigens are removed). However, corticosteroid therapy is more efficacious. Furthermore, it is less expensive to employ 6‐mercaptopurine as the next modality in steroid failures. Branched‐chain amino acid infusions may have some effect on hepatic encephalopathy, but again, lactulose is less expensive. Nutritional support is one area of medicine in which there has been far more enthusiasm than the data justify. Disease‐associated malnutrition probably is a secondary phenomenon, not an important cause of morbidity. The widespread use of this modality cannot be justified in a cost‐constrained health care system.

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Long-term treatment of latent portosystemic encephalopathy with branched-chain amino acids

Cited by 120 publications

References 26 publications

Clinical science workshop: targeting the gut-liver-brain axis

Clinical science workshop: targeting the gut-liver-brain axis

Hepatic encephalopathy as a complication of liver disease

Nutritional support

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