Probiotics for patients with hepatic encephalopathy

McGee, Richard G; Bakens, Anouk; Wiley, Kerrie; Riordan, Stephen M.; Webster, Angela C

doi:10.1002/14651858.cd008716.pub2

Cited by 88 publications

(65 citation statements)

References 184 publications

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“…Lactulose is used to acidify feces and sequester ammonia as ammonium, but lactulose is poorly tolerated, resulting in poor adherence (13). In a mouse model of thioacetamide-induced liver injury, a lactobacillus probiotic has been reported to reduce ammonia levels and mortality (14), but these benefits have not been extended to human studies (15,16). While promising, studies of probiotic therapies in humans described to date have suffered from methodological limitations, did not document long-term effects, and showed consistently minimal effects on outcome, motivating efforts to engineer more resilient and effective bacterial communities.…”

Section: Introductionmentioning

confidence: 99%

Engineering the gut microbiota to treat hyperammonemia

Shen¹,

Albenberg²,

Bittinger³

et al. 2015

J. Clin. Invest.

164

130

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Section: Introductionmentioning

confidence: 99%

Engineering the gut microbiota to treat hyperammonemia

Shen¹,

Albenberg²,

Bittinger³

et al. 2015

J. Clin. Invest.

164

130

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“…Вместе с тем отмечено существенное снижение концентрации аммиака. Авторы пришли к заключе-нию о необходимости проведения дальнейших ран-домизированных клинических исследований [17].…”

Section: результаты исследования и обсуждениеunclassified

Experience of Ornithine Aspartate (Hepa-Merz) and Probiotics Bioflorum Forte in the Treatment of Non-Severe Forms of Alcoholic and Non-Alcoholic Fatty Liver Disease

Ильченко

Мельникова

Журавлева

2016

Arhivʺ vnutrennej mediciny

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“…Loguercio et al 36,37 showed that long-term administration of Enterococcus faecium (SF68) is at least as useful as lactulose for the chronic treatment of chronic HE. In a meta-analysis by McGee et al 38 …”

Section: Probioticsmentioning

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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Probiotics for patients with hepatic encephalopathy

Abstract: Trusted evidence. Informed decisions. Better health.

Cited by 88 publications

References 184 publications

Engineering the gut microbiota to treat hyperammonemia

Engineering the gut microbiota to treat hyperammonemia

Experience of Ornithine Aspartate (Hepa-Merz) and Probiotics Bioflorum Forte in the Treatment of Non-Severe Forms of Alcoholic and Non-Alcoholic Fatty Liver Disease

Management of Overt Hepatic Encephalopathy

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