Nutrition principles and recommendations in different types of hepatic encephalopathy

Pazgan−Simon, Monika; Zuwała−Jagiełło, Jolanta; Serafińska, Syłwia; Simon, Krzysztof

doi:10.5114/ceh.2016.57759

Cited by 4 publications

(5 citation statements)

References 14 publications

(16 reference statements)

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“…The four organizations recommend a protein intake of 1.2–1.5 g/kg/day. In particular, lipids in the diet are beneficial to patients with HE, as they have been shown to have beneficial effects on gut microbiota and bowel transit time [ 15 ].…”

Section: Linkage Of Gut Microbiota With Hepatic Encephalopathymentioning

confidence: 99%

“…In addition, although the management of HE through pharmacological approaches and nutritional methods is being studied [ 14 , 15 ], the link with the intestinal microflora has not been clearly identified. We explore the association of HE with the gut microbiota based on the gut–liver-brain axis and evaluate the therapeutic management of HE with a focus on clinical research data.…”

Section: Introductionmentioning

confidence: 99%

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The Link between Gut Microbiota and Hepatic Encephalopathy

Won

Gupta

et al. 2022

IJMS

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Hepatic encephalopathy (HE) is a serious complication of cirrhosis that causes neuropsychiatric problems, such as cognitive dysfunction and movement disorders. The link between the microbiota and the host plays a key role in the pathogenesis of HE. The link between the gut microbiome and disease can be positively utilized not only in the diagnosis area of HE but also in the treatment area. Probiotics and prebiotics aim to resolve gut dysbiosis and increase beneficial microbial taxa, while fecal microbiota transplantation aims to address gut dysbiosis through transplantation (FMT) of the gut microbiome from healthy donors. Antibiotics, such as rifaximin, aim to improve cognitive function and hyperammonemia by targeting harmful taxa. Current treatment regimens for HE have achieved some success in treatment by targeting the gut microbiota, however, are still accompanied by limitations and problems. A focused approach should be placed on the establishment of personalized trial designs and therapies for the improvement of future care. This narrative review identifies factors negatively influencing the gut–hepatic–brain axis leading to HE in cirrhosis and explores their relationship with the gut microbiome. We also focused on the evaluation of reported clinical studies on the management and improvement of HE patients with a particular focus on microbiome-targeted therapy.

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Section: Linkage Of Gut Microbiota With Hepatic Encephalopathymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Link between Gut Microbiota and Hepatic Encephalopathy

Won

Gupta

et al. 2022

IJMS

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“…Retinol deficiency may be caused by reduced intestinal absorption and hepatic clearance of vitamins. Vitamin A is stored in stellate cells and its deficiency may promote collagen release and fibrosis [ 31 ]. Vitamin A deficiency can cause night blindness, photophobia and increased risk of neoplastic complications.…”

Section: Assessment Of Nutritional Statusmentioning

confidence: 99%

Nutrition Assessment and Management in Patients with Cirrhosis and Cognitive Impairment: A Comprehensive Review of Literature

Faccioli¹,

Nardelli²,

Gioia³

et al. 2022

JCM

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Hepatic encephalopathy (HE) represents a common complication of liver cirrhosis. Protein-calorie malnutrition is frequently encountered in the cirrhotic patient and its most obvious clinical manifestation is sarcopenia. This condition represents a risk factor for HE occurrence because skeletal muscle acts as an alternative site for ammonium detoxification. Preventive intervention through an adequate assessment of nutritional status should be carried out at early stages of the disease and in a multidisciplinary team using both non-instrumental methods (food diary, anthropometric measurements, blood chemistry tests) and instrumental methods (bioimpedance testing, DEXA, CT, indirect calorimetry, dynamometry). Dietary recommendations for patients with HE do not differ from those for cirrhotic patient without HE. Daily caloric intake in the non-obese patient should be 30–40 Kcal/Kg/day with a protein intake of 1–1.5 g/Kg/day, especially of vegetable origin, through 4–6 meals daily. In patients with HE, it is also essential to monitor electrolyte balance, supplementing any micronutrient deficiencies such as sodium and zinc, as well as vitamin deficiencies because they can cause neurological symptoms similar to those of HE. In light of the critical role of nutritional status, this aspect should not be underestimated and should be included in the diagnostic–therapeutic algorithm of patients with HE.

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“…In patients with recurrent HE with cirrhosis, rifaximin (550 mg twice a day) can be added to lactulose to alter gut microbiota. No nutrition recommendations are made concerning Mn reduction [166]. Human prion diseases are mostly classified into inherited, sporadic, and acquired types.…”

Section: Hepatic Encephalopathy (He)mentioning

confidence: 99%

Copper, Iron, and Manganese Toxicity in Neuropsychiatric Conditions

Tarnacka

Jopowicz

Maślińska

2021

IJMS

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Copper, manganese, and iron are vital elements required for the appropriate development and the general preservation of good health. Additionally, these essential metals play key roles in ensuring proper brain development and function. They also play vital roles in the central nervous system as significant cofactors for several enzymes, including the antioxidant enzyme superoxide dismutase (SOD) and other enzymes that take part in the creation and breakdown of neurotransmitters in the brain. An imbalance in the levels of these metals weakens the structural, regulatory, and catalytic roles of different enzymes, proteins, receptors, and transporters and is known to provoke the development of various neurological conditions through different mechanisms, such as via induction of oxidative stress, increased α-synuclein aggregation and fibril formation, and stimulation of microglial cells, thus resulting in inflammation and reduced production of metalloproteins. In the present review, the authors focus on neurological disorders with psychiatric signs associated with copper, iron, and manganese excess and the diagnosis and potential treatment of such disorders. In our review, we described diseases related to these metals, such as aceruloplasminaemia, neuroferritinopathy, pantothenate kinase-associated neurodegeneration (PKAN) and other very rare classical NBIA forms, manganism, attention-deficit/hyperactivity disorder (ADHD), ephedrone encephalopathy, HMNDYT1-SLC30A10 deficiency (HMNDYT1), HMNDYT2-SLC39A14 deficiency, CDG2N-SLC39A8 deficiency, hepatic encephalopathy, prion disease and “prion-like disease”, amyotrophic lateral sclerosis, Huntington’s disease, Friedreich’s ataxia, and depression.

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Nutrition principles and recommendations in different types of hepatic encephalopathy

Cited by 4 publications

References 14 publications

The Link between Gut Microbiota and Hepatic Encephalopathy

The Link between Gut Microbiota and Hepatic Encephalopathy

Nutrition Assessment and Management in Patients with Cirrhosis and Cognitive Impairment: A Comprehensive Review of Literature

Copper, Iron, and Manganese Toxicity in Neuropsychiatric Conditions

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