Hepatic encephalopathy in patients with liver cirrhosis: Is there a role of malnutrition?

Portal hypertension is the main consequence of liver cirrhosis, leading to severe complications such as variceal hemorrhage, ascites or hepatic encephalopathy. As an attempt to decompress the portal venous system, portal flow is derived into the systemic venous system through spontaneous portosystemic shunts (SPSSs), bypassing the liver. In this review, we aim to provide an overview of the published reports in relation to the prevalence and physiopathology behind the appearance of SPSS in liver cirrhosis, as well as the complications derived from its formation and its management. The role of SPSS embolization is specifically discussed, as SPSSs have been assessed as a therapeutic target, mainly for patients with recurrent/persistent hepatic encephalopathy and preserved liver function. Furthermore, different aspects of the role of SPSS in liver transplantation, as well as in candidates for transjugular intrahepatic portosystemic shunt are reviewed. In these settings, SPSS occlusion has been proposed to minimize possible deleterious effects, but results are so far inconclusive.

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The impact of PNPLA3 and TM6SF2 in cirrhosis related complications

10.1101/2021.01.07.425655 ◽

2021 ◽

Author(s):

Haruki Uojima ◽

Xue Shao ◽

Taeang Arai ◽

Yuji ogawa ◽

Toru Setsu ◽

...

Keyword(s):

Liver Cirrhosis ◽

Liver Disease ◽

Hepatic Encephalopathy ◽

Odds Ratio ◽

Fatty Liver Disease ◽

Nonalcoholic Fatty Liver ◽

Fibrosis Progression ◽

Cirrhotic Patients ◽

The Impact

Patatin-like phospholipase domain-containing 3 (PNPLA3) and transmembrane 6-superfamily member 2 (TM6SF2) polymorphisms have major impact for fibrosis due to steatohepatitis. However, there are scant data about correlations between cirrhosis-related complications and the polymorphisms of these genes. Therefore, we aimed to determine the role of the PNPLA3 and TM6SF2 polymorphisms in fibrosis progression for patients with liver cirrhosis. A multicenter study was performed at six hospitals in Japan enrolling 400 patients with liver cirrhosis caused by virus (n = 157), alcohol (n = 104), nonalcoholic fatty liver disease (NAFLD) (n = 106), or autoimmune disease (n = 33). These cirrhotic patients included those with complications of variceal bleeding, hepatic ascites, and/or hepatic encephalopathy and those without. To assess the role of the PNPLA3 and TM6SF2 polymorphisms in patients with cirrhosis related complications, we calculated the odds ratio and relative risk for the rs738409 and rs58542926 polymorphisms. We also accessed whether or not the interaction between these two polymorphisms contributed to cirrhosis related complications. As a result, the odds ratio for complications in the NAFLD group significantly increased in the presence of the rs738409 GG genotype when the CC genotype was used as the reference. There were no significant risks between complications and the presence of the rs738409 G allele in the virus or alcohol groups. There were no significant risks of complications in the frequency of the rs58542926 T polymorphism regardless of the etiology of liver cirrhosis. The interaction between the trs738409 and rs58542926 polymorphisms had the highest odds ratio of 2.415 for complications in the rs738409 GG + rs58542926 (CT+TT) group when rs738409 (CC+CG) + TM6SF2 CC was used as the reference in the NAFLD group.

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The effectiveness of oral zinc supplementation in patients with liver cirrhosis and hepatic encephalopathy

EURASIAN JOURNAL OF CLINICAL SCIENCES ◽

10.28942/ejcs.v2i2.79 ◽

2020 ◽

Vol 2 (3) ◽

pp. 38-41

Author(s):

Zaur Orujov

Keyword(s):

Liver Cirrhosis ◽

Hepatic Encephalopathy ◽

Zinc Supplementation ◽

Scientific Data ◽

Decompensated Cirrhosis ◽

Zinc Ions ◽

Biochemical Reactions ◽

Medical Practitioners ◽

Long Time

The role of zinc in biochemical reactions in the human body and the need for sufficient intake of zinc have been known to science for long time. Zinc is a cofactor of more than 300 biochemical reactions, including those occurring in the liver. The human genome encodes about 3,000 zinc proteins. At least thirty proteins homeostatically control the vesicular accumulation and intracellular distribution of zinc, as well as the concentration of zinc ions (1). In 20% of patients with compensated and 50% of patients with decompensated cirrhosis of the liver, both quantitative and qualitative nutritional problems are observed (2). There is still not much work and recommendations on the diet of patients with hepatic encephalopathy in the modern doctor’s arsenal. A review of articles describing the effectiveness of adding zinc to the diet of patient with cirrhosis and hepatic encephalopathy, as we know, has not been conducted yet. The purpose of this review is a detailed analysis of the available scientific data on the effectiveness of zinc in patients with hepatic encephalopathy and, if it is possible, the development of specific recommendations for medical practitioners, as well as identification of perspective directions for further researches.

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Hepatic encephalopathy: issues relevant to clinical practice

Medical Council ◽

10.21518/2079-701x-2021-15-104-108 ◽

2021 ◽

pp. 104-108

Author(s):

M. V. Maevskaya

Keyword(s):

Liver Cirrhosis ◽

Clinical Practice ◽

Hepatic Encephalopathy ◽

Clinical Signs ◽

Ammonia Concentration ◽

High Concentration ◽

Expert Opinions ◽

Diagnostic Role ◽

Cirrhotic Patients

Hepatic encephalopathy (HE) remains one of the most serious complications of liver cirrhosis. Its clinical spectrum sometimes creates difficulties in the optimal diagnosis at the patient’s bedside and treatment. To present new data on the field of clinical management of cirrhotic patients with hepatic encephalopathy. The role of ammonia in the diagnosis of HE is still under discussion. In clinical practice, in patients with suspected overt HE, normal ammonia concentration can be used to exclude this diagnosis. In contrast, a high concentration of ammonia in the absence of clinical signs of HE should not serve as a criterion for this diagnosis and as a guide for treatment. A separate issue for discussion is the covert HE. The simplest and most affordable test for screening for covert HE and evaluating the effectiveness of therapy is the animal naming test, which can be done on bedside by physician or caregivers. Patients with covert HE need treatment that is similar in approach to overt HE. The diagnosis of overt HE and the methods of its therapy are well known. According to Russian recommendations, depending on the disease course in a certain patient, lactulose, rifaximin, L-ornithine L-aspartate can be used as first-line drugs, which is applicable to the treatment of both overt and latent PE. The main issues on the management of HE in liver cirrhosis relate to the diagnostic role of ammonia, optimal diagnosis and treatment strategy for covert HE, therapy of choice for both overt and latent HE. There are expert opinions and consensus documents on all these issues. Treatment of overt and latent PE is carried out according to the same principles. Drugs of choice: lactulose, rifaximin and L-Ornithine L-Aspartate.

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Role of probiotics in the treatment of minimal hepatic encephalopathy in patients with HBV-induced liver cirrhosis

Journal of International Medical Research ◽

10.1177/0300060518776064 ◽

2018 ◽

Vol 46 (9) ◽

pp. 3596-3604 ◽

Cited By ~ 14

Author(s):

Xiaoxue Xia ◽

Jiang Chen ◽

Jiayun Xia ◽

Bin Wang ◽

Hua Liu ◽

...

Keyword(s):

Liver Cirrhosis ◽

Hepatic Encephalopathy ◽

Minimal Hepatic Encephalopathy ◽

Treated Group ◽

Mucosal Barrier ◽

Overt Hepatic Encephalopathy ◽

Probiotic Treatment ◽

B Virus ◽

Number Connection Test

Objective This study was performed to investigate the role of probiotics ( Clostridium butyricum combined with Bifidobacterium infantis) in the treatment of minimal hepatic encephalopathy (MHE) in patients with hepatitis B virus (HBV)-induced liver cirrhosis. Methods Sixty-seven consecutive patients with HBV-induced cirrhosis without overt hepatic encephalopathy were screened using the number connection test and digit symbol test. The patients were randomized to receive probiotics (n = 30) or no probiotics (n = 37) for 3 months. At the end of the trial, changes in cognition, intestinal microbiota, venous ammonia, and intestinal mucosal barriers were analyzed using recommended systems biology techniques. Results The patients’ cognition was significantly improved after probiotic treatment. The predominant bacteria ( Clostridium cluster I and Bifidobacterium) were significantly enriched in the probiotics-treated group, while Enterococcus and Enterobacteriaceae were significantly decreased. Probiotic treatment was also associated with an obvious reduction in venous ammonia. Additionally, the parameters of the intestinal mucosal barrier were obviously improved after probiotic treatment, which might have contributed to the improved cognition and the decreased ammonia levels. Conclusion Treatment with probiotics containing C. butyricum and B. infantis represents a new adjuvant therapy for the management of MHE in patients with HBV-induced cirrhosis.

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The risk of cirrhosis and its complications based on PNPLA3 rs738409 G allele frequency

Digestive Diseases ◽

10.1159/000521062 ◽

2021 ◽

Author(s):

Xue Shao ◽

Haruki Uojima ◽

Taeang Arai ◽

Yuji Ogawa ◽

Toru Setsu ◽

...

Keyword(s):

Liver Cirrhosis ◽

Hepatic Encephalopathy ◽

Odds Ratio ◽

Fatty Liver Disease ◽

Wild Type ◽

Nonalcoholic Fatty Liver ◽

Entire Cohort ◽

Significant Difference ◽

Background Data

Background: Data regarding the influence of patatin-like phospholipase domain-containing 3 (PNPLA3) polymorphism for patients with liver cirrhosis (LC) are scarce. Objective: This study assesses the role of the PNPLA3 polymorphism for the development of LC and its complications by the findings of genetic examinations. Methods: Patients with LC caused by virus (n = 157), alcohol (n = 104), nonalcoholic fatty liver disease (NAFLD) (n = 106), or autoimmune disease (n = 33) and without LC (n = 128) were enrolled. LC were composed of the present and absent of complications, such as variceal bleeding, hepatic ascites, and/or hepatic encephalopathy. To assess the role of the PNPLA3 polymorphism, odds ratio (OR) for the rs738409 variant was calculated for the patients between (i) with LC and without LC in the entire cohort, and (ii) the present and absent of complications in the patients with LC. Results: There was a significant difference among the patients without LC and those with alcohol, NAFLD related LC in the frequency of G alleles (p < 0.001, both). According to complications of LC, the OR for NAFLD related cirrhosis significantly increased in the presence of the two mutated alleles (OR = 3.165; p = 0.046) when the wild type was used as the reference. However, there were no significant risks for the complications in the virus and alcohol related cirrhosis unless there was a presence of G alleles. Conclusion: The PNPLA3 polymorphism was associated with the risk of NAFLD related LC and its complications.

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Catabolism of Human Fibrinogen Fragment D in Normal Subjects and Patients with Liver Cirrhosis

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650106 ◽

1980 ◽

Vol 44 (03) ◽

pp. 146-149 ◽

Cited By ~ 3

Author(s):

Nicole Ardaillou ◽

Jeannine Yvart ◽

Philippe Le Bras ◽

Marie-José Larrieu

Keyword(s):

Liver Cirrhosis ◽

Clearance Rate ◽

Plasma Clearance ◽

Normal Subjects ◽

Fractional Catabolic Rate ◽

Human Fibrinogen ◽

Plasma Pool ◽

Catabolic Rate ◽

Chloramine T

SummaryThe catabolism of human fragment D, (FgD), obtained by plasmin digestion of fibrinogen has been investigated in normal subjects and patients with liver cirrhosis and the results compared with those obtained for fibrinogen (Fg). Fg was labelled with I-125 and Fg D with I-131 using the chloramine T method. The plasma disappearance curves of both labelled proteins fitted a two exponential curve. In controls the plasma clearance rate of Fg D was greater than that of Fg as shown by the marked difference between the half-lives of these two tracers: 8,9 and 83,5 hours for Fg D and Fg respectively. The fractional catabolic rate of Fg D was 3.38 times the plasma pool per day. In nine patients with liver cirrhosis, catabolism of Fg was not modified. In contrast, catabolism of Fg D was significantly reduced with a half life of 13.0 hours and a low fractional catabolic rate. These results suggest the role of the liver in the catabolism of Fg D in man.

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