scholarly journals Usefulness of Carnitine Supplementation for the Complications of Liver Cirrhosis

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1915
Author(s):  
Tatsunori Hanai ◽  
Makoto Shiraki ◽  
Kenji Imai ◽  
Atsushi Suetugu ◽  
Koji Takai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Carnitine Deficiency ◽  
Carnitine Supplementation ◽  
Constant Attention ◽  
Carnitine Level ◽  
Muscle Cramps ◽  
Cirrhotic Patients

Carnitine is a vitamin-like substance that regulates lipid metabolism and energy production. Carnitine homeostasis is mainly regulated by dietary intake and biosynthesis in the organs, including the skeletal muscle and the liver. Therefore, liver cirrhotic patients with reduced food intake, malnutrition, biosynthetic disorder, and poor storage capacity of carnitine in the skeletal muscle and liver are more likely to experience carnitine deficiency. In particular, liver cirrhotic patients with sarcopenia are at a high risk for developing carnitine deficiency. Carnitine deficiency impairs the important metabolic processes of the liver, such as gluconeogenesis, fatty acid metabolism, albumin biosynthesis, and ammonia detoxification by the urea cycle, and causes hypoalbuminemia and hyperammonemia. Carnitine deficiency should be suspected in liver cirrhotic patients with severe malaise, hepatic encephalopathy, sarcopenia, muscle cramps, and so on. Importantly, the blood carnitine level does not always decrease in patients with liver cirrhosis, and it sometimes exceeds the normal level. Therefore, patients with liver cirrhosis should be treated as if they are in a state of relative carnitine deficiency at the liver, skeletal muscle, and mitochondrial levels, even if the blood carnitine level is not decreased. Recent clinical trials have revealed the effectiveness of carnitine supplementation for the complications of liver cirrhosis, such as hepatic encephalopathy, sarcopenia, and muscle cramps. In conclusion, carnitine deficiency is not always rare in liver cirrhosis, and it requires constant attention in the daily medical care of this disease. Carnitine supplementation might be an important strategy for improving the quality of life of patients with liver cirrhosis.

scholarly journals Pilot study of orphenadrine as a novel treatment for muscle cramps in patients with liver cirrhosis

2017 ◽  
Vol 6 (3) ◽  
pp. 422-427 ◽  
Author(s):  
Sherief Abd-Elsalam ◽  
Ferial El-Kalla ◽  
Lobna A Ali ◽  
Samah Mosaad ◽  
Walaa Alkhalawany ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Side Effects ◽  
Safety And Efficacy ◽  
Muscle Cramps ◽  
Novel Treatment ◽  
Significant Difference ◽  
Before And After ◽  
Cirrhotic Patients ◽  
To Receive

Background and aims Muscle cramps markedly affect the quality of life in cirrhotic patients with no available highly effective treatment. The aim of this study was to assess the safety and efficacy of orphenadrine in the treatment of muscle cramps in cirrhotic patients. Methods The study enrolled 30 liver cirrhosis patients complaining of frequent muscle cramps (≥3 per week), who were randomized to receive either orphenadrine 100 mg or calcium carbonate 500 mg twice daily as a control for one month. Severity, frequency, and duration of the muscle cramps were assessed before and after treatment as well as recurrence after washout of the drug for two weeks. Side effects were recorded. Results One month after treatment with orphenadrine; the frequency of muscle cramps decreased significantly to 0.6 ± 0.74 per week compared to 12.53 ± 6.01 at baseline ( p < 0.001), the duration of muscle cramps decreased from 1 min to 0.1 min after treatment ( p < 0.001). The pain score improved significantly from a score of 8/10 to 0/10 ( p < 0.001). The side effects were few, such as dry mouth, drowsiness, and nausea, with no significant difference between their occurrences in the two groups. Conclusion Orphenadrine is safe and effective in treatment of muscle cramps in patients with liver cirrhosis.

scholarly journals Low Serum 25-Hydroxy Vitamin D (25-OHD) and Hepatic Encephalopathy in HCV-Related Liver Cirrhosis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Mohamed Abd Ellatif Afifi ◽  
Ahmed Mohamed Hussein ◽  
Mahmoud Rizk
Keyword(s):  
Vitamin D ◽  
Liver Cirrhosis ◽  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Wide Spectrum ◽  
The Other ◽  
Vitamin D Levels ◽  
25 Hydroxy Vitamin D ◽  
Cirrhotic Patients ◽  
Low Serum

Background. Patients with liver cirrhosis experience a large variety of metabolic disorders associated with more hepatic decompensation. Hepatic encephalopathy (HE) is a significant complication in liver cirrhosis patients, presenting a wide spectrum of neuropsychological symptoms. A deficiency of 25-hydroxy vitamin D (25-OHD) in the general population is associated with a loss of cognitive function, dementia, and Alzheimer’s disease. Aim of the Study. Our study aims to check the relationship between low serum 25-OHD and HE in patients with HCV-related liver cirrhosis and assess its link with patient mortality. Patients and Methods. This study was observationally carried out on 100 patients with HCV-related liver cirrhosis. The patients were divided into 2 groups: Group A—included 50 HCV-related cirrhotic patients with HE, and Group B—included 50 HCV-related cirrhotic patients without HE. Assessment of disease severity using the end-stage liver disease (MELD) model and Child Turcotte Pugh (CTP) scores were done, and 25-OHD levels were measured. Comparison of vitamin D levels in different etiologies and different CTP categories was made using one-way ANOVA. Pearson’s correlation between the level of vitamin D and other biomarkers was applied. Results. There was a statistically significant Vitamin D level difference between the two groups. A lower level of vitamin D was observed in the HE group where the severe deficiency was 16%, while it was 6% in the other group and the moderate deficiency was 24% in HE group as compared to 10% in the other group. The insufficient vitamin D level represented 46% of the non-HE group while none of the HE group falls in this category. Vitamin D level was statistically higher in Grade 1 HE than in Grade 2 which is higher than in Grades 3 to 4. Vitamin D level was also significantly higher in those who improved from HE as compared to those who died. Conclusion. The lower levels of 25-OHD were associated with the higher incidence of HE in cirrhotic HCV patients. The worsening vitamin D deficiency was associated with increased severity of the liver disease, so vitamin D may be considered a prognostic factor for the severity of liver cirrhosis and high mortality rate in HE patients.

scholarly journals Hepatic Encephalopathy: From the Pathogenesis to the New Treatments

2014 ◽  
Vol 2014 ◽  
pp. 1-16 ◽  
Author(s):  
Juan Cordoba
Keyword(s):  
Clinical Trials ◽  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Prospective Studies ◽  
Hepatic Dysfunction ◽  
Short Term ◽  
Multiple Factors ◽  
Short Term Mortality ◽  
Cirrhotic Patients ◽  
New Treatments

Hepatic encephalopathy is a frequent and serious complication of liver cirrhosis; the pathophysiology of this complication is not fully understood although great efforts have been made during the last years. There are few prospective studies on the epidemiology of this complication; however, it is known that it confers with high short-term mortality. Hepatic encephalopathy has been classified into different groups depending on the degree of hepatic dysfunction, the presence of portal-systemic shunts, and the number of episodes. Due to the large clinical spectra of overt EH and the complexity of cirrhotic patients, it is very difficult to perform quality clinical trials for assessing the efficacy of the treatments proposed. The physiopathology, clinical manifestation, and the treatment of HE is a challenge because of the multiple factors that converge and coexist in an episode of overt HE.

scholarly journals The impact of PNPLA3 and TM6SF2 in cirrhosis related complications

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.

scholarly journals HEPATIC ENCEPHALOPATHY

2018 ◽  
Vol 25 (12) ◽  
pp. 1857-1862
Author(s):  
Ashok Kumar Lohano ◽  
Shamsuddin Shaikh ◽  
Nazia Arain
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Serum Sodium Level ◽  
Cross Sectional Study ◽  
Inclusion Criteria ◽  
Exclusion Criteria ◽  
Cross Sectional ◽  
Medicine Department ◽  
Grade Ii ◽  
Cirrhotic Patients

Objectives: To determine the prevalence and relation to severity of hyponatremia in liver cirrhotic patients associated with hepatic encephalopathy. Study Design: Cross sectional study. Place and Duration of Study: Medicine Department of Peoples University of Medical and Health Sciences Nawabshah from 26th October 2016 to 25th April 2017. Material and Methods: All patients of either gender with 15 to 70 years associated liver cirrhosis, were included in the study. Diagnosis of liver cirrhosis was confirmed by laboratory and ultrasonographic findings. Exclusion criteria were patients outside of patient range, patients with hepatocellular carcinoma, or anotherco morbid. Sodium levels were measured by 2cc bloodsample by blood from cubital vein preferably. Encephalopathy was evaluated via West Haven classification. All the data were entered into SPSS 20 version and were analyzed by using the same software. Results: A total of 369 patients met the inclusion criteria. Among them were 129 males and 240 females. The overall mean age of study subjects was 57.07±9.23 years. The overall mean duration of hepatic encephalopathy was 2.53±0.733 days. The overall mean serum sodium level for study subjects was 129.59±7.11 mEq/L. Most of the study subjects, 83.5% had HCV, 12.7% patients were HBV positive whereas 3% were positive for HBV as well as HCV. 26 patients had grade 1 encephalopathy, 30 patients had grade II encephalopathies, 258 patients had grade III encephalopathies, and 55 patients had grade IV encephalopathy. In our study, 73.2% study subjects were observed with hyponatremia. Out of 270 study subjects found with hyponatremia, 25.2% had mild hyponatremia, 44.8% had moderate hyponatremia, and 30% had severe hyponatremia. The results showed that there was a significant association of hyponatremia with viral markers (p=0.030), duration of hepatic encephalopathy (p=0.102) and grades of hepatic encephalopathy (p=0.746). Conclusion: We concluded hyponatremia is frequently found in patients with cirrhosis liver. Significant correlation of hyponatremia with the severity of hepatic encephalopathy.

scholarly journals Loss of Skeletal Muscle Mass Affects the Incidence of Minimal Hepatic Encephalopathy: A Case Control Study

2020 ◽  
Author(s):  
Masakuni Tateyama ◽  
Hideaki Naoe ◽  
Motohiko Tanaka ◽  
Kentaro Tanaka ◽  
Satoshi Narahara ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Mass Loss ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Lumbar Vertebra ◽  
Minimal Hepatic Encephalopathy ◽  
Skeletal Muscle Index ◽  
Muscle Mass Loss

Abstract Background: Sarcopenia is a syndrome characterized by progressive and systemic decreases in skeletal muscle mass and muscle strength. The influence or prognosis of various liver diseases in this condition have been widely investigated, but little is known about whether sarcopenia and/or muscle mass loss are related to minimal hepatic encephalopathy.Methods: To clarify the relationship between minimal hepatic encephalopathy and sarcopenia and/or muscle mass loss in patients with liver cirrhosis. Ninety-nine patients with liver cirrhosis were enrolled. Minimal hepatic encephalopathy was diagnosed by a neuropsychiatric test. Skeletal mass index was calculated by dividing muscle area at the third lumbar vertebra by the square of height in meters.Results: MHE was detected in 48 cases (48.5%) and sarcopenia in 6 cases (6.1%). Patients were divided into two groups, with or without MHE. Comparing groups, no significant differences were seen in serum ammonia concentration or rate of sarcopenia. Skeletal muscle index was smaller in patients with minimal hepatic encephalopathy (46.4 cm2/m2) than in those without (51.2 cm2/m2, P = 0.027). Skeletal muscle index represented a predictive factor related to minimal hepatic encephalopathy (<50 cm2/m2; odds ratio 0.300, P = 0.002).Conclusions: Muscle mass loss was related to minimal hepatic encephalopathy, although sarcopenia was not. Measurement of muscle mass loss might be useful to predict MHE.

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