scholarly journals Myoadenylate deaminase deficiency associated to a liver cirrhosis: A possible cause of neurological dysfunction resembling a hepatic encephalopathy

2015 ◽  
Vol 2 (2) ◽  
Author(s):  
Marco Fiore ◽  
Lorenzo Andreana ◽  
Nicola Coppola ◽  
Annarosa Floreani
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Neurological Dysfunction ◽  
Myoadenylate Deaminase Deficiency ◽  
Myoadenylate Deaminase ◽  
Possible Cause

Effects of SNPs in HE-relevant genes on the development of hepatic encephalopathy in patients with liver cirrhosis

2019 ◽  
Author(s):  
MS Jördens ◽  
V Keitel ◽  
A Mertens ◽  
B Görg ◽  
D Häussinger
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy

scholarly journals Innumerable cerebral microbleeds in hepatitis B virus-related decompensated liver cirrhosis: a case report

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chi Hyuk Oh ◽  
Jin San Lee
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Brain Mri ◽  
Cerebral Microbleeds ◽  
Amyloid Angiopathy ◽  
Decompensated Liver Cirrhosis ◽  
B Virus ◽  
The Brain

Abstract Background Cerebral microbleeds (CMBs) are small, rounded, dark-signal lesions on brain MRI that represent cerebral hemosiderin deposits resulting from prior microhemorrhages and are neuroimaging biomarkers of cerebral amyloid angiopathy (CAA). Here, we report a case of innumerable CMBs in a patient with hepatic encephalopathy underlying decompensated liver cirrhosis. Case presentation An 83-year-old woman diagnosed with hepatitis B virus-related liver cirrhosis 40 years before was referred to our neurology clinic for progressive disorientation of time and place, personality changes, and confusion with somnolence over 2 weeks. Based on the laboratory, neuroimaging, and electrophysiological findings, we diagnosed the patient with hepatic encephalopathy, and her symptoms recovered within 12 h after proper medical management. Brain MRI showed innumerable CMBs in the bilateral frontal, parietal, temporal, and occipital lobes. Since the distribution of CMBs in the patient was mainly corticosubcortical and predominantly in the posterior cortical regions, and the apolipoprotein E genotype was ε4/ε4, we speculated that CAA and hepatic encephalopathy coexisted in this patient. Conclusions We suggest that severe liver dysfunction associated with long-term decompensated liver cirrhosis may be related to an increased number of CMBs in the brain. Our findings indicate that decompensated liver cirrhosis may be a risk factor for the development of CMBs and corroborate a link between the liver and the brain.

scholarly journals Myoadenylate deaminase deficiency does not affect muscle anaplerosis during exhaustive exercise in humans

2001 ◽  
Vol 533 (3) ◽  
pp. 881-889 ◽  
Author(s):  
Mark A. Tarnopolsky ◽  
Gianni Parise ◽  
Martin J. Gibala ◽  
Terry E. Graham ◽  
James W. E. Rush
Keyword(s):  
Exhaustive Exercise ◽  
Myoadenylate Deaminase Deficiency ◽  
Myoadenylate Deaminase ◽  
Exercise In Humans

scholarly journals L-Carnitine for the Treatment of Overt Hepatic Encephalopathy in Patients with Advanced Liver Cirrhosis

2018 ◽  
Vol 64 (5) ◽  
pp. 321-328 ◽  
Author(s):  
Kazuto TAJIRI ◽  
Yuka FUTSUKAICHI ◽  
Saito KOBAYASHI ◽  
Satoshi YASUMURA ◽  
Terumi TAKAHARA ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Overt Hepatic Encephalopathy ◽  
Advanced Liver Cirrhosis

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

2008 ◽  
Vol 14 (21) ◽  
pp. 3438 ◽  
Author(s):  
Evangelos Kalaitzakis ◽  
Einar Björnsson
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy

Sarcopenia predicts minimal hepatic encephalopathy in patients with liver cirrhosis

2017 ◽  
Vol 47 (13) ◽  
pp. 1359-1367 ◽  
Author(s):  
Tatsunori Hanai ◽  
Makoto Shiraki ◽  
Satoshi Watanabe ◽  
Takahiro Kochi ◽  
Kenji Imai ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Minimal Hepatic Encephalopathy

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 The Role of L-ornithine-L-aspartate in the Management of Minimal Hepatic Encephalopathy among Patients with Liver cirrhosis: a Systemic review and Meta-analysis

2018 ◽  
Vol 52 (1) ◽  
Author(s):  
Henry Winston C. Li ◽  
Maria Ana Louise M. Naidas ◽  
Karen Anjela M. Mondragon ◽  
Ruter M. Maralit
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Meta Analysis ◽  
Block Design ◽  
Cochrane Collaboration ◽  
Minimal Hepatic Encephalopathy ◽  
Systemic Review ◽  
Cochrane Library ◽  
P Value ◽  
Picture Completion

Objective. To evaluate the efficacy of L-ornithine-L-aspartate (LOLA) in improving minimal hepatic encephalopathy in adult patients with liver cirrhosis. Methods. A search in PubMed, Cochrane Library, Google Scholar, and Medline was made obtaining four qualified randomized controlled trials. Studies included adult cirrhotic patients with minimal hepatic encephalopathy measured by the number connection test (NCT-A, B), figure connection test (FCT-A, B), picture completion, block design test, and critical flicker frequency (CFF) testing with a cut-off score of <39Hz. Methodologic assessment of studies was performed using Cochrane Collaboration Risk of Bias Tool and Review Manager (RevMan) version 5.3 for statistical analysis. Results. Of the 29 studies identified, 4 fulfilled the inclusion criteria, which entailed analysis of 238 participants (LOLA: 116, Control: 122). Three out of the four studies were used in meta-analysis and one study was analyzed separately due to a difference in the neuropsychometric measure. The metaanalysis favored experimental group (LOLA), with a mean difference of 2.29 (95% CI 0.72 – 3.86), p-value = 0.004, and an I2 of 18%. Conclusion. LOLA provided great potential in managing encephalopathy since treating earlier related to better survival and prevention of disease progression. The results of our study supported such evidence and its use may be encouraged.

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