Hepatic Encephalopathy Research Articles

Correlation of Serum Zinc Levels with Hepatic Encephalopathy Severity in Patients with Decompensated Liver Cirrhosis: A Prospective Observational Study from Egypt.

A vital trace element, zinc, is involved in several metabolic and enzymatic functions, such as antioxidant defense and ammonia detoxification. Zinc metabolism is disturbed by liver cirrhosis, especially when it is decompensated, contributing to systemic complications, including hepatic encephalopathy (HE). This study aimed to assess serum zinc levels in patients with decompensated liver cirrhosis and evaluate their correlation with the severity of cirrhosis and HE grades. This prospective observational study included 100 patients with decompensated liver cirrhosis and 100 healthy controls between December 2022 and June 2023. Serum zinc levels and other biochemical parameters were measured using standard laboratory methods. Liver cirrhosis severity was evaluated using the Child-Pugh score, and HE was graded using the West Haven criteria. Correlations between zinc levels, clinical parameters, and disease severity were analyzed statistically by Spearman's correlation and Kruskal-Wallis tests. Serum zinc levels were significantly lower in cirrhotic patients compared to controls (21.7 ± 24.3µg/dL vs. 85.9 ± 32.6µg/dL, P < 0.0001). Zinc levels inversely correlated with both Child-Pugh class (r = - 0.84, P < 0.001) and HE grade (r = - 0.78, P < 0.001). Patients with advanced Child-Pugh Class C or HE Grade 3 had severe zinc deficiency. A strong positive correlation was observed between serum zinc and albumin levels (r = 0.843, P < 0.0001), underscoring albumin's role in zinc transport. Serum zinc deficiency is strongly correlated with the severity of liver cirrhosis and HE. Therefore, routine zinc assessment and supplementation should be considered in cirrhotic patients, especially those with hypoalbuminemia or advanced HE for better outcomes.

A prolonged activated partial thromboplastin time indicates poor short-term prognosis in patients with hepatic encephalopathy: insights from the MIMIC database

A prolonged activated partial thromboplastin time indicates poor short-term prognosis in patients with hepatic encephalopathy: insights from the MIMIC database

Edaravone reduces brain injury in hepatic encephalopathy by upregulation of Nrf2/HO-1 and inhibition of NF-κB, iNOS/NO and inflammatory cytokines.

Brain damage is the most important complication in patients with hepatic encephalopathy (HE). Oxidative stress and inflammation are essential factors in the progression of brain injury caused by HE. The aim of this study was to investigate the potential therapeutic effect of edaravone and its underlying mechanisms against brain injury associated with HE in mice. HE was induced by the injection of thioacetamide (200 mg/kg) for 2 days and then mice treated with edaravone (10 or 20 mg/kg/day, ip) for four consecutive days. The brain tissues were dissected for histopathological, biochemical, ELISA, RT-qPCR and immunofluorescence analysis. The results showed that edaravone improved the locomotor function and ameliorated brain histopathological changes in mice with HE. Edaravone inhibited oxidative stress markers by increasing the levels of glutathione, catalase, superoxide dismutase, glutathione reductase and the upregulation of nuclear erythroid 2-related factor (Nrf2)/HO-1 pathway in the brain tissue. Administration of edaravone significantly decreased the expression of p-NF-κB and iNOS. Edaravone treatment reduced the levels of NO, MPO and MMP-9 in the brain of mice. Additionally, the brain levels and expressions of inflammatory cytokines IL-1β, IL-6, TNF-α and IFN-γ were downregulated in mice treated with edaravone. These results suggest that edaravone exerts significant neuroprotection by modulating of inflammatory and oxidative responses in HE and may serve as a promising agent for the treatment of brain injury associated with HE.

Late Onset Hepatic Encephalopathy after Living Donor Liver Transplant: Successful Reversal by Plug Embolization of Shunt—A Report of Two Cases

AbstractIn liver transplant (LT) recipients, development of portosystemic (PS) shunts can lead to hepatic encephalopathy. Here we report the cases of two patients who presented with hepatic encephalopathy 11 and 15 years after LT. Plug-assisted embolization of PS shunt led to significant improvement in their clinical and neurological symptoms, highlighting the importance of monitoring for PS shunts in long-term LT follow-up.

Clinical Characteristics of Hepatitis B Virus-Associated Hepatocellular Carcinoma Patients in Southwest Nigeria

Hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) is a major cause of morbidity and mortality in West Africa, but its presentation is poorly understood. In this study, we describe the clinical characteristics of HBV-associated HCC patients in Lagos, Nigeria. Data for all cases were collected at the emergency and gastroenterology units (2017–2019), considering chronic carriers as controls. Clinical data and routine biochemical and radiologic test results were extracted from the files. The serum biomarkers (Osteopontin, AFP-L3, DCP) were investigated. For some cases, the hepatitis B viral load was determined. The mean age of the cases (n = 92) was 41.4 years, compared to 39.9 years for the controls (n = 100). Clinically, 69.5% of cases presented with ascites, 66.3% had nodules occupying &gt;50% of the liver, and 67.4% had moderate hepatic encephalopathy. The mean viral load and the median values of Osteopontin, AFP-L3, and DCP for the cases were significantly higher than for the controls (p &lt; 0.001). The area under the curve, sensitivity, and specificity were significantly higher for Osteopontin, compared with DCP and AFP-L3 (p &lt; 0.001). Most HCC patients presented at a late disease stage, when the prognosis is usually poor. Especially Osteopontin seems to have potential for early HCC detection and could possibly complement AFP and abdominal ultrasound scan for risk-group screening.

Comparative efficacy of pre-emptive TIPS and elective TIPS in EGVB patients with cirrhosis: A single-center retrospective study.

Transjugular intrahepatic portosystemic shunt (TIPS) is the main method to prevent the rebleeding of esophagogastric varices. Many studies have demonstrated that pre-emptive TIPS (p-TIPS) is superior to medicine combined with endoscopic standard therapy in the efficacy of high-risk patients, but very few relevant studies reported whether p-TIPS is more effective than elective TIPS. This study aims to compare the efficacy and prognosis of p-TIPS and elective TIPS for the treatment of esophagogastric variceal bleeding (EGVB) patients with cirrhosis. In this retrospective study, clinical data of 92 patients with cirrhosis who accepted TIPS treatment after EGVB of cirrhosis were collected. According to the different times of TIPS, the patients were divided into the p-TIPS group and the elective TIPS group. The following information is documented: clinical manifestations and laboratory examination at 1, 3, and 6 months after the operation, survival state, the rates of rebleeding at 6 weeks and 6 months, and postoperative complications and serious adverse events during follow-up. The Child-Pugh score (P = 0.002) and MELD score (P = 0.006) in the p-TIPS group were significantly lower than those in the elective TIPS group in the 6th month after treatment. The rate of no gastric coronary vein embolization in the p-TIPS group was higher than in the elective TIPS group (P = 0.034). The hospitalized days (P < 0.001) and hospitalized costs (P < 0.001) were significantly lower in the p-TIPS group than in the elective TIPS group. No significant differences were observed between the two groups concerning rebleeding, overt hepatic encephalopathy, ascites, complications, and serious adverse events, occurrence. The p-TIPS contributes to liver function recovery and enhances patient survival benefits at 6-months postoperation in the treatment of EGVB compared with elective TIPS, without increasing the incidence of complications and adverse events.

Use of Transjugular Intrahepatic Portosystemic Shunt (TIPS) to Provide for Safe Pancreaticoduodenectomy in Patients with Portal Hypertension.

Pancreaticoduodenectomy (PD) is a complex operation associated with high morbidity, especially in the setting of hepatic fibrosis/cirrhosis and portal hypertension. Portal hypertension can be a near-certain contraindication for PD, potentially precluding patients with resectable malignancy from a curative operation. Transjugular intrahepatic portosystemic shunt (TIPS) is an artificial path between the portal vein and suprahepatic veins for decreasing the portal pressure, defined as a hepatic venous pressure gradient > 5mmHg. TIPS can be used as a bridge to facilitate the safe performance of PD. This is a single-institution retrospective analysis of patients treated with TIPS prior to PD from July 2011 to July 2022. The patient's preoperative management, perioperative course, and postoperative complications were analyzed and reported. Out of 1140 patients in a pancreatic resection database, four underwent preoperative TIPS before PD. The cohort included two males and two females, with a mean age of 66years and body mass index of 30.2. All patients had portal hypertension, with a reduction in the mean gradient following TIPS, 13mmHg to 2.5mmHg. Three patients had cirrhosis, and one had portal thrombosis. The median estimated blood loss and operative time were 275mL and 267min, respectively. Postoperatively, one patient experienced a grade IIIa complication and three developed hepatic encephalopathy at a median of 98days. All patients received chemo-radiation (two neoadjuvant, three adjuvant) and developed recurrent metastatic disease at a median of 13.5months. Median overall survival was 21.8months. TIPS in patients with portal hypertension should be considered as a bridge to a safe PD for patients with peri-ampullary adenocarcinoma.

Inequalities in developing cirrhosis complications over time: A cohort study.

Current knowledge of cirrhosis progression is derived from outdated data. We examined the progression patterns of cirrhosis in a contemporary cohort. We conducted a retrospective cohort study of adult patients diagnosed with compensated cirrhosis at 130 Veterans Affairs healthcare facilities from 10/1/2010 to 08/30/2015, with follow-up through 08/31/2023. A semi-Markov multistate model with 7 states and 15 transitions was used to evaluate progression from compensated cirrhosis to ascites, hepatic encephalopathy, variceal bleeding, hepatocellular carcinoma (HCC), multiple complications, or death, considering age and etiology (cured/active HCV, alcohol, metabolic dysfunction-associated steatotic liver disease [MASLD]) as time-varying factors. Results: We identified 24,679 patients with compensated cirrhosis. Over a median follow-up of 5.3 years, 49.8% progressed to a single complication, with ascites (30.3%) being the most common, and 3.1% progressed to multiple complications. A total of 12.9% transitioned directly to death from non-liver-related causes, while 26% remained compensated. The two-year risk of transitioning to death was 13.5%, exceeding the risk of any complication state. Younger patients and those with alcohol-related cirrhosis had faster progression, while older patients and those with active HCV had a higher incidence of HCC. Transition rates were similar for patients with alcohol and MASLD. In a contemporary cirrhosis cohort, half of patients progressed, while others remain compensated, and a large fraction transitioned directly to death, with age and etiology significantly influencing outcomes. These data highlight the importance of interventions in the high-yield period before the first complication.

Simvastatin and Rifaximin in Decompensated Cirrhosis: A Randomized Clinical Trial.

There are no useful treatments to prevent the development of severe complications of liver cirrhosis. Simvastatin and rifaximin have shown beneficial effects in liver cirrhosis. To assess whether simvastatin combined with rifaximin improves outcomes in patients with decompensated cirrhosis. Double-blind, placebo-controlled, phase 3 trial conducted among patients with decompensated cirrhosis in 14 European hospitals between January 2019 and December 2022. The last date of follow-up was December 2022. Patients were randomly assigned to receive simvastatin, 20 mg/d, plus rifaximin, 1200 mg/d (n = 117), or identical-appearing placebo (n = 120) for 12 months in addition to standard therapy, stratified according to Child-Pugh class B or C. The primary end point was incidence of severe complications of liver cirrhosis associated with organ failure meeting criteria for acute-on-chronic liver failure. Secondary outcomes included transplant or death and a composite end point of complications of cirrhosis (ascites, hepatic encephalopathy, variceal bleeding, acute kidney injury, and infection). Among the 237 participants randomized (Child-Pugh class B: n = 194; Child-Pugh class C: n = 43), 72% were male and the mean age was 57 years. There were no differences between the 2 groups in terms of development of acute-on-chronic liver failure (21 [17.9%] vs 17 [14.2%] patients in the treatment and placebo groups, respectively; hazard ratio, 1.23; 95% CI, 0.65-2.34; P = .52); transplant or death (22 [18.8%] vs 29 [24.2%] patients in the treatment and placebo groups, respectively; hazard ratio, 0.75; 95% CI, 0.43-1.32; P = .32); or development of complications of cirrhosis (50 [42.7%] vs 55 [45.8%] patients in the treatment and placebo groups, respectively; hazard ratio, 0.93; 95% CI, 0.63-1.36; P = .70). Incidence of adverse events was similar in both groups (426 vs 419; P = .59), but 3 patients in the treatment group (2.6%) developed rhabdomyolysis. The addition of simvastatin plus rifaximin to standard therapy does not improve outcomes in patients with decompensated liver cirrhosis. ClinicalTrials.gov Identifier: NCT03780673.

Update on the Complications and Management of Liver Cirrhosis

Liver cirrhosis represents the advanced pathological stage of chronic liver disease, characterized by the progressive destruction and regeneration of the hepatic parenchyma over years, culminating in fibrosis and disruption of the vascular architecture. As a leading global cause of morbidity and mortality, it continues to affect millions worldwide, imposing a substantial burden on healthcare systems. Alcoholic/nonalcoholic fatty liver disease and chronic viral hepatitis infection, hepatitis C (HCV) in particular, remain leading causes of cirrhosis. Despite significant advances in understanding the pathogenesis of cirrhosis, its management is still complex due to the multifaceted complications, including ascites, hepatic encephalopathy, variceal bleeding, and hepatocellular carcinoma, all of which severely compromise the patient outcomes and quality of life. This review aims at filling a critical gap by providing a comprehensive summary of the latest evidence on the complications and management of liver cirrhosis. Evidence-based therapies targeting both the etiologies and complications of cirrhosis are essential for improving outcomes. While liver transplantation is considered a definitive cure, advancements in pharmacological therapies offer promising avenues for halting and potentially reversing disease progression. This review summarizes the latest management strategies for cirrhosis and its associated complications, emphasizing the importance of early intervention and novel therapeutic options for improving outcomes and quality of life in affected individuals.

TIPS and hepatic encephalopathy in patients with cirrhosis.

Despite a better understanding in its prognosis and pathogenesis, hepatic encephalopathy (HE) remains one of the major complications of Transjugular Intrahepatic Portosystemic Shunt (TIPS) with a prevalence ranging from 35 to 50%. Its epidemiology differs according to the indication for TIPS (salvage/rescue TIPS, preemptive (pTIPS) or elective TIPS). In salvage/rescue TIPS, the prognosis is linked to that of bleeding, and HE should not be a contraindication to TIPS, especially as bleeding is a common precipitating factor of HE. In pTIPS, i.e. TIPS performed within the 72h after stabilization of acute variceal bleeding in high-risk patients, the risk rebleeding and HE is reduced, when compared to endoscopic and drugs treatment. As a consequence, the Baveno VII recommendations state that HE at admission should not be considered as a contraindication to pTIPS placement. In elective situations, such as refractory (intractable ascites (intolerance to diuretics) or resistant ascites (i.e. despite optimal diuretic treatment (spironolactone 400mg/d and Furosemide 160mg/d combined with low-salt treatment (< 5.2g/day) or recurrent ascites (the need for at least 3 paracenteses per year) and secondary prophylaxis of variceal bleeding, it is recommended to systematically look for risk factors for HE, and chronic or refractory HE remain not recommended to TIPS in most centers. Chronic HE involves persistent neurological symptoms with fluctuating acute episodes. Recurrent HE refers to repeated episodes occurring within 6 months, while refractory HE is resistant to standard treatments, often requiring more aggressive management (Vilstrup et al. 2014). A careful selection of patients is mandatory before elective TIPS decision. Risk factors must be identified and corrected if possible before any TIPS decision is made. Management of HE after TIPS is based on identification of precipitating factors, curative treatment with lactulose as first-line therapy and rifaximin as second-line therapy, and nutritional management. In elective TIPS, prophylactic administration of rifaximin is recommended in order to decrease the risk of further HE development in selected patients (not in everyone, at least according to Baveno VII). Liver transplantation (LT) should be discussed with a multidisciplinary team as an alternative option to TIPS in case of high-risk of post-TIPS HE, and in case of refractory HE after TIPS.

The role of multifocal visual evoked potential in detection of minimal hepatic encephalopathy in patients with compensated liver cirrhosis.

Minimal hepatic encephalopathy (MHE) is one of the most debilitating complications of hepatic cirrhosis, and visual electrophysiology, visual evoked potential (VEP) has long been used for MHE diagnosis. This technique only produces a summed response that is greatly dominated by the macular region. Multifocal visual evoked potential (mfVEP) imaging minimizes these limitations because it allows topographic recording of the optic nerve and visual cortex. The aim of this study was to detect minimal hepatic encephalopathy among cirrhotic patients using the mfVEP in comparison to the validated psychometric hepatic encephalopathy score (PHES), paired associative learning (PAL) and the Benton visual retention test (BVRT). Forty-five patients with compensated hepatic cirrhosis were enrolled in our study and compared to 45 normal controls who were matched for age, sex and educational level. Both groups underwent psychological tests (PHES, PAL, BVRT) and neurophysiological tests (mfVEP). 1According to the validated PHES, 14 patients were found to have MHE, 15 patients were found to have abnormal mfVEP, and abnormalities in the BVRT and PAL were found in 11 and 10 patients, respectively. 2-mfVEP showed the highest sensitivity in the detection of MHE in reference to the PHES. 3- The mfVEP test and potentially the BVRT have the advantage of detecting subtle abnormalities in non-MHE cirrhotic patients, for further research and follow-up are needed. mfVEP demonstates promising results for objective early detection of MHE, with a sensitivity of approximately 92.9%.

A new prognostic model based on serum apolipoprotein AI in patients with HBV-ACLF and acutely decompensated liver cirrhosis

Background/AimTo investigate the prognostic value of circulating apolipoprotein AI (apoAI) levels and develop a new prognostic model in individuals with acute-on-chronic liver failure (ACLF) and acute decompensation (AD) of liver cirrhosis caused by hepatitis B virus (HBV) infection.MethodsBaseline levels of serum lipids were measured, and data concerning the presence of complications were collected from 561 HBV-ACLF and AD patients. Survival analysis was conducted by log-rank test. Proportional hazards model was used to perform multivariate analysis. The dynamics of serum apoAI levels were also explored in 37 HBV-ACLF patients.ResultsIn the cohort, the negatively correlation was found between the Model for End-Stage Liver Disease (MELD) score and serum apoAI levels (r = -0.7946, P < 0.001). Circulating apoAI concentration was an independent risk factor for 90-day survival according to Cox multivariate analysis. A new prognostic score-integrated serum lipid profile for ACLF patients (Lip-ACLF score = 0.86×International Normalized Ratio (INR) + 0.0034×total bilirubin (TBIL) (µmol/L) + 0.99× hepatorenal syndrome (HRS) (HRS: no/1; with/2) + 0.50×hepatic encephalopathy (HE) (grade/ponint: no/1; 1–2/2; 3–4/3) − 2.97×apoAI (g/L) + 5.2) was subsequently designed for the derivation cohort. Compared to MELD score, Child-Turcotte-Pugh (CTP) score or apoAI, Lip-ACLFs was superior for the prediction of 90-day outcomes (receiver operating characteristic curve (ROC): 0.930 vs. 0.885, 0.833 or 0.856, all P < 0.01), as was the validation cohort (ROC 0.906 vs. 0.839, 0.857 or 0.837, all P < 0.05). In Kaplan‒Meier survival analysis, low apoAI levels (< 0.42 g/L) at baseline indicated poor prognosis in ACLF and AD patients. Among the 37 patients, the deceased individuals were characterised with significantly decreased serum apoAI levels during the follow-up test compared with those at baseline (P < 0.05), whereas in patients with a good prognosis, the serum apoAI levels remained stable during the follow-up.ConclusionIn HBV-ACLF and AD patients, lower serum apoAI levels suggest greater disease severity and 90-day mortality risk. For predicting the short-term prognosis of these patients, the new Lip-ACLF score might serve as a potential model.

Cell-cell communications in the brain of hepatic encephalopathy: The neurovascular unit.

Many patients with liver diseases are exposed to the risk of hepatic encephalopathy (HE). The incidence of HE in liver patients is high, showing various symptoms ranging from mild symptoms to coma. Liver transplantation is one of the ways to overcome HE. However, not all patients can receive liver transplantation. Moreover, patients who have received liver transplantation have limitations in that they are vulnerable to hepatocellular carcinoma, allograft rejection, and infection. To find other therapeutic strategies, it is important to understand pathological factors and mechanisms that lead to HE after liver disease. Oxidative stress, inflammatory response, hyperammonaemia and metabolic disorders seen after liver diseases have been reported as risk factors of HE. These are known to affect the brain and cause HE. These peripheral pathological factors can impair the blood-brain barrier, cause it to collapse and damage the neurovascular unit component of multiple cells, including vascular endothelial cells, astrocytes, microglia, and neurons, leading to HE. Many previous studies on HE have suggested the impairment of neurovascular unit and cell-cell communication in the pathogenesis of HE. This review focuses on pathological factors that appear in HE, cell type-specific pathological mechanisms, miscommunication/incorrect relationships, and therapeutic candidates between brain cells in HE. This review suggests that regulating communications and interactions between cells may be important in overcoming HE.

Exploring the link between liver cirrhosis and liver metastasis in colorectal cancer.

301 Background: Colorectal cancer (CRC) is the third most common cancer and the second most common cause of cancer mortality in the world. Although it is now associated with improved outcomes due to advancements in treatment modalities, CRC continues to be the most common source of liver metastasis. Previous studies have shown cirrhotic livers to be at reduced risk of metastatic disease. Our study aims to investigate the association between colorectal cancer and liver metastasis in the presence of concomitant liver cirrhosis. Methods: The National Inpatient Sample (NIS) was queried to identify all hospitalizations with colorectal cancer utilizing ICD-10 codes C18.x, C19.x, and C20.x from 2016 to 2020 and were further classified based on the presence or absence of cirrhosis. Demographic and clinical data were analyzed using chi-squared tests, independent sample t-tests, and binary logistic regression (adjusted for age, gender, and Charlson comorbidity index or CCI). The primary outcome studied was liver metastasis. Secondary outcomes were hepatic encephalopathy, portal hypertension, and spontaneous bacterial peritonitis. Statistical significance is indicated by a p-value less than 0.05. Results: A total of 255,599 hospitalizations with colorectal cancer were identified. Out of these, 5,370 (2.1%) had liver cirrhosis and 250,229 (97.9%) did not. Hospitalizations with CRC and concomitant cirrhosis had higher comorbidities as per the Charlson Comorbidity Index (10.5 vs 8.1, p-value&lt;0.001) and higher mortality rates (8.5% vs 4.2%, p-value&lt;0.001). Higher rates of liver metastasis (26.5 vs 23.4, p &lt;0.001) and portal hypertension (26.1% vs 0.3%, p&lt;0.001) were observed in the cirrhosis subgroup. This subgroup also has a significantly higher risk of SBP (2.8% vs 0.2%, p &lt;0.001). Conclusions: This is a large retrospective study analyzing the impact of cirrhosis on liver metastasis in patients with colorectal cancer. Patients with concomitant cirrhosis consistently have increased liver metastasis and worse outcomes. The results of this study imply that diligent CRC screening is of utmost importance in patients with cirrhosis. Patients with CRC and coexisting cirrhosis would benefit from routine surveillance such as carcinoembryonic antigen (CEA) screening or CT scans to allow early detection of liver metastases which could potentially improve outcomes. Colorectal Cancer Patients No Cirrhosis (N=250,229) Cirrhosis (N=5,370) p-value Age (in years) 65.79 ± 13.8 65.04 ± 10.9 &lt;.001 Sex (Female) 47.3% 36.8% &lt;.001 Charlson Comorbidity Index 8.1 ± 3.6 10.5 ± 3.7 &lt;.001 Mortality 4.2% 8.5% &lt;.001 Length of Stay 6.6 ± 7.2 7.4 ± 7.2 &lt;.001 Liver Metastasis 23.4% 26.5% &lt;.001 Hepatic Encephalopathy 0.0% 0.2% &lt;.001 Portal hypertension 0.3% 26.1% &lt;.001 Spontaneous Bacterial Peritonitis (SBP) 0.2% 2.8% &lt;.001

Malnutrition and Associated Factors Among Patients With Cirrhosis at a Tertiary Care Center in Addis Ababa Ethiopia: An Ordinal Logistic Regression Analysis.

Cirrhosis is an irreversible stage of liver damage that decreases the ability of the liver to store and metabolize nutrients. Malnutrition is a common problem in patients with cirrhosis and increases the risk of mortality. This study aimed to assess malnutrition and associated factors among patients with cirrhosis at Tikur Anbessa Specialized Hospital, Addis Ababa, Ethiopia. A cross-sectional study was conducted at Tikur Anbessa Specialized Hospital. All patients with cirrhosis who were admitted to the hospital from August to November were included. Royal Free Hospital Global Assessment tool (RFH-GA) was used to assess nutritional status. Data were entered in Epi-data software version 4.6.0.2 and analyzed with STATA version 17/MP. Ordinal logistic regression analysis was fitted to determine factors associated with nutritional status. Statistical significance was declared at p value < 0.05. The prevalence of moderate malnutrition and severe malnutrition were 36.67% and 14.29%, respectively. Patients with ascites were five times at a higher risk of being severely malnourished (AOR = 5.08; 95% CI = 2.66-9.67). The odds of severe malnutrition decrease by 0.35 times for patients without a history of previous hospitalization (AOR = 0.35; 95% CI = 0.18-0.68). The odds of being in the higher category of nutritional status (severe malnutrition) are 10 times higher for patients with hepatic encephalopathy (AOR = 10.43; 95% CI = 4.66-23.31). As the level of creatinine blood urea nitrogen (Cr-BUN) increases, the risk of malnutrition increases by 2.57 times (AOR = 2.57; 95% CI = 1.02-5.78). Malnutrition is high among cirrhotic patients at Tikur Anbessa Specialized Hospital. Ascites, history of hospitalization, Cr-BUN, and hepatic encephalopathy are significant predictors of malnutrition.

Portal vein intimal thickening in patients with cirrhosis is associated with indicators of portal hypertension.

The exact pathophysiology of portal vein thrombosis (PVT), a common complication of cirrhosis, remains largely unknown. We previously found that cirrhotic PVT consists of fibrotic intimal thickening of the portal vein wall rather than of true fibrin-rich thrombus. We hypothesized that this portal vein intimal thickening is secondary to portal hypertension and/or to local inflammatory responses. The intimal thickness of right and left portal branches was measured in hilar liver samples from 232 cirrhotic patients without PVT who underwent liver transplantation. The relation between intimal thickness and pre-transplant clinical variables was studied with linear regression. CT-scans of 25 patients prior to liver transplantation were reanalysed for portal vein and portal hypertension-related characteristics. Median right intimal thickness was 129 (1 - 300 (IQR)) μm, median left intimal thickness was 112 (1 - 230) μm and there was correlation between intimal thickness in the right and left branches in individual patients (r = 0.30, P<.001). Intimal thickness of the portal vein was associated with a history of variceal bleeding, hepatic encephalopathy or ascites, etiology of disease and statin use. Other factors, including duration of liver disease, presence of infection, or radiological characteristics were not significantly associated with intimal thickness. Intrahepatic portal vein intimal thickness is highly variable in patients with cirrhosis, but relatively consistent between right and left portal branches. The association between intimal thickness and history of variceal bleeding suggests that portal hypertension may contribute to initiation of intimal thickening, and consequently to the development of PVT.

567 Post-transplant hepatic encephalopathy after recurrent cirrhosis

567 Post-transplant hepatic encephalopathy after recurrent cirrhosis

Efficacy and safety of rifaximin for the prophylaxis of hepatic encephalopathy: A meta-analysis.

The efficacy of rifaximin in the prevention of overt hepatic encephalopathy (HE) has not been established. The aim of this study was to access the efficacy and safety of rifaximin in the prophylaxis of HE. We conducted a meta-analysis search of the Cochrane Library, PubMed, ClinicalTrials.gov, Web of Science, and EMBASE as of March 2022. We pooled data by random-effects DerSimonian-Laird models to calculate hazard ratios (relative risks, RRs) for mortality, incidence of HE, and adverse events. Fourteen randomized controlled trials were included in the study. Rifaximin helped prevent HE (RR = -0.47, 95% confidence interval [CI]: -0.68 to -0.26) in patients with cirrhosis, but did not reduce mortality (RR = 0.03, 95% CI: -0.32 to 0.39) or increase the occurrence of adverse events (RR = -0.08, 95% CI: 0.22-0.07). Subgroup analysis showed that rifaximin was effective in both the primary (RR = 1.17, 95% CI: 1.06-1.29) and secondary (RR = 1.17, 95% CI: 1.06-1.29) prevention of HE. Moreover, subgroup analysis found that rifaximin helped prevent HE in alcohol-related (RR = -0.59, 95% CI: -0.87 to -0.32) or virus-associated (RR = -0.41, 95% CI: -0.71 to -0.11), and underwent transjugular intrahepatic portosystemic shunt (RR = -0.51, 95% CI: -0.76 to -0.27) or non-transjugular intrahepatic portosystemic shunt (RR = -0.35, 95% CI: -0.66 to -0.05) cirrhotic patients. Subgroup analyzed by the intervention, rifaximin versus placebo (RR = -0.43, 95% CI: -0.73 to -0.14) and rifaximin+lactulose versus lactulose (RR = -0.57, 95% CI: -0.68 to -0.26) were statistically significant prevention of HE, rather than rifaximin versus lactulose (RR = -0.44, 95% CI: -1.0 to 0.11). Rifaximin is beneficial for primary and secondary prevention of HE, but it does not reduce mortality or increase the incidence of adverse events in patients with end-stage cirrhosis caused by virus or alcohol.

Hepatic encephalopathy and spontaneous bacterial peritonitis are associated with increased liver-related readmissions in cirrhosis

Hepatic encephalopathy and spontaneous bacterial peritonitis are associated with increased liver-related readmissions in cirrhosis