Plasma lipidomics and fungal peptide-based community analysis identifies distinct signatures of early mortality in acute liver failure.

Background And Aims: Acute liver failure (ALF) has high mortality predominantly due to compromised immune system and increase vulnerability to bacterial and fungal infections.

Method: Plasma lipidome and fungal peptide-based-community (mycobiome) analysis were performed in Discovery cohort (40-ALF, 5-healthy) and validated in a validation cohort of 230-ALF using High-resolution-mass-spectrometry, artificial-neural-network (ANN) and machine-learning (ML).

Results: Untargeted lipidomics identified 2,013 lipids across 8 lipid-groups.

Cilostazol counteracts mitochondrial dysfunction in hepatic encephalopathy rat model: Insights into the role of cAMP/AMPK/SIRT1/ PINK-1/parkin hub and p-CREB /BDNF/ TrkB neuroprotective trajectory.

A devasting stage of chronic hepatic dysfunction is strictly correlated with neurological impairment, signifying hepatic encephalopathy (HE). HE is a multifactorial condition; therefore, hyperammonemia, oxidative stress, neuroinflammation, and mitochondrial dysfunction interplay in HE's progressive development. Cilostazol (Cilo) has shown promising neuroprotective and hepatoprotective effectiveness in different neuronal and hepatic disorders; however, its efficiency against HE hasn't yet been explored.

Reversibility of structural and functional alterations of hepatic encephalopathy.

Hepatic Encephalopathy (HE) is a frequent complication of chronic liver disease. Type C HE mainly appears in episodes; only seldom chronic persistent forms occur. HE can lead to hospitalization and it has a huge impact on the health related quality of life.

CD47 signaling induces hepatic cell death and microglia activation during hepatic encephalopathy.

Acute liver failure results from severe hepatic injury and can lead to neurological dysfunction known as hepatic encephalopathy (HE). Thrombospondin-1 can contribute to HE by increasing cerebral edema and microglia activation in the azoxymethane (AOM) mouse model. CD47 is a receptor for TSP1 and can directly modulate inflammation in numerous disease states.

Value of systemic inflammation markers for the detection of minimal and prediction of overt hepatic encephalopathy after TIPS insertion.

Development of overt hepatic encephalopathy (oHE) is a particularly feared complication when considering treatment with transjugular intrahepatic portosystemic shunt (TIPS). However, the pathophysiology of HE, in particular after TIPS-insertion, is complex and valid predictors remain scarce. We aimed to investigate whether systemic inflammation markers (SIM) are linked to minimal (mHE) and overt HE (oHE) development before and after TIPS.

Sarcomatoid hepatocellular carcinoma with subdiaphragmatic metastasis misdiagnosed as liver abscess: A case report.

Rationale: Sarcomatoid hepatocellular carcinoma (SHC) is a rare subtype of hepatocellular carcinoma. Its imaging findings often resemble those of liver abscess, making preoperative diagnosis particularly challenging. To date, there have been no documented cases of SHC with subdiaphragmatic metastases.

Ceftriaxone encephalopathy in a very elderly dialysis patient.

Ceftriaxone is widely used clinically but it can potentially cause ceftriaxone encephalopathy in individuals who are on dialysis. We describe ceftriaxone encephalopathy in a dialysis patient. The 87-year-old Japanese woman had a 9-year dialysis history.

Development and Validation of a New Model Including Inflammation Indexes for the Long-Term Prognosis of Hepatitis B-Related Acute-On-Chronic Liver Failure.

Acute-on-chronic liver failure (ACLF) is a severe condition characterized by a systemic inflammatory response and associated with high mortality. Currently, there is no reliable prediction model for long-term prognosis in ACLF. This study aimed to develop and validate a prognostic model incorporating inflammation indexes to predict the long-term outcome of patients with hepatitis B virus-related ACLF (HBV-ACLF).

Dodder ( sp.) extract prevents cognitive deficits in a rat model of hepatic encephalopathy.

Objective: In our study, the protective effect of dodder plant extract against encephalopathy induced by cholestatic liver disease model was investigated.

Methods: Spraque Dawley rats were used in the study. For the cholestatic liver disease model, the bile duct ligation (BDL) was applied.

Insights and future directions in studying intestinal microbiota post-transjugular intrahepatic portosystemic shunt for hepatitis B virus-related portal hypertension.

The gut microbiota (GM) plays a major role in the progression and treatment response of liver diseases, with diverse compositions based on different etiologies. In China, hepatitis B virus (HBV) infection is the leading cause of cirrhosis and affects the GM composition in patients with cirrhosis-related portal hypertension (PH). However, a few studies have been conducted on GM alterations after transjugular intrahepatic portosystemic shunt (TIPS) in patients with HBV-related PH.

Mechanisms and implications of recompensation in cirrhosis.

Decompensated cirrhosis has long been considered the irreversible end stage of liver disease, characterised by further decompensating events until death or liver transplantation. However, the observed clinical improvements after effective antiviral treatments for HBV and HCV and after sustained alcohol abstinence have changed this paradigm, leading to the concept of "recompensation" of cirrhosis. Recompensation of cirrhosis was recently defined by Baveno VII as (i) cure of the primary liver disease aetiology; (ii) disappearance of signs of decompensation (ascites, encephalopathy and portal hypertensive bleeding) off therapy; and (iii) stable improvement of liver function tests (bilirubin, international normalised ratio and albumin).

The Misdiagnosis and Underdiagnosis of Hepatic Encephalopathy.

Patients with cirrhosis are at risk of developing hepatic encephalopathy (HE), which can present with a wide range of symptoms, including confusion, lethargy, inappropriate behavior, and altered sleep patterns. In addition to HE, patients with cirrhosis are at risk of developing mild cognitive impairment, dementia, and delirium, which have features closely resembling HE. Given the similar presentation of these conditions, misdiagnosis can and does occur.

Liver Transplantation for Acute Liver Failure due to Mushroom Poisoning.

Background/aims: Liver transplantation is a life-saving approach in some cases of mushroom poisoning, which is one of the important causes of acute liver failure. However, debate continues regarding the timing of liver transplantation. The aim of this study is to retrospectively evaluate the results of patients who underwent liver transplantation due to mushroom poisoning.

The burden of hepatic encephalopathy and the use of albumin as a potential treatment.

As a potential sequela of cirrhosis, hepatic encephalopathy (HE) significantly impacts the lives of patients and caregivers and places a substantial burden on the healthcare system. With an increasing incidence over time and a cumulative effect on cognition, HE adversely effects quality of life, morbidity and mortality in patients with cirrhosis. HE can range from minimal or covert (MHE/CHE) to overt and symptomatic (OHE).

Down the road towards hepatic encephalopathy. Urea synthesis - the liver workhorse of nitrogen metabolism.

Urea synthesis is an irreversible, essential for maintenance of health and life, and highly regulated liver function with a very high capacity for production of the end-product urea-nitrogen. The set-point of urea synthesis in relation to its overall substrate, the prevailing blood concentration of L-α-amino acids, contributes to determine whole-body nitrogen balance and the size and composition of the plasma free amino acid pool. Ammonia is definitively eliminated from the body by urea synthesis.

Systems of care that improve outcomes for people with hepatic encephalopathy.

Hepatic encephalopathy (HE) is a critical neuropsychiatric complication of liver cirrhosis with a significant impact on patient quality of life and survival. The global prevalence of cirrhosis and associated HE necessitates a comprehensive understanding of the condition and effective systems of care to optimize outcomes. This review addresses the epidemiology, classification, diagnosis, and management of HE, with an emphasis on systems of care that improve outcomes for people with HE.

Down the road towards hepatic encephalopathy. The elusive ammonia- what determines the arterial concentration?

Elevated arterial ammonia is associated with several complications of liver disease as it predicts mortality for in-patients and decompensation, hospitalization and death in out-patients with cirrhosis. In this review, our aim was to estimate how the individual organs contribute to arterial ammonia based on published data from human studies. The brain removes ammonia from arterial blood in a concentration-dependent fashion.

A Novel Scoring System for Assessing In-Hospital Mortality Risk in Patients With Liver Cirrhosis.

Background Mortality among patients with liver cirrhosis has recently increased in Indonesia. However, predicting the prognosis of patients hospitalized with liver cirrhosis remains a clinical challenge due to its variability and dependence on multiple factors. A simple and accurate method is required to identify high-risk patients.

Effects of cholestasis and hyperammonemia on dendritic spine density and turnover in rat hippocampal neurons.

Adults and children with cholestatic liver disease are at risk for type C hepatic encephalopathy (HE) and may present lifelong neurocognitive impairment. While the underlying cellular and molecular mechanisms are still incompletely understood, ammonium and bile acids (BAs) seem to play a key role in this pathology, by crossing the blood-brain-barrier and modifying neuronal homeostasis and synaptic plasticity. This experimental study aimed to investigate the effects of ammonium and BAs on dendritic spines of rat hippocampal CA1 neurons.

A transient blood IL-17 increase triggers neuroinflammation in cerebellum and motor incoordination in hyperammonemic rats.

Patients with liver cirrhosis may show minimal hepatic encephalopathy (MHE) with motor incoordination which is reproduced in hyperammonemic rats. Hyperammonemia induces peripheral inflammation which triggers neuroinflammation and enhanced GABAergic neurotransmission in cerebellum and motor incoordination. The mechanisms involved remain unknown.

Brain reserve in hepatic encephalopathy: Pathways of damage and preventive strategies through lifestyle and therapeutic interventions.

Brain reserve is an important concept to understand the variability of damage associated with brain-related diseases and includes the adaptation of cognitive processes to preserve brain function. A good cognitive reserve might delay the onset of clinical manifestations of neurodegenerative diseases as well as hepatic encephalopathy, improving the quality of life in patients with chronic liver diseases. By stimulating activities and maintaining overall health, individuals may be able to enhance their brain's resilience to age-related changes and pathology.

Hyperammonaemic encephalopathy due to non-functioning urea cycle as a complication to gastric bypass surgery.

Hyperammonaemic encephalopathy in the absence of liver failure is a major diagnostic challenge. A rare cause is as a complication to previous gastric bypass surgery, a condition reported to be associated with high mortality. In this case report, we present the exhaustive diagnostic work-up and clinical reversal of deep and recurrent hyperammonaemic encephalopathy in a patient with previous gastric bypass surgery.