Minimal encephalopathy in hereditary hemorrhagic telangiectasia patients with portosystemic vascular malformations.

Background: Hereditary hemorrhagic telangiectasia (HHT) is characterized by telangiectasia and larger vascular malformations. Liver malformations are the most frequent visceral involvement including the presence of portosystemic malformations (PSM) that can cause hepatic encephalopathy. Minimal hepatic encephalopathy (mHE) is characterized by alterations of brain function in neuropsychological or neurophysiological tests and decreases quality of life.

Liver assistive devices in acute liver failure: Current use and future directions.

Acute liver failure (ALF) is a rare syndrome where rapid deterioration of liver function occurs after an acute insult in a patient without prior chronic liver disease and leads to jaundice, hepatic encephalopathy (HE), and oftentimes multiorgan failure (MOF). At this time, the only definitive treatment for ALF is LT but some patients, particularly APAP-induced ALF patients, may have ongoing regenerative capacity of the liver and may not require LT with ongoing supportive management. As a result, extracorporeal liver support (ECLS) has been a topic of interest both as a bridge to LT and as a bridge to spontaneous recovery and aims to remove damaging toxins that further aggravate liver failure, stimulate regeneration of the liver, and improve pathophysiologic consequences of liver failure.

Evaluation and management of neurological complications in acute liver failure.

Neurological complications in acute liver failure are the most common cause of mortality in this group of patients. Almost all neurologic complications arise from underlying increase in intracranial pressure in ALF. In addition to symptomatic management, the treatment relies on measures to bring down ICP.

Advanced strategies for intensive care management of acute liver failure.

Acute liver failure (ALF) is defined as the loss of hepatic function in conjunction with hepatic encephalopathy and coagulopathy. There is histological evidence of profound hepatocyte damage. If it is not aggressively managed, ALF can be fatal within a few days.

Coagulopathy in acute liver failure.

Acute liver failure (ALF) is a rare but rapidly progressing syndrome, marked by severe liver dysfunction and altered mental status. While definitions of ALF vary across different guidelines, with timelines ranging from 4 to 26 weeks between jaundice onset and encephalopathy, the key defining features remain encephalopathy and coagulopathy. Elevated coagulation markers, particularly prothrombin time and international normalized ratio, have traditionally been associated with bleeding risks.

Investigating cognitive impairments and hippocampal proteome alterations in aged male rats with TAA-Induced minimal hepatic encephalopathy.

The aging population faces a gradual decline in physical and mental capacities, with an increased risk of liver cirrhosis and chronic liver diseases leading to hepatic encephalopathy (HE). The intertwining of physiological manifestations of aging with the pathophysiology of HE significantly impairs cognitive ability, reduces quality of life, and increases mortality. Hence, effective therapeutic intervention is imperative.

Stem cell transplantation therapy for advanced liver damage-associated neurodegenerative disorders.

Hepatic encephalopathy and other neurodegenerative disorders have profound implications for extensive liver impairment, calling for new ways of treating the condition. The application of stem cell transplantation to treat these severe disorders is a new and encouraging technique. This review article digs deep into the subject of stem cell transplantation therapy, neurodegenerative disorders associated with advanced liver damage, and liver transplantation.

Contribution of extracellular vesicles to neuroinflammation and cognitive and motor deficits in hyperammonemia and hepatic encephalopathy.

Cirrhotic patients can present hepatic encephalopathy (HE), showing motor and cognitive deficits. Hyperammonemia and peripheral inflammation are known to induce neuroinflammation and alter neurotransmission, which finally induces neurological impairment in HE. However, the mechanisms by which the deleterious effects of peripheral inflammation are transmitted to the brain are not well understood.

Extracellular vesicles from mesenchymal stem cells improve neuroinflammation and neurotransmission in hippocampus and cognitive impairment in rats with mild liver damage and minimal hepatic encephalopathy.

Background: Patients with steatotic liver disease may show mild cognitive impairment. Rats with mild liver damage reproduce this cognitive impairment, which is mediated by neuroinflammation that alters glutamate neurotransmission in the hippocampus. Treatment with extracellular vesicles (EV) from mesenchymal stem cells (MSC) reduces neuroinflammation and improves cognitive impairment in different animal models of neurological diseases.

Bacterial infection adversely increases the risk of decompensation in patients with hepatitis B virus-related compensated cirrhosis: a retrospective study.

Background: Hepatitis B virus related compensated cirrhosis generally has a favorable prognosis until decompensation occurs. Bacterial infections are prevalent in Hepatitis B virus related decompensated cirrhosis.Bacterial infection and decompensated hepatitis B cirrhosis are mutually reinforcing.

Increasing incidence of mycotoxicosis in South-Eastern Germany: a comprehensive analysis of mushroom poisonings at a University Medical Center.

Background: Mushrooms, an integral component of human diets, range from esteemed delicacies to potentially lethal toxins. The risk of severe poisoning from misidentified species, poses a significant challenge. For clinicians, recognizing mushroom poisoning amidst nonspecific symptoms and determining the specific mushroom ingested are critical yet complex tasks.

Role of astrocytes and microglia in hepatic encephalopathy associated with advanced chronic liver disease: lessons from animal studies.

Hepatic encephalopathy, defined as neuropsychiatric dysfunction secondary to liver disease, is a frequent decompensating event in cirrhosis. Its clinical impact is highlighted by a notable increase in patient mortality rates and a concomitant reduction in overall quality of life. Systemically, liver disease, liver function failure, portosystemic shunting, and associated multi-organ dysfunction result in the increase of disease-causing neurotoxins in the circulation, which impairs cerebral homeostasis.

The Role of Vitamin D Deficiency in Hepatic Encephalopathy: A Review of Pathophysiology, Clinical Outcomes, and Therapeutic Potential.

Hepatic encephalopathy (HE) is a neuropsychiatric condition frequently associated with cirrhosis and portosystemic shunting (PSS). It imposes a significant clinical and economic burden, with increasing attention toward identifying modifiable factors that could improve outcomes. Emerging evidence suggests that vitamin D deficiency (VDD), prevalent in patients with cirrhosis, may contribute to the development and severity of HE.

Graft inflow modulation in recipients with portal hypertension.

The extended application of living donor liver transplantation (LDLT) has revealed the problem of graft size mismatching, potentially leading to the "small-for-size syndrome" (SFSS). SFSS is a rare dysfunction that may affect a partial liver graft, characterized by coagulopathy, cholestasis, ascites, and encephalopathy. A key role in the physiopathology of SFSS is played by portal hypertension (PHT) to which a small allograft is submitted after reperfusion, resulting in sinusoidal congestion and hemorrhage.

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.

Predicting the risk of mortality in children with dengue-induced hepatitis admitted to the paediatric intensive care unit.

Background: Dengue-associated acute liver failure (PALF) accounts for a high mortality rate in children admitted to the pediatric intensive care unit (PICU). To date, there is a lack of data on clinical algorithms for estimating the risk of mortality in pediatric patients with dengue-induced severe hepatitis (DISH).

Aim: To determine the prevalence of PALF and identify the predictors of mortality among patients with DISH.

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.