Use of albumin infusion for cirrhosis-related complications. An international position statement

Background & Aims: Numerous studies have evaluated the role of human albumin (HA) in managing various liver cirrhosis-related complications. However, their conclusions remain partially controversial, probably because HA was evaluated in different settings, including indications, patient characteristics, and dosage and duration of therapy. Methods: Thirty-three investigators from 19 countries with expertise in the management of liver cirrhosis-related complications were invited to organise an International Special Interest Group. A three-round Delphi consensus process was conducted to complete the international position statement on the use of HA for treatment of liver cirrhosis-related complications. Results: Twelve clinically significant position statements were proposed. Short-term infusion of HA should be recommended for the management of hepatorenal syndrome, large volume paracentesis, and spontaneous bacterial peritonitis in liver cirrhosis. Its effects on the prevention or treatment of other liver cirrhosis-related complications should be further elucidated. Long-term HA administration can be considered in specific settings. Pulmonary oedema should be closely monitored as a potential adverse effect in cirrhotic patients receiving HA infusion. Conclusions: Based on the currently available evidence, the international position statement suggests the potential benefits of HA for the management of multiple liver cirrhosis-related complications and summarises its safety profile. However, its optimal timing and infusion strategy remain to be further elucidated. Impact and implications: Thirty-three investigators from 19 countries proposed 12 position statements on the use of human albumin (HA) infusion in liver cirrhosis-related complications. Based on current evidence, short-term HA infusion should be recommended for the management of HRS, LVP, and SBP; whereas, long-term HA administration can be considered in the setting where budget and logistical issues can be resolved. However, pulmonary oedema should be closely monitored in cirrhotic patients who receive HA infusion

Time course of collagen peak in bile duct-ligated rats

<p>Abstract</p> <p>Background</p> <p>One of the most useful experimental fibrogenesis models is the "bile duct-ligated rats". Our aim was to investigate the quantitative hepatic collagen content by two different methods during the different stages of hepatic fibrosis in bile duct-ligated rats on a weekly basis. We questioned whether the 1-wk or 4-wk bile duct-ligated model is suitable in animal fibrogenesis trials.</p> <p>Methods</p> <p>Of the 53 male Wistar rats, 8 (Group 0) were used as a healthy control group. Bile duct ligation (BDL) had been performed in the rest. Bile duct-ligated rates were sacrificed 7 days later in group 1 (10 rats), 14 days later in group 2 (9 rats), 21 days later in group 3(9 rats) and 28 days later in group 4 (9 rats). Eight rats underwent sham-operation (Sham). Hepatic collagen measurements as well as serum levels of liver enzymes and function tests were all analysed.</p> <p>Results</p> <p>The peak level of collagen was observed biochemically and histomorphometricly at the end of third week (P < 0.001 and P < 0.05). Suprisingly, collagen levels had decreased with the course of time such as at the end of fourth week (P < 0.01 and P < 0.05).</p> <p>Conclusion</p> <p>We have shown that fibrosis in bile duct-ligated rats is transient, i.e. reverses spontaneously after 3 weeks. This contrasts any situation in patients where hepatic fibrosis is progressive and irreversible as countless studies performed by many investigators in the same animal model.</p

Oxygen-sensing neurons reciprocally regulate peripheral lipid metabolism via neuropeptide signaling in <i>Caenorhabditis elegans</i>

<div><p>The mechanisms by which the sensory environment influences metabolic homeostasis remains poorly understood. In this report, we show that oxygen, a potent environmental signal, is an important regulator of whole body lipid metabolism. <i>C</i>. <i>elegans</i> oxygen-sensing neurons reciprocally regulate peripheral lipid metabolism under normoxia in the following way: under high oxygen and food absence, URX sensory neurons are activated, and stimulate fat loss in the intestine, the major metabolic organ for <i>C</i>. <i>elegans</i>. Under lower oxygen conditions or when food is present, the BAG sensory neurons respond by repressing the resting properties of the URX neurons. A genetic screen to identify modulators of this effect led to the identification of a BAG-neuron-specific neuropeptide called FLP-17, whose cognate receptor EGL-6 functions in URX neurons. Thus, BAG sensory neurons counterbalance the metabolic effect of tonically active URX neurons via neuropeptide communication. The combined regulatory actions of these neurons serve to precisely tune the rate and extent of fat loss to the availability of food and oxygen, and provides an interesting example of the myriad mechanisms underlying homeostatic control.</p></div

Mapping artificial intelligence adoption in hepatology practice and research: challenges and opportunities in MENA region

BackgroundArtificial intelligence (AI) is increasingly relevant to hepatology, yet real-world adoption in the Middle East and North Africa (MENA) is uncertain. We assessed awareness, use, perceived value, barriers, and policy priorities among hepatology clinicians in the region.MethodsA cross-sectional online survey targeted hepatologists and gastroenterologists across 17 MENA countries. The survey assessed clinical and research applications of AI, perceived benefits, clinical and research use, barriers, ethical considerations, and institutional readiness. Descriptive statistics and thematic analysis were performed.ResultsOf 285 invited professionals, 236 completed the survey (response rate: 82.8%). While 73.2% recognized the transformative potential of AI, only 14.4% used AI tools daily, primarily for imaging analysis and disease prediction. AI tools were used in research by 39.8% of respondents, mainly for data analysis, manuscript writing assistance, and predictive modeling. Major barriers included inadequate training (60.6%), limited AI tool access (53%), and insufficient infrastructure (53%). Ethical concerns focused on data privacy, diagnostic accuracy, and over-reliance on automation. Despite these challenges, 70.3% expressed strong interest in AI training., and 43.6% anticipating routine clinical integration within 1–3 years.ConclusionMENA hepatologists are optimistic about AI but report limited routine use and substantial readiness gaps. Priorities include scalable training, interoperable infrastructure and standards, clear governance with human-in-the-loop safeguards, and region-specific validation to enable safe, equitable implementation

The Prevalence and Risk Factors Associated with Post-infective Irritable Bowel Syndrome (PI-IBS) Developed in Hospitalized Patients Due to Acute Bacterial Gastroenteritis

[Abstract not Available

The effects of Valsalva manoeuvres on venepuncture pain

Background and objective: Stimulating the vagus nerve reduces pain. The purpose of this study was to evaluate the effect of a Valsalva. manoeuvre, which stimulates the vagus nerve, on perception of pain during peripheral venous cannulation in adult patients. Methods: This was a prospective randomized clinical trial. One hundred and ten patients scheduled for elective surgery were randomly divided into two groups. Half of the patients, Group A, underwent venepuncture during a Valsalva manoeuvre and the other half of the patients, Group B, underwent venepuncture without performing a Valsalva manoeuvre. Patients made a pain assessment using a 0-10 point numerical rating scale. Results: The numerical rating scale score was 1.5 +/- 1.2 for Group A and 3.1 +/- 1.9 for Group B, the difference being statistically significant (P < 0.0001). Conclusions: On the basis of data from this study, the Valsalva manoeuvre may be of the value before venous cannulation as a simple and practical method to reduce pain from venous cannulation

Pathophysiology of NASH

Rapid advances on molecular studies, manipulation of the mouse genome, the development of a number of animal models, and using these in studies of nonalcoholic fatty liver disease (NAFLD) have provided important insights into the pathogenesis of this relatively common disorder. One of the most crucial advances was to recognize the links among obesity, insulin resistance, inflammation and NAFLD. A growing body of literature has shown that insulin resistance and its liver-related consequence, NAFLD, could be the result of generalized inflammation. Genetic and behavioral factors contribute to increased visceral adipose tissue where increased oxidative stress and lipid peroxidation may contribute to dysregulated production of adipocytokines, fatty acids, and bioactive lipids. This chain of these events may contribute to local and peripheral insulin resistance, a central underlying pathophysiological process that may both cause and result from increased peripheral lipolysis and elevated free fatty acid concentrations in the circulation. Abnormally elevated free fatty acids taken up by organs other than adipose tissue, such as liver and skeletal muscle, contributes to steatosis of these organs (ectopic lipogenesis). Increased muscle and hepatocellular lipid content provides substrates for oxidative stress and lipid peroxidation, and also promotes insulin resistance in both liver and muscle by disturbing their downstream insulin signaling cascades. Insulin resistance further increases peripheral lipolysis in adipose tissue, further elevates circulating free fatty acids, inhibits hepatic fatty acid ß-oxidation and increases de novo synthesis of both fatty acids and triglycerides in the liver. Excessively produced triglycerides in the liver are either stored as fat droplets or secreted into the plasma as very-low-density lipoproteins. If this complex mechanism of hepatic fat synthesis and secretion capacity is overwhelmed, excessive triglycerides accumulate within the hepatocytes and manifests as NAFLD. A fatty liver is sensitive to hepatocellular injury and sustained injury can manifest as nonalcoholic steatohepatitis (NASH), NASH-associated cirrhosis, and NASH-associated hepatocellular carcinoma. Specific depletion of hepatic natural killer T cells with consequent proinflammatory cytokine polarization of liver cytokine production might be one reason for this increased hepatic sensitivity against various stimuli. Only a minority of patients with NAFLD have the necroinflammatory changes of NASH. The development of NASH in patients with NAFLD may be the consequence of secondary abnormalities such as injured and dysfunctional mitochondria, generation of reactive oxygen species with down-regulation or consumption of antioxidants causing oxidative stress and lipid peroxidation, increased activity of cytochrome P450 2E1, disturbed production of adipocytokines, and the effects of gut-derived cytotoxic products. The dynamic interplay of these processes in the pathogenesis of NAFLD remains incompletely understood and is an area of active research. © 2008 by Nova Science Publishers, Inc. All rights reserved