Recompensation in cirrhosis: unravelling the evolving natural history of nonalcoholic fatty liver disease.

Recompensation has gained increasing attention in the field of cirrhosis, particularly in chronic liver disease with a definite aetiology. The current global prevalence of obesity and nonalcoholic fatty liver disease (NAFLD) is increasing, but there is currently a lack of a clear definition for recompensation in NAFLD-related cirrhosis. Here, we provide an up-to-date perspective on the natural history of NAFLD, emphasizing the reversible nature of the disease, summarizing possible mechanisms underlying recompensation in NAFLD, discussing challenges that need to be addressed and outlining future research directions in the field. Recompensation is a promising goal in patients with NAFLD-related cirrhosis, and further studies are needed to explore its underlying mechanisms and uncover its clinical features.

Editorial: The Metabolic (Dysfunction)-Associated Fatty Liver Disease (MAFLD) and Non-Alcoholic Fatty Liver Disease (NAFLD) Debate: Why the American Association for the Study of Liver Diseases (AASLD) and European Association for the Study of the Liver (EASL) Consensus Process is Not Representative.

A debate has recently arisen in hepatology on the redefinition of fatty liver disease associated with metabolic dysfunction. The definition of metabolic (dysfunction)-associated fatty liver disease (MAFLD) has been widely endorsed by multiple stakeholders and societies. More importantly, although robust evidence supports the utility of the definition of MAFLD in clinical practice and research, and for increasing awareness of liver disease, controversy still abounds. Recently, the American Association for the Study of Liver Diseases (AASLD) and the European Association for the Study of the Liver (EASL) have undertaken similar consensus approaches for MAFLD. However, there are serious concerns with these regional consensus approaches. The views of hepatologists from the Middle East, North Africa, and sub-Saharan Africa are not represented. Also, the selection of experts raises concerns regarding the validity of the outcomes of the expert consensus process. We conclude that unless the process has global involvement, there will be no incentive for global adherence to these regional recommendations. This Editorial aims to highlight these concerns and to call for those involved in leading the AASLD and EASL consensus process to be more inclusive, which may facilitate the adoption of more unified recommendations that have global clinical importance.

Allopurinol potentiates the hepatoprotective effect of metformin and vitamin E in fructose-induced fatty liver in rats.

AIM OF THE STUDY: Non-alcoholic fatty liver disease (NAFLD) is a challenging health problem. Hyperuricemia is a key player in the pathogenesis of NAFLD. This study investigated the effect of allopurinol (uric acid synthesis inhibitor) in combination with metformin and vitamin E in prevention of fructose induced-fatty liver in rats. MATERIAL AND METHODS: Rats were divided into 7 groups: control group, fructose group (model group of NAFLD), allopurinol-treated group, metformin-treated group, vitamin E-treated group, metformin plus vitamin E-treated group and a combination group (received allopurinol plus metformin plus vitamin E). Development of NAFLD was assessed biochemically by serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) as well as by histopathological examination. Oxidative stress parameters [reduced glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA)], and the inflammatory mediators tumor necrosis factor α (TNF-α) and inducible nitric oxide synthase (iNOS) were assessed, along with serum levels of uric acid and triglyceride (TG). RESULTS: Combination of allopurinol plus metformin plus vitamin E significantly attenuated fatty changes compared to their respective monotherapy. Interestingly, though all treated groups showed significant attenuation in the oxidative stress markers, TNF-α level and iNOS immunostaining in hepatic tissue, along with a significant decrease in the levels of uric acid and TG, the combination group showed a further significant decrease in the serum level of uric acid and iNOS immunostaining compared to other treated regimens. CONCLUSIONS: Allopurinol synergistically increases the protective effect of metformin and vitamin E in treatment of NAFLD, namely via reduction of uric acid synthesis and iNOS expression.

Prevalence of Eosinophilic Esophagitis in Adult Patients with Upper Gastrointestinal Symptoms in a Locality in Upper Egypt.

BACKGROUND/AIMS: Eosinophilic esophagitis (EoE) is gaining importance in the diagnosis of upper gastrointestinal (UGI) symptoms. Diagnosis is based on the clinical presentation of esophageal dysfunction and pathological findings in the absence of other causes of tissue eosinophilia. Our study was designed to evaluate EoE prevalence in patients with UGI symptoms in our locality (El-Minia, Egypt). METHODS: This single-center, cross-sectional study recruited all patients with UGI symptoms who agreed for endoscopic evaluation. Esophageal biopsy samples were obtained and histological evaluation for the presence of eosinophils was performed for every patient. EoE was defined when at least 15 eosinophils were present in a single high-power field, in the absence of other causes of esophageal eosinophilia. RESULTS: Between 2013 and 2015, 218 of 476 adult patients with UGI symptoms underwent upper endoscopy after giving consent. Among the 218 patients, only 4 (1.87%) had the diagnosis of EoE based on the presence of eosinophils in esophageal biopsies and exclusion of other causes of esophageal eosinophilia. Three patients with EoE presented mainly with dysphagia (75%) and/or other UGI symptoms, such as heartburn. CONCLUSIONS: We observed a low prevalence of EoE in our locality. The diagnosis of EoE should be considered in patients with dysphagia and/or heartburn.

Biomarkers of Barrett's esophagus.

Barrett's esophagus is the strongest risk for esophageal adenocarcinoma (EAC). Metaplasia in patients with BE may progress to dysplasia and then invasive carcinoma. Well-defined diagnostic, progressive, predictive, and prognostic biomarkers are needed to identify the presence of the disease, estimate the risk of malignant transformation, and predict the therapeutic outcome and survival of EAC patients. There are many predictive and prognostic markers that lack substantial validation, and do not allow stratification of patients with gastroesophageal reflux disease in clinical practice for outcome and effectiveness of therapy. In this short review we summarize the current knowledge regarding possible biomarkers, focusing on the pathophysiologic mechanisms to improve prognostic and therapeutic approaches.

Hepato-cardiac disorders.

Understanding the mutual relationship between the liver and the heart is important for both hepatologists and cardiologists. Hepato-cardiac diseases can be classified into heart diseases affecting the liver, liver diseases affecting the heart, and conditions affecting the heart and the liver at the same time. Differential diagnoses of liver injury are extremely important in a cardiologist's clinical practice calling for collaboration between cardiologists and hepatologists due to the many other diseases that can affect the liver and mimic haemodynamic injury. Acute and chronic heart failure may lead to acute ischemic hepatitis or chronic congestive hepatopathy. Treatment in these cases should be directed to the primary heart disease. In patients with advanced liver disease, cirrhotic cardiomyopathy may develop including hemodynamic changes, diastolic and systolic dysfunctions, reduced cardiac performance and electrophysiological abnormalities. Cardiac evaluation is important for patients with liver diseases especially before and after liver transplantation. Liver transplantation may lead to the improvement of all cardiac changes and the reversal of cirrhotic cardiomyopathy. There are systemic diseases that may affect both the liver and the heart concomitantly including congenital, metabolic and inflammatory diseases as well as alcoholism. This review highlights these hepatocardiac diseases.