The prevalence of metabolic-associated fatty liver disease (MAFLD) is increasing globally due to factors such as urbanization, obesity, poor nutrition, sedentary lifestyles, healthcare accessibility, diagnostic advancements, and genetic influences. Research on MAFLD and HCC risk factors, pathogenesis, and biomarkers has been conducted through a narrative review of relevant studies, with a focus on PubMed and Web of Science databases and exclusion criteria based on article availability and language. Steatosis marks the early stage of MASH advancement, commonly associated with factors of metabolic syndrome such as obesity and type 2 diabetes. Various mechanisms, including heightened lipolysis, hepatic lipogenesis, and consumption of high-calorie diets, contribute to the accumulation of lipids in the liver. Insulin resistance is pivotal in the development of steatosis, as it leads to the release of free fatty acids from adipose tissue. Natural compounds hold promise in regulating lipid metabolism and inflammation to combat these conditions. Liver fibrosis serves as a significant predictor of MASH progression and HCC development, underscoring the need to target fibrosis in treatment approaches. Risk factors for MASH-associated HCC encompass advanced liver fibrosis, older age, male gender, metabolic syndrome, genetic predispositions, and dietary habits, emphasizing the requirement for efficient surveillance and diagnostic measures. Considering these factors, it is important for further studies to determine the biochemical impact of these risk factors in order to establish targeted therapies that can prevent the development of HCC or reduce progression of MASH, indirectly decreasing the risk of HCC.

Isolated pancreatic tuberculosis (TB) remains a rarity despite the high incidence of tuberculosis in many of the African and Asian countries. Presentation as discrete pancreatic mass often masquerades as pancreatic neoplasm and diagnosis may require histology. Extra-hepatic portal hypertension due to splenic vein thrombosis complicating pancreatic TB has been reported in the literature. We report here a case of isolated pancreatic TB with pancreatic head mass mimicking neoplasm with extra-hepatic portal hypertension. The possibility of TB should be considered in the list of differential diagnoses of pancreatic mass and an endoscopic, ultrasound-guided biopsy might help to clinch the diagnosis of this potentially curable disease.

Substance use disorders are a global health problem with detrimental effects on one’s health, wealth, and stealth. It includes the use of prescribed medications or the use of illicit drugs in excess amounts or for excess durations associated with complex neuropsychiatric and/or physical manifestations. It affects every organ in the body, and the liver is no exception to the deleterious effects of substance abuse. The mechanism of liver injury varies from agent to agent and may include direct toxic effects, oxidative stress, and inflammatory responses. The hepatic involvement ranges from asymptomatic liver enzyme elevation and fatty liver disease to hepatitis, liver failure, and cirrhosis. Alcohol, the most frequent agent implicated in substance use disorder, is also a prototype hepatotoxin, capable of inducing the whole spectrum of liver diseases. Cigarette smoke contains numerous harmful chemicals, including carcinogens, which can induce liver injury, fibrosis, and HCC. Cocaine, particularly in acute overdose, can result in ischemic hepatonecrosis, while it can also result in clinically inapparent transaminasemia. Marijuana and opiates, despite being associated with numerous deleterious effects, are rarely implicated in clinically apparent liver injury. Individuals with substance use disorder are also prone to viral hepatitis and hepatic insults secondary to hypotension, hypoxia, and other systemic ailments. Liver transplant candidacy in individuals with substance use disorder is a highly complex arena, with guidelines balancing abstinence requirements against evolving evidence on outcomes. This review article provides a thorough analysis of the hepatotoxic repercussions stemming from the agents commonly implicated in substance abuse disorders.

Glucagon-like peptide-1 (GLP-1), an incretin hormone, plays a crucial role in glucose homeostasis by stimulating insulin secretion, suppressing glucagon release, and delaying gastric emptying. Its therapeutic potential was long realized, leading to the development of the first GLP-1 receptor agonist, exenatide, followed by liraglutide, dulaglutide, semaglutide, and tirzepatide. Semaglutide is available as a weekly subcutaneous injection with high bioavailability. Semaglutide is the only GLP-1 agonist available for oral therapy, used in the treatment of type 2 diabetes mellitus (T2DM). Semaglutide has demonstrated broad clinical efficacy beyond glycemic control, including weight reduction, cardiovascular risk reduction, and, most recently, in the treatment of metabolic dysfunction-associated steatohepatitis (MASH). Semaglutide therapy is associated with the resolution of steatohepatitis and improvement in hepatic fibrosis in patients with MASH. Alongside resmetirom, semaglutide is currently approved for the treatment of non-cirrhotic MASH with moderate-to-advanced fibrosis. Safety considerations include gastrointestinal intolerance, hypoglycemia, rare pancreaticobiliary events, and theoretical concerns of thyroid C-cell tumors, though human risk remains minimal. In summary, semaglutide extends the armamentarium of the hepatologist against the most common liver disease worldwide.

Acetaminophen, or paracetamol, ranks among the most extensively utilized analgesic and antipyretic medications globally. The administration of acetaminophen to individuals with underlying liver disease has long sparked concerns regarding the potential risk of hepatotoxicity. However, the available literature and recommendations consider it a safe option in all forms of liver diseases and is deemed safe when used at recommended doses. This article aims to offer a concise review of the pharmacokinetics, toxicity profile, and the intricate considerations surrounding the safety of acetaminophen in patients with liver disease. By delving into the liver-acetaminophen interactions, we seek to provide a nuanced perspective on the use of acetaminophen in this critical patient population.

Acute esophageal necrosis or black esophagus is an uncommon clinical entity, diagnosed at the upper gastrointestinal endoscopy with the presence of strikingly black necrotic esophagus. Very often no definite etiology will be identified even though a large list of potential associations has been postulated. Upper gastrointestinal bleeding is the most common clinical presentation, others being epigastric pain, retrosternal chest discomfort and dysphagia. Only about a hundred cases of acute esophageal necrosis have been described in medical literature till this date. We report a case of acute esophageal necrosis in an elderly female who had presented with hematemesis.