Alcohol consumption is the most prevalent aetiology for liver cirrhosis in Europe and the third leading risk factor for overall mortality.1,2 In fact, alcoholic liver cirrhosis accounts for almost half a million deaths a year worldwide, corresponding to 50% of all cases of cirrhosis, according to the World Health Organization (WHO).3 Alcoholic liver disease (ALD) is multifaceted, with several cofactors influencing its progression. Patients abusing alcohol can simultaneously have viral hepatitis B or C, or a genetic disease, such as alpha-1 antitrypsin deficiency or haemochromatosis.

Jaundice can be caused by abnormalities in any of the steps comprising the formation, metabolism and excretion of bilirubin. In addition, these processes may be functioning properly, but jaundice can be seen because of an obstruction of the biliary tree at any point, from its intrahepatic origins to its end at the ampulla of Vater. For this reason, it is clear that numerous conditions can result in jaundice. When faced with a patient presenting with jaundice a reasonable and careful diagnostic approach is, therefore, warranted to elucidate the underlying cause of this sign. Conventional wisdom may be that “jaundice by itself never killed anyone,” but it is imperative to find the cause as soon as possible, as prompt intervention saves lives in many cases.

Hepatitis C virus (HCV) infection remains an important global health concern. It is estimated that there are approximately 50 million people infected with HCV globally, with around 1 million new infections each year and about 242,000 deaths annually attributed to HCV-related complications. Most acute HCV infections (55–85%) become chronic due to the virus’s effective evasion strategies, with spontaneous clearance being rare once chronicity is established. This condition often progresses silently, with many individuals unaware of their infection until advanced liver damage has occurred. If left untreated, HCV can lead to severe complications, including liver cirrhosis and hepatocellular carcinoma (HCC). HCV transmission occurs mainly through percutaneous exposure to infected blood. HCV can also spread from mother to infant (vertical transmission) and, less frequently, via sexual contact.1,2 In recent years, the introduction of oral direct-acting antivirals (DAAs), with remarkable safety and effectiveness profiles, has led to a sustained virological response (SVR) in virtually all (>97%) HCV-infected patients, regardless of HCV genotype or disease stage. However, significant barriers remain, such as issues with diagnosis, access to treatment and awareness of the disease.

Here, we discuss some of the misconceptions in HCV management and provide a practical management approach grounded in evidence and clinical experience.

Ulcerative colitis (UC) is a lifelong inflammatory bowel disease (IBD) of unknown origin characterized by alternating flare and remission periods. An acute severe episode, so-called acute severe UC (ASUC), may happen in approximately one-quarter of patients during their life.1 Notably, more than 25% of ASUC episodes correspond to the index presentation of the disease. Patients with ASUC should be promptly identified by the modified Truelove and Witts criteria recommended by the most recent international guidelines and admitted rapidly to a digestive unit. Indeed, ASUC is a life-threatening condition still leading to a 1% death rate in Western countries. In the current article, we will discuss the most frequent and/or relevant mistakes in managing patients admitted for an ASUC episode and how to avoid them. The manuscript is based on the available evidence and expert opinion when evidence is lacking.

Tissue sampling during endoscopic procedures is a fundamental aspect of investigating digestive diseases, with histological examination playing a crucial role in almost every case. Given its prevalence, the potential for mistakes is significant. Therefore, understanding the appropriate indications, techniques, and consequences of tissue sampling is essential for gastroenterologists. Key questions to consider before taking a biopsy or acquiring tissue include: Why? What for? How? How many?

This manuscript addresses these critical questions by detailing the eight most frequent and correctable mistakes in tissue acquisition during endoscopy. The recommendations provided are largely supported by existing guidelines and evidence, with some insights drawn from the authors' professional experience.

Biological therapy has revolutionised the treatment of moderate to severe inflammatory bowel disease (IBD), namely Crohn’s disease (CD) and ulcerative colitis (UC). However, up to one-third of patients with IBD are primary non-responders, and up to half can lose response over time.These unwanted outcomes can be explained by either pharmacodynamic (mechanistic failure) or pharmacokinetic (PK) issues with or without the development of anti-drug antibodies (ADA), so-called immunogenicity.1 Reactive therapeutic drug monitoring (TDM), defined as the measurement of drug concentrations and anti-drug antibody (ADA) levels in the setting of primary non-response (PNR) or secondary loss of response (SLR), can help to explain better and manage these unwanted outcomes. However, it would make sense to try to prevent PNR and SLR by routinely measuring drug concentrations and ADA to achieve and maintain a targeted therapeutic drug concentration, the so-called proactive TDM. Here we discuss some common mistakes and significant errors to avoid when utilising TDM of biologics in patients with IBD. The discussion is based on evidence, whenever possible, and our clinical experience and perception of the field.