Refractory coeliac disease (RCD) is characterized by the persistence or recurrence of symptoms and signs of malabsorption associated with villous atrophy in patients with coeliac disease who have adhered to a strict gluten-free diet (GFD) for more than 12 months.^1–3 Serology is usually negative or, in a small percentage of cases, positive at a low titre.⁴ Splenic hypofunction, a risk factor for RCD, can be indicated by Howell–Jolly bodies and pitted red cells in a peripheral blood smear. A reduced spleen size visible on ultrasound examination also provides direct evidence of hyposplenism.⁵ 

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.

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is a subclassification of steatotic liver disease (SLD), defined as the presence of excess triglyceride storage in the liver in conjunction with at least one cardiometabolic risk factor and no other discernible cause.1 Cirrhosis secondary to MASH is the most common cause of liver disease in the world and is the fastest-growing indication for liver transplantation, but it also has a >50% recurrence rate post-transplantation.

The term ‘gastroparesis’ was first coined by Kassander in 1958 to describe the fact that barium did not leave the stomach of patients with diabetes for over 24 hours — so-called ‘gastroparesis diabeticorum’. Nowadays it refers to a delay in gastric emptying that is associated with symptoms primarily of nausea and vomiting as well as the absence of mechanical obstruction. In 1958, 21 cases were described, but in 2019, 5 million US individuals were diagnosed as having gastroparesis. This rapid increase in prevalence is likely to have occurred because it has become much easier to measure gastric emptying and to attribute symptoms to this without necessarily thinking through differentials. The incidence of hospital admissions for patients labelled as having gastroparesis is rapidly rising, increasing at a much faster rate than admissions for patients with nausea and vomiting, gastro-oesophageal reflux disease, gastritis or gastric ulcers, which are all remaining relatively static. Gastroparesis therefore represents a major healthcare burden. Gastroparesis can be idiopathic or is most frequently caused by diabetes (type 1 more than type 2) or surgical procedures that can disrupt the vagus nerve (e.g. Billroth gastrectomy, oesophagectomy, gastric bypass surgery and fundoplication). In this article, I describe the mistakes most frequently made in patients who have a suspected diagnosis of gastroparesis. I base my discussion on the available evidence as well as clinical experience in the field. 

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.

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.

Chronic gastritis is a common condition that occurs when an inflammatory infiltrate is present in the gastric mucosa. Diverse factors can cause such inflammation to develop, including food, common bacteria (particularly Helicobacter pylori) and even some viruses. Although the inflammatory infiltrate itself may not cause a disease per se, in some cases gastritis will evolve into atrophic gastritis, ulcers or gastric cancer. Clinicians therefore need to be aware of when gastritis is a harmless condition that can be left alone and when further action is required. In addition, many patients and some clinicians use the term ‘chronic gastritis’ to describe symptoms, mostly those of dyspepsia. This misuse of the terminology can lead to the erroneous conclusion that a diagnosis is being discussed and not a symptom. Here we address these mistakes and some of the others that are frequently made when managing patients with chronic gastritis. We discuss how to avoid making the mistakes to ensure that patients are managed adequately while reducing over treatment.