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.

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. 

Proton pump inhibitors (PPIs), first introduced with omeprazole in 1988, revolutionized the treatment of gastric acid-related conditions like gastro-oesophageal reflux disease, gastroduodenal ulcers, and Helicobacter pylori infections. Despite their effectiveness, PPIs are often prescribed for conditions without a proven link to gastric acid, such as dyspepsia and upper abdominal discomfort. Long-term use of PPIs has raised safety concerns, including risks of vitamin and mineral malabsorption, pneumonia, gastrointestinal infections, and dementia. This Mistakes In article addresses nine common mistakes in PPI use and aims to clarify misconceptions about their use.

Acute diverticulitis is an inflammatory complication of diverticulosis and can either be uncomplicated or complicated. Making the distinction between uncomplicated and complicated acute diverticulitis is essential because treatment strategies differ between the two. Here, we discuss 10 mistakes frequently made when managing patients with acute diverticulitis. We focus on using the correct terminology, diagnostic preference and several treatment options, such as omitting or administering antibiotics, radiological interventions and various aspects of surgery. Acute diverticulitis is an important topic because its incidence is rising worldwide and it is becoming a considerable burden on healthcare systems. Most of the discussion included here is evidence-based, supplemented with many years’ combined clinical experience where 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.

Malnutrition frequently occurs in patients who have chronic liver disease and worsens their prognosis. There are multiple causes of malnutrition in the context of cirrhosis: low dietary intake, malabsorption, metabolic alterations and modification of substrate utilisation. Sarcopenia, which is defined by loss of muscle mass and function, is a major component of malnutrition in patients with cirrhosis. Sarcopenia adversely affects the number and severity of complications, quality of life, the outcome of liver transplantation and the overall survival rate of patients with advanced liver disease. Physicians should be aware of the clinical and prognostic relevance of nutritional status, how to promptly recognise malnutrition and sarcopenia in patients with liver cirrhosis and how to appropriately manage these conditions. Here we discuss some mistakes that are frequently made regarding nutrition in chronic liver disease, and we provide evidence and experience-based approaches to avoid them.