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.

Adequate nutrition is essential for the homeostasis of fluids and nutrients, growth and thriving, especially in children. While the underlying principle of percutaneous endoscopic gastrostomy (PEG) placement is the same for both adults and children—providing a means of enteral feeding through the stomach—the indications, considerations and techniques differ owing to anatomical differences, age-dependent physiological concerns, and the age- and disease-specific needs of the child.

If feeding via nasogastric tube (NGT) or naso-jejunal tube (NJT) is necessary for a prolonged time, placement of a PEG or percutaneous endoscopic gastro-jejunal (PEG-J) tube should be considered. A PEG tube also allows the delivery of medications and venting of the stomach when needed. Nutrition via PEG facilitates the transition to out-of-hospital care and improves the quality of life (QoL) for children and families while improving the outcome of children with chronic diseases.

There are recent clinical guidelines providing guidance for PEG tube placement in children, but little advice on, e.g., choosing the right device for the right patient, details on postoperative management, removal of the PEG tube and other specific cases. The following article provides a combination of evidence-based data and the authors’ clinical 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.

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. 

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.