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.

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.

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.

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. 

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.