The complexity of managing inflammatory bowel disease (IBD) stems from the heterogeneity of Crohn’s disease and ulcerative colitis. This leads to differences in disease course, complications, and treatment responses among patients. Current treatment strategies rely on a trial-and-error approach, but there's a need for personalized therapy. Efforts have been made to develop reliable prognostic and predictive biomarkers to overcome disease heterogeneity. This article discusses common mistakes in biomarker development, interpretation, and application in IBD, emphasizing evidence-based insights and lessons learned from other fields.

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.

Hepatitis B virus (HBV) infection is the most common chronic viral infection in the world. Despite the availability of a preventative vaccine, more than 250 million people worldwide are chronically infected with HBV. The complications of chronic HBV infection—cirrhosis and hepatocellular cancer (HCC)—account for more than 850,000 deaths per year. HBV is transmitted haematogenously and sexually, with the majority of HBV infections being transmitted vertically (or perinatally) in high prevalence regions. HBV infection acquired at birth or in early childhood results in chronicity in >95% of cases, whereas only 5–10% of those who are infected in adulthood will progress to chronic infection. 

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. 

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.