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.

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 

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.

Liver function tests (LFTs) are routinely used to screen for liver disease. A correct interpretation of LFT abnormalities may suggest the cause, severity, and prognosis of an underlying disease. Once the diagnosis has been established, sequential LFT assessment can be used to assess treatment efficacy. Abnormal LFTs are frequently encountered in clinical practice, since elevation of at least one LFT occurs in more than 20% of the population.1 Many patients with abnormal LFTs, however,  do not suffer from structural liver disease, since these tests can be influenced by factors unrelated to significant liver damage or liver function loss. During normal pregnancy, for example, serum albumin levels fall due to plasma volume expansion, and alkaline phosphatase (ALP) levels rise due to placental influx. Patients who have elevated transaminase levels may not suffer from liver disease, but rather from cardiac or skeletal muscle damage. Conversely, patients who suffer from advanced liver disease, such as chronic hepatitis or compensated liver cirrhosis, may have normal LFTs.