Coeliac disease is an autoimmune disorder triggered by gluten, which activates an immune reaction against the autoantigen tissue transglutaminase (TG2) in genetically predisposed subjects. Genetic susceptibility to coeliac disease has been proven by its close linkage with major histocompatibility complex (MHC) class II human leukocyte antigen (HLA) DQ2 and DQ8 haplotypes. The identification of biomarkers for coeliac disease (e.g. endomysial antibodies [EmA] and antibodies to TG2 [anti-TG2]) has changed the epidemiology of coeliac disease from being a rare to a frequent condition, with an expected prevalence of 1% in the worldwide population. Coeliac disease can be difficult to diagnose because symptoms vary from patient to patient, and the majority of patients who have coeliac disease remain undiagnosed. Small intestinal biopsy remains the gold standard for coeliac disease diagnosis, and a delayed diagnosis in the elderly can be considered a risk factor for complications. Complicated coeliac disease is not so frequent, but for those who have it, the prognosis is very poor, with a low rate of survival after 5 years.

Familial Mediterranean fever (FMF), also called periodic disease, Armenian disease, etc., is a prototypical autoinflammatory disorder where the underlying mechanism is the dysfunction of innate immunity, resulting in unprovoked episodes of inflammation.¹ Although considered rare worldwide, it is prevalent in people of Mediterranean origin; however, one can expect to encounter patients in all parts of the modern world. FMF is a monogenic disease with autosomal recessive inheritance.² Unlike other monogenic disorders, the diagnosis remains largely clinical, and it is important to understand the limitations of genetic testing. Another distinguishing feature is the well-established effectiveness of lifelong monotherapy with colchicine in preventing attacks and complications.³

Barrett’s oesophagus is a premalignant condition of the distal oesophagus predisposing to oesophageal adenocarcinoma. Given the potential for malignant progression and the poor prognosis of eosophageal adenocarcinoma when diagnosed at a symptomatic stage, patients with known Barrett oesophagus undergo regular endoscopic surveillance to detect neoplastic progression at an early and preferably endoscopically, treatable stage. Endoscopic management of early Barrett oesophagus neoplasia consists of a combination of endoscopic imaging, endoscopic resection and endoscopic ablation. Below we discuss a number of mistakes that are frequently made when managing Barrett oesophagus neoplasia and how to avoid them. Much of this discussion draws on existing guidelines (for background reading, check the ESGE Barrett oesophagus guideline), but in many instances the underlying evidence (even in the guideline) is missing and therefore many of our practically driven recommendations are based on common sense and our experience in this field.