The rate of CRBSI did not differ from larger centres in Denmark but the rate of thrombotic events was higher than expected. Parenteral therapy can safely and effectively be offered to patients with IF in smaller centres.

Epstein-Barr virus (EBV) infects the vast majority of the human population. The primary infection in immunocompetent individuals is typically asymptomatic or presenting as infectious mononucleosis. Here, an 18-year-old man without medical history was admitted with mild non-specific symptoms of infection presenting primarily with severe dysphagia and epigastric pain. Gastroscopy revealed severe, extensive, ulcerative oesophagitis with suspicion of Crohn’s disease. However, a diagnosis of primary EBV infection presenting as severe ulcerative oesophagitis and without systemic symptoms of infectious mononucleosis was made based on dynamic changes in EBV serology (shift from IgM to IgG positivity), EBV-specific immunohistochemical staining, and PCR analysis of biopsy specimens. This rare manifestation of primary EBV in an immunocompetent patient was treated symptomatically and resolved within a few weeks, and should be considered a differential diagnosis at otherwise unexplained ulcerative oesophagitis in younger individuals.

Background and Aim Normalizing health‐related quality of life (QoL) and fatigue are important long‐term treatment targets in inflammatory bowel disease (IBD). We examined their evolution in relation to changes in disease activity during vedolizumab therapy. Methods Cohort study of biologically refractory IBD patients treated with vedolizumab. Patients were prospectively evaluated at all infusions by Short Health Scale (SHS) (QoL questionnaire covering four health dimensions) (n = 79), visual analogous scale for fatigue (VAS‐F) (n = 30), and clinical disease activity. Objective disease assessment was carried out after 1 year or at treatment failure. Results Patients in steroid‐free clinical remission at end of induction improved significantly in all SHS items already from week 2 with full implementation by week 14 (“Symptoms” 59% improvement, P < 0.001; “Function” 63%, P < 0.001; “Worries” 59%, P < 0.001; “Well‐being” 40%, P < 0.01). Then, SHS remained stable at background levels (< 20) for 1 year (improvements 67%; 65%; 62%; 57%; P < 0.001). Combined clinical‐objective remission at 1 year was associated with highest SHS improvements (64–72%; P < 0.001). Of note, early SHS improvements preceded manifestation of clinical remission in most patients (22 of 33; 67%). Clinical response materialized into late (week 6 or later) and minor SHS improvements (31–46%, P < 0.001). Fatigue improved steadily over 6 months to background levels (VAS‐F < 4) among patients in clinical remission (45% decrease) or clinical‐objective remission (41%). SHS and VAS‐F impairment remained elevated in patients without effect of therapy. Conclusion QoL rapidly improves and predicts later significant clinical‐objective efficacies of vedolizumab at end of induction and 1 year. Fatigue improves slowly after remission is attained.

Small bowel villous atrophy is most often caused by celiac disease in the Western world, but other diseases should be explored in patients without positive serology. Adult-onset autoimmune enteropathy (AIE) is a rare cause of villous atrophy first known in children with T-cell dysregulation but also seen in adults with autoimmune predispositions. Here, an 82-year-old woman with autoimmune thyroiditis was admitted with weight loss and watery diarrhoea not responding to diet change. Endoscopy revealed villous atrophy both in the duodenum and in the ileum, but no positive celiac serology. A diagnosis of autoimmune enteropathy was made based on chronic diarrhoea not responding to diet change, autoimmune predisposition, villous atrophy, typical histological findings, and no evidence of immunodeficiency or medications causing villous atrophy. The patient was treated to good effect with corticosteroids but needed total parenteral nutrition while admitted. AIE should be considered in villous atrophy without positive celiac serology.