ObjectiveTo document changes in the clinical features of coeliac disease (CD) at presentation over the last 25 years.DesignObservational study.Patients802 subjects diagnosed between 1993 and 2017 at a single general hospital.Outcome measuresDate of diagnosis, age, sex, postcode, symptoms, haematinic deficiency, smoking status, serology, family history and autoimmune phenomena.ResultsThe incidence of diagnosed CD rose threefold during the course of the study, with a rising prevalence of positive coeliac serology and positive family history of CD, and a falling prevalence of symptoms and haematinic deficiencies. There was little change in the female predominance, age at diagnosis or high prevalence of other autoimmune conditions over the 25 years, and a paucity throughout of cigarette smokers, particularly heavy smokers. A cohort of patients with seronegative CD was identified who shared many of the characteristics of seropositive CD, but with a significantly older age at diagnosis and a higher prevalence of cigarette smokers.ConclusionThere have been major changes in the epidemiology of CD over the last 25 years, of relevance to both our understanding of the aetiopathogenesis of CD and the requirement for service provision. The implications are discussed.

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A 26 year old, Caucasian, female student nurse presented with facial pains and vesicular rash, and over the following three days developed focal faciobrachial twitches. She was febrile, with an erythematous rash. Neurological examination was normal. MRI showed a non-enhancing lesion in the right medulla. CSF was normal with negative viral PCR. EEG demonstrated no seizure activity.A month earlier she was treated with steroids and antibiotics for acute liver injury and maculopapular rash, of presumed allergic aetiology. On that admission, deficiency of Immunoglobulins A and G was noted prompting diagnosis of Common Variable Immune Deficiency, treated with IVIg.Her conscious level deteriorated rapidly, requiring ventilation 10 days after admission. Repeat MRI showed a new subcortical inflammatory lesion. EEG showed new background slowing, and progressed to electrographic status, which continued despite six anticonvulsants, IV Propofol and Midazolam. Sequential imaging showed progressive deterioration with widespread inflammation and oedema, and consequent herniation. Life-support was withdrawn one month after presentation.Post-mortem demonstrated T-lymphocytic inflammation with inclusion bodies suggesting viral encephalitis. Electron microscopy demonstrated filamentous viral particles. Measles PCR was positive in brain tissue and CSF, diagnosing Measles Inclusion Body Encephalitis. Serum measles IgM, previously reported as negative, was re-evaluated and tested positive.