Coeliac disease (CD) is caused by a CD4 T helper cell type 1 (Th1) response in the small intestinal mucosa to dietary gluten. As the major Th1 inducing cytokine, interleukin 12, is undetectable in CD gut mucosa, the mechanism by which Th1 eVector cells are generated remains unknown. Interferon (IFN) , a cytokine capable of promoting IFN-synthesis, has been implicated in the development of Th1 mediated immune diseases. Here we report a case of CD-like enteropathy in a patient receiving IFN-for chronic myeloid leukaemia. Morphological assessment of duodenal biopsies taken from the patient showed total villous atrophy, crypt cell hyperplasia, and a high number of CD3 + intraepithelial lymphocytes. Both antigliadin antibodies and antiendomysial antibodies were positive. RNA analysis revealed pronounced expression of IFN-. Withdrawal of gluten from the diet resulted in a patchy improvement in intestinal morphology, normalisation of laboratory parameters, and resolution of clinical symptoms. By western blot analysis, IFN-protein was seen in the duodenal mucosa from untreated CD patients but not in controls. This was associated with marked expression of IFN-protein in CD mucosa. Collectively, these results suggest a role for IFN-in promoting Th1 responses to gluten. (Gut 2001;48:425-429)

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Klebsiella oxytoca was recently described as the causative organism for antibiotic-associated hemorrhagic colitis (AAHC). It is currently not known if this novel gastrointestinal infection exists in children. AAHC is usually preceded by antibiotic treatment with penicillins, which are frequently prescribed for pediatric patients. In contrast to colitis caused by Clostridium difficile, colitis caused by K oxytoca is usually segmental and located predominantly in the right colon. Patients with AAHC typically present with abdominal pain and almost always bloody diarrhea. We present here the case of an adolescent patient who developed acute abdominal pain and bloody diarrhea after antibiotic treatment for acute urinary infection with amoxicillin-clavulanate. Right-sided colitis was verified by abdominal sonography. Stool culture tested negative for common gastrointestinal pathogens but yielded K oxytoca. Toxin production of the isolated strain was verified in a cell-culture assay. Cessation of the causative antibiotic treatment led to rapid improvement and cessation of bloody diarrhea within 3 days. We report here the first (to our knowledge) pediatric case of K oxytoca infection causing AAHC. Establishing the diagnosis of AAHC by culturing K oxytoca and demonstrating right-sided colitis with noninvasive imaging studies might prevent unnecessary invasive procedures in children with bloody diarrhea.

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Children and adolescents with T1DM have a lower frequency of PCA than is reported for adults. Compared to healthy controls, they seem to be at increased risk for developing PCA, in particular if positive for TPOAb, but overt clinical disease is rare in children with T1DM.