ObjectiveTo study the association between Dientamoebafragilis colonisation and faecal calprotectin to see whether the parasite is a harmless commensal or a gut pathogen.DesignCross-sectional study of previously collected stool samples.Setting and patientsTwo hundred stool samples originated from children aged 5–19 years with chronic abdominal pain and diarrhoea, who were seen in paediatric clinics in the Netherlands and Belgium and in whom somatic gastrointestinal disorders were excluded. Another 122 samples came from a healthy community-based reference population of the same age. All stool samples were analysed with real-time PCR for the detection of D. fragilis and with an ELISA for calprotectin—a biomarker of gastrointestinal inflammation.Main outcome measuresPrevalence of D. fragilis colonisation and results of stool calprotectin testing.ResultsD. fragilis was detected in 45% (95% CI 38% to 51%) of patients and in 71% (95% CI 63% to 79%) of healthy children. Median (IQR) concentrations of calprotectin in patients and healthy children with a positive PCR result were not different from those with a negative PCR result (40 (40–55) μg/g vs 40 (40–75) μg/g, respectively).ConclusionSince D. fragilis colonisation is most prevalent in healthy children and is not associated with an increase in faecal calprotectin concentration, our data do not support the inference that D. fragilis is a pathogenic parasite. Routinely testing for D. fragilis in children with chronic abdominal pain should therefore be discouraged.

Background & Aims Sclerosing cholangitis (SC) is a severe liver disease leading to destruction of bile ducts. It is believed to run a milder course in children than in adults. To test this assumption, we evaluated time‐to‐complication curves in two independent paediatric‐onset cohorts from the same geographical area. Methods Short‐term disease outcomes were evaluated with an online clinical registry that was filled with data on children with SC diagnosed between 2000 and 2017 and who were followed bi‐annually thereafter. Long‐term disease outcomes were evaluated in a paediatric‐onset subcohort derived from a previously published population‐based study from the Netherlands. Time‐to‐complication in the first cohort was defined as the time from diagnosis until portal hypertension, biliary obstructions and infections, development of malignancy, or liver transplantation, whichever came first. In the second cohort time‐to‐complication was defined as the time until liver transplantation or PSC‐related death. Results Median age at diagnosis in the first cohort (n = 86) was 12.3 years. In the first 5 years post‐diagnosis 23% of patients developed complications. The patients in the population‐based study (n = 683) were stratified into those diagnosed before the age of 18 years (‘paediatric‐onset’ subcohort, n = 43) and those diagnosed after the age of 18 years (‘adult‐onset’ subcohort, n = 640). Median age at diagnosis was 14.6 and 40.2 years, respectively. Median time‐to‐complication in the paediatric‐onset and adult‐onset subcohorts was not statistically different. Conclusion Paediatric and adult‐onset SC run a similar long‐term disease course. Paediatricians who treat children with SC should monitor them closely to recognize early complications and control long‐term sequelae.

Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.