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Background/aims Percutaneous endoscopic gastrostomy with push technique (PEG-T) is increasingly used in pediatric patients. In a retrospective study of PEG-T (cohort 1) we reported frequent complications related to T-fasteners and tube dislodgment. The aim of this study was to assess complications after implementation of a strict treatment protocol, and to compare these with the previous retrospective study. Materials and methods The study is a prospective study of PEG-T placement performed between 2017 and 2020 (cohort 2) in pediatric patients (0–18 years). Complications were recorded during hospital stay, fourteen days and three months postoperatively, graded according to the Clavien-Dindo classification and categorized as early (30 days). Results In total 82 patients were included, of which 52 (60%) had neurologic impairments. Median age and weight were 2.0 years [6 months-18.1 years] and 13.4 kg [3.5–51.5 kg], respectively. There was a significant reduction in median operating time from 28 min [10–65 min] in cohort 1 to 15 min [6–35 min] in cohort 2 (p

Background and aim: Modern treatment strategies for inflammatory bowel disease (IBD) are postulated to change the natural disease course. Inception cohort studies are the gold standard for investigating such changes. We have initiated a new population-based inception cohort study; Inflammatory bowel disease in South Eastern Norway III (IBSEN III). In this article, we describe the study protocol and baseline characteristics of the cohort. Methods: IBSEN III is an ongoing, population-based observational inception cohort study with prospective follow-up. Adult and pediatric patients with suspected IBD in the South-Eastern Health Region of Norway (catchment area of 2.95 million inhabitants in 2017), during the 3-year period from 2017 to 2019, were eligible for inclusion. Comprehensive clinical, biochemical, endoscopic, demographic, and patient-reported data were collected at the time of diagnosis and throughout standardized follow-up. For a portion of the patients, extensive biological material was biobanked. Results: The study included 2168 patients, of whom 1779 were diagnosed with IBD (Crohn's disease: 626, ulcerative colitis: 1082, IBD unclassified: 71). In 124 patients, there were subtle findings indicative of, but not diagnostic for, IBD. The remaining 265 patients were classified as symptomatic non-IBD controls. Conclusion: We have included patients in a comprehensive population-based IBD cohort from a catchment population of 2.95 million, and a unique biobank with materials from newly diagnosed and treatment-naïve IBD patients and symptomatic non-IBD controls. We believe this cohort will add important knowledge about IBD in the years to come.

OBJECTIVES We aimed to study whether the incidence of pediatric celiac disease (CD) in South-Eastern Norway changed from 2000 to 2010. We also examined whether there was a change in symptoms and histopathological morphology in the duodenal biopsies during the same period. METHODS In 3 hospitals in South-Eastern Norway, records from pediatric patients (0-14.9 years) diagnosed with CD during two 3-year periods (2000-2002 and 2008-2010) were reviewed. Only cases with a duodenal biopsy diagnosis of CD classified as Marsh grade 2 and 3a-c were included. Frequencies of symptoms, anthropometric data, and laboratory results were compared, in addition to re-examinations of histological sections from one of the hospitals. RESULTS A total of 400 cases were diagnosed with a female to male ratio of 1.5:1. The incidence rate for 2000 to 2002 was 15.9 cases per 100,000 person-years (95% confidence interval 12.8-19.4), compared with 45.5 cases per 100,000 person-years during 2008 to 2010 (95% confidence interval 40.5-50.9), P

Christine Olbjørn,1,2 Milada Cvancarova Småstuen,3 Espen Thiis-Evensen,4 Britt Nakstad,1,2 Morten Harald Vatn,5 Jørgen Jahnsen,2,6 Petr Ricanek,2,6 Simen Vatn,2,6 Aina EF Moen,5 Tone M Tannæs,5 Jonas C Lindstrøm,7 Johan D Söderholm,8 Jonas Halfvarson,9 Fernando Gomollón,10 Christina Casén,11 Magdalena K Karlsson,11 Rahul Kalla,12 Alex T Adams,12,13 Jack Satsangi,12,13 Gøri Perminow14 1Department of Pediatric and Adolescent Medicine, Akershus University Hospital, Lørenskog, Norway; 2Institute of Clinical Medicine, Campus Ahus, University of Oslo, Oslo, Norway; 3Faculty of Health Sciences, Oslo Metropolitan University, Oslo, Norway; 4Department of Gastroenterology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; 5Department of Clinical Molecular Biology (EpiGen), Division of Medicine, Akershus University Hospital, Lørenskog, and University of Oslo, Oslo, Norway; 6Department of Gastroenterology, Akerhus University Hospital, Lørenskog, Norway; 7Institute of Clinical Medicine, University of Oslo, Health Services Research Unit, Akershus University Hospital, Lørenskog, Norway; 8Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden; 9Department of Clinical and Experimental Medicine, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden; 10Digestive Diseases Unit, IIS Aragón, Zaragoza, Spain; 11Genetic-Analysis AS, Oslo, Norway; 12Gastrointestinal Unit, Centre for Genomics and Molecular Medicine, University of Edinburgh, Edinburgh, UK; 13Translational Gastroenterology Unit, Experimental Medicine Division, University of Oxford, Oxford, UK; 14Department of Pediatrics, Oslo University Hospital, Ullevål, Oslo, Norway Purpose: Imbalance in the microbiota, dysbiosis, has been identified in inflammatory bowel disease (IBD). We explored the fecal microbiota in pediatric patients with treatment-naïve IBD, non-IBD patients with gastrointestinal symptoms and healthy children, its relation to IBD subgroups, and treatment outcomes.Patients and methods: Fecal samples were collected from 235 children below 18 years of age. Eighty children had Crohn’s disease (CD), 27 ulcerative colitis (UC), 3 IBD unclassified, 50 were non-IBD symptomatic patients, and 75 were healthy. The bacterial abundance of 54 predefined DNA markers was measured with a 16S rRNA DNA-based test using GA-Map™ technology at diagnosis and after therapy in IBD patients.Results: Bacterial abundance was similarly reduced in IBD and non-IBD patients in 51 of 54 markers compared to healthy patients (P

Objective: To describe the prevalence of serological markers in newly diagnosed treatment naïve pediatric inflammatory bowel disease (IBD), their utility in differentiating Crohn’s disease (CD), ulcerative colitis (UC) and symptomatic non-IBD patients and whether serological markers are associated with early TNF blocker treatment. Material and methods: Ninety-six children and adolescents < 18 years, 58 with IBD and 38 symptomatic non-IBD controls were included. At diagnosis and after 1-2 years, serological antibodies (anti–Saccharomyces cerevisiae antibodies (ASCA), perinuclear anti-neutrophil cytoplasmic antibody (pANCA), flagellin expressed by Clostridial phylum (anti-CBir), outer membrane porin of Escherichia coli (anti-OmpC), Pseudomonas fluorescens associated sequence (anti-I2)), CRP, ESR, and fecal calprotectin were analyzed. The choice of treatment was made at the discretion of the treating pediatrician. Results: Of the IBD patients 20 (36%) and 26 (47%) were positive for ASCA and pANCA compared to 3(8%), p

The present population based adult cohort was part of a new prospective study of patients with inflammatory bowel disease (IBD) in South-Eastern Norway, the Inflammatory Bowel South-Eastern Norway II study, investigating disease characteristics in an attempt to improve our knowledge regarding factors related to early clinical phenotype and disease activity.Patients suspected to have IBD on the basis of predefined symptoms, including abdominal pain, diarrhea, and/or blood in stool for more than 10 days were examined at the local hospital. Colonoscopy with biopsies was performed and blood and stool samples were taken.In ulcerative colitis (UC) patients, the median Simple Clinical Colitis Activity Index (SCCAI) was 4 (range 0-10) in mild and 6 (range 0-14) in patients with moderate or severe endoscopic activity of inflammation (p = 0.002). The calprotectin concentration in feces was significantly related to the SCCAI (p = 0.034) and the Mayo endoscopic subscore (p = 0.031). There was a significant association between the C-reactive protein (CRP) value, leucocytes and thrombocytes and the SCCAI, but only leucocytes were significantly associated with the Mayo endoscopic subscore. In Crohn's disease (CD) patients, there was no statistical significant association between the Harvey-Bradshaw Index (HBI) and the endoscopic grade of mucosal inflammation (p = 0.8). The calprotectin concentration in feces was significantly related to the endoscopic activity score (p = 0.004), but not to the HBI (p = 0.5). HBI was significantly related to the CRP value (p = 0.047) and thrombocytes (p = 0.03).In UC, both biochemical and fecal markers are related to disease activity and extent of disease, whereas in CD, the fecal calprotectin concentration is a reliable marker of mucosal affection, but not for systemic disease activity.

Inflammatory bowel disease (IBD) of pediatric and adult onset differs in several aspects although little knowledge exists about pathogenic disparity. Regulatory T cells (Tregs) characterized as CD4+CD25+Foxp3+ are modulators of gut homeostasis, but their role in human IBD remains unclear.To evaluate the mucosal distribution of Foxp3+ and CD25+ cells in untreated pediatric IBD patients at the time of diagnosis.Untreated pediatric (n = 14) and adult (n = 12) Crohn's disease (CD) patients were prospectively included together with age-matched symptomatic controls. Colonic and ileal mucosal biopsies collected at diagnosis were studied by immunohistochemistry for enumeration of T cells and for mucosal expression of Foxp3 and CD25. Multicolor immunofluorescence staining was performed in situ to phenotype Foxp3+ cells as Tregs and characterize the CD25+ cells.The density of mucosal T cells displayed only small variations, while that of Foxp3+ cells and CD25+ cells was increased in CD patients. Multicolor immunofluorescence showed that most CD25+ cells were macrophages. Interestingly, in the ileum of pediatric CD patients the density of Foxp3+ cells was significantly higher than in adult CD patients. Co-expression of Foxp3 and CD25, as well as Foxp3 and CTLA-4, indicated that the Foxp3+ cells were Tregs.Mucosal numbers of Foxp3(+) Tregs and activated (CD25+) macrophages are elevated in both pediatric and adult ileal CD. The greater increase of ileal Foxp3+ Tregs in pediatric CD than in adult CD might contribute to the relatively less frequent phenotype of isolated ileal enteritis in CD children.

The presence of Mycobacterium avium subspecies paratuberculosis (MAP) has previously been inferred in the genesis of Crohn's disease (CD), and a higher incidence of MAP PCR positivity has been demonstrated in the gut and peripheral blood of CD patients than in healthy individuals. The objective of this prospective study was to assess the potential etiological role of MAP in the pathogenesis of CD.The presence of mycobacteria was assessed in bowel biopsies from newly diagnosed, treatment naïve Norwegian patients with IBD, including CD and ulcerative colitis (UC), as compared to a hospital-based cohort of CD and UC patients. Biopsies were collected from the small and large bowel in 354 individuals with suspected IBD. Detection of mycobacteria was performed by long-term cultivation in combination with direct detection by MAP IS900-specific PCR.Among the specimens included from the patients with early IBD, samples from only two of the patients with CD (2.7%) and two of the non-IBD controls (1.5%) exhibited a positive growth signal. None of the CD patients and only one of the non-IBD controls was MAP PCR positive. Only the single PCR positive non-IBD control was also mycobacterial culture positive with Mycobacterium avium subsp. hominissuis. In the referral patients with long-term IBD, the prevalence of growth signal and MAP PCR positivity was higher (52 and 9%, respectively).These findings demonstrate the paucity of MAP in the gut of treatment naïve CD patients. This study does not provide evidence for a role of MAP in early IBD.

Background: Pediatric inflammatory bowel disease (IBD) may be phenotypically different from adult IBD. In IBD lesions, macrophages are overactivated, suggesting involvement of innate immunity in the pathogenesis. Here, mucosal macrophages were studied in selected untreated pediatric patients compared with adults from a population-based Norwegian cohort of IBD patients. Age-matched non-IBD controls were also included. Methods: Untreated children (

IMPORTANCE: Blood markers and fecal calprotectin are used in the diagnostic workup for inflammatory bowel disease (IBD) in pediatric patients. Any added diagnostic value of these laboratory markers remains unclear.OBJECTIVE: To determine whether adding laboratory markers to evaluation of signs and symptoms improves accuracy when diagnosing pediatric IBD.DATA SOURCES: A literature search of MEDLINE and EMBASE from inception through September 26, 2016. Studies were identified using indexing terms and free-text words related to child, target condition IBD, and diagnostic accuracy.STUDY SELECTION: Two reviewers independently selected studies evaluating the diagnostic accuracy of more than 1 blood marker or fecal calprotectin for IBD, confirmed by endoscopy and histopathology or clinical follow-up, in pediatric patients with chronic gastrointestinal symptoms. Studies that included healthy controls and/or patients with known IBD were excluded.DATA EXTRACTION AND SYNTHESIS: Individual patient data from each eligible study were requested from the authors. In addition, 2 reviewers independently assessed quality with Quality Assessment of Diagnostic Accuracy Studies-2.MEAN OUTCOMES AND MEASURES: Laboratory markers were added as a single test to a basic prediction model based on symptoms. Outcome measures were improvement of discrimination by adding markers as a single test and improvement of risk classification of pediatric patients by adding the best marker.RESULTS: Of the 16 eligible studies, authors of 8 studies (n = 1120 patients) provided their data sets. All blood markers and fecal calprotectin individually significantly improved the discrimination between pediatric patients with and those without IBD, when added to evaluation of symptoms. The best marker-fecal calprotectin-improved the area under the curve of symptoms by 0.26 (95% CI, 0.21-0.31). The second best marker-erythrocyte sedimentation rate-improved the area under the curve of symptoms by 0.16 (95% CI, 0.11-0.21). When fecal calprotectin was added to the model, the proportion of patients without IBD correctly classified as low risk of IBD increased from 33% to 91%. The proportion of patients with IBD incorrectly classified as low risk of IBD decreased from 16% to 9%. The proportion of the total number of patients assigned to the intermediate-risk category decreased from 55% to 6%.CONCLUSIONS AND RELEVANCE: In a hospital setting, fecal calprotectin added the most diagnostic value to symptoms compared with blood markers. Adding fecal calprotectin to the diagnostic workup of pediatric patients with symptoms suggestive of IBD considerably decreased the number of patients in the group in whom challenges in clinical decision making are most prevalent.

Germline loss-of-function mutations in the transcription factor signal transducer and activator of transcription 3 ( STAT3 ) cause immunodeficiency, whereas somatic gain-of-function mutations in STAT3 are associated with large granular lymphocytic leukemic, myelodysplastic syndrome, and aplastic anemia. Recently, germline mutations in STAT3 have also been associated with autoimmune disease. Here, we report on 13 individuals from 10 families with lymphoproliferation and early-onset solid-organ autoimmunity associated with 9 different germline heterozygous mutations in STAT3 . Patients exhibited a variety of clinical features, with most having lymphadenopathy, autoimmune cytopenias, multiorgan autoimmunity (lung, gastrointestinal, hepatic, and/or endocrine dysfunction), infections, and short stature. Functional analyses demonstrate that these mutations confer a gain-of-function in STAT3 leading to secondary defects in STAT5 and STAT1 phosphorylation and the regulatory T-cell compartment. Treatment targeting a cytokine pathway that signals through STAT3 led to clinical improvement in 1 patient, suggesting a potential therapeutic option for such patients. These results suggest that there is a broad range of autoimmunity caused by germline STAT3 gain-of-function mutations, and that hematologic autoimmunity is a major component of this newly described disorder. Some patients for this study were enrolled in a trial registered at www.clinicaltrials.gov as #NCT00001350.

Objective: Pediatric Crohn’s disease (CD) is often debilitating, with upper gastrointestinal involvement and complications over time. Treatment with TNF blockers can induce and maintain remission. We wanted to evaluate the outcome of patients medically treated for CD to investigate whether clinical, endoscopic and biochemical factors at diagnosis are associated with the early initiation of treatment with the TNF blocker infliximab. Materials and Methods: Patients aged

Wnt signaling regulates small intestinal stem cell maintenance and Paneth cell differentiation. In patients with ileal Crohn's disease (CD), a decrease of Paneth cell α-defensins has been observed that is partially caused by impaired TCF-4 and LRP6 function. Here we show reduced expression of the Wnt signaling effector TCF-1 (also known as TCF-7) in patients with ileal CD. Reporter gene assays and in vitro promoter binding analysis revealed that TCF-1 activates α-defensin HD-5 and HD-6 transcription in cooperation with β-catenin and that activation is mediated by three distinct TCF binding sites. EMSA analysis showed binding of TCF-1 to the respective motifs. In ileal CD patients, TCF-1 mRNA expression levels were significantly reduced. Moreover, we found specifically reduced expression of active TCF-1 mRNA isoforms. Tcf-1 knockout mice exhibited reduced cryptdin expression in the jejunum, which was not consistently seen at other small intestinal locations. Our data provide evidence that TCF-1-mediated Wnt signaling is disturbed in small intestinal CD, which might contribute to the observed barrier dysfunction in the disease.

The knowledge about correlation patterns between the fecal microbiota and inflammatory bowel diseases (IBD)—comprising the two subforms Crohn's disease (CD) and ulcerative colitis (UC)—for newly diagnosed untreated children is limited. To address this knowledge gap, a selection of faecal specimens (CD,n=27and UC,n=16) and non-IBD controls (n=30) children (age < 18 years) was analysed utilising bacterial small subunit (SSU) rRNA. We found, surprising age dependence for the fecal microbiota correlating to IBD. The most pronounced patterns were thatE. coliwas positively (R2=0.16,P=0.05) and Bacteroidetes, negatively (R2=0.15,P=0.05) correlated to age for CD patients. For UC, we found an apparent opposite age-related disease correlation for bothBacteroidesandEscherichia. In addition, there was an overrepresentation ofHaemophilusfor the UC children. From our, results we propose a model where the aetiology of IBD is related to an on-going immunological development in children requiring different age-dependent bacterial stimuli. The impact of our findings could be a better age stratification for understanding and treating IBD in children.

Tap-water has recently been identified as an important epidemiological parameter in inflammatory bowel disease (IBD). Whether bacteria present in tap-water are involved in IBD still remains unknown. To address this question, the dominant microbiota in tap-water samples from households of patients with IBD, and from those of non-IBD control patients, were screened. Tap-water from both pediatric patients (

OBJECTIVES Adult ileal Crohn's disease (CD) is characterized by a specific decrease in ileal Paneth cell alpha-defensins. In addition to NOD2, we previously identified a disturbance of the Wnt-signaling transcription factor TCF-4 as a major mechanism for this deficiency. The aim of this study was to evaluate human alpha-defensin-5 (HD-5) and TCF-4 in an independent cohort of pediatric CD patients. METHODS Expression levels of HD-5 and TCF-4 mRNA were quantified by real-time PCR in biopsies from newly diagnosed untreated pediatric CD patients (

Objective. Owing to rising incidence rates in inflammatory bowel disease (IBD), there has been increased interest in causal relationships in pediatric disease. The present population-based inception cohort was recruited in the Oslo area from 2005 to 2007, with the aim of conducting a detailed characterization of treatment-naive patients at diagnosis. Material and methods. After an invitation was extended to all general practitioners in the catchment area, patients aged 18 years with suspected IBD were diagnosed by proximal and distal endoscopy, MRI, demographic, clinical, and histological and molecular characteristics. Symptomatic non-IBD patients served as controls. Results. Of 100 pediatric patients, 62 had IBD (39 Crohn's disease (CD), 19 ulcerative colitis (UC), 4 IBD unclassified (IBDU)) and 38 other diseases. Median age at diagnosis for IBD was 13.1 years (56.4% males), median symptom duration 6 months, and 69% L3 (Vienna classification). With 195,000 children aged 18 years in the catchment area, the incidence rate of IBD per 100,000/years inhabitants was 10.9 (6.8 for CD, 3.6 for UC, and 0.6 IBDU) and for those aged 16 years (178,500) the incidence rate was 10.6. The higher NOD2 allele frequency among children may partly contribute to the increase. Conclusions. The results indicate a marked rise in the incidence of CD in contrast to no increase in UC in South-Eastern Norway, compared with the figures from the last 15 years. Time from onset of symptoms to diagnosis still represents a challenge for early characterization in IBD.

The results of recent research suggest that there is an increasing incidence of inflammatory bowel disease (IBD) among children. Newly diagnosed IBD was compared between two consecutive 6-year periods in the same catchment area of southeastern Norway.Children subjected to endoscopy from 1993 to 2004 were recorded retrospectively in the first 6-year period and prospectively for the subsequent period. The mean size of the child population under 16 years in the area was 70,500. The study reports on incidence numbers, age at diagnosis, disease distribution and clinical presentation at diagnosis.There were 23 incident cases of IBD in the first period and 25 in the subsequent period. The rates of Crohn's disease (CD) for the two periods were, respectively, 1.95 and 3.64, and for ulcerative colitis (UC) 3.67 and 2.05/100,000 children/year. Total incidence rates of IBD for the two periods were 5.6 and 5.7, respectively, similar to the findings of the IBSEN study of 1990-94. The change in CD and UC rates from the first to the second period can be explained by better methods of diagnosis.The total incidence of IBD was not changed between time periods, whereas a trend towards an increase in CD and a reduction in UC was recorded. The incidence rates are in accordance with previously reported national and international data from the past decade. The extent of disease in CD and UC may indicate a serious prognosis of IBD among children.

s of the 3rd International Symposium on Pediatric Inflammatory Bowel Disease S411 end-tidal carbon dioxide(ETCO2) were recorded. We also examine retrospectively whether additional sedative drugs needed during colonoscopy because of pain or body motion, the abdominal pain within 24 hours after colonoscopy, and whether the underlying disease got worse within 1 week. Results: In the CO2 group, the abdominal circumference increased only an average of 0.9cm and no severe ETCO2 increased. There were no patient who had postcolonoscopy abdominal pain within 24 hours in the CO2 group, whereas two patients in the air group. Only in the air group, diarrhea and blood feces got worse suddenly after colonoscopy. Conclusions: This study indicates that CO2 insufflation can reduse abdominal pain after colonoscopy and is safe to use in sedated pediatric patients. P-048 Cut-off value of fecal calprotectin in pediatric patients with inflammatory bowel disease G. Veres *, D. Giczi, A. Cseh, D. Szabo, K.E. Muller, N. Csepregi, A. Arato. Semmelweis University, Ist Dept of Pediatrics, Budapest, Hungary Introduction: Fecal calprotectin is a neutrophil-derived S-100 protein correlating with intestinal inflammation. Aims: The primary aim of our prospective study was to compare fecal calprotectin levels in pediatric patients with inflammatory bowel disease (IBD: Crohn’s disease, CD and ulcerative colitis, UC) with healthy controls to determine the best cut-off value to distinguish IBD patients from controls. Our secondary aim was to correlate fecal calprotectin to disease activity scores (PCDAI, PUCAI) and laboratory markers. Methods: Fecal calprotectin was measured by quantitative lateral flow assay in 81 pediatric patients with IBD (CD: 65, UC: 14, median age: 15.8 years) and in 67 healthy controls (median age 11.3 years). In addition, disease activity scores (PCDAI, PUCAI) and laboratory markers were also determined. Results: Fecal calprotectin was significantly increased in patients with IBD (median: 784 mg/g, 25 75 pc: 292.5 1754 mg/g), in CD (800 mg/g, 365.5 1620 mg/g), in UC (207.5 mg/g, 100 207.5 mg/g) when compared with controls (100 mg/g, 100 100 mg/g). The best cut-off value was defined: 192.5 mg/g. Fecal calprotectin and platelet count correlated positively in patients with UC. There was no correlation between fecal calprotectin and disease activity indexes (PCDAI, PUCAI) or laboratory markers studied (CRP, PCDAI, PUCAI). Conclusions: Fecal calprotectin is a reliable, non-invasive marker in patients with IBD with the cut-off level of 200 mg/g. Disease activity indexes were not correlated with fecal calprotectin. Positive correlation of platelet count and calprotectin may have diagnostic relevance in patients with UC. P-049 Reproducibility of serologic antibody activity at diagnosis and after treatment in pediatric ulcerative colitis and Crohn’s disease C. Olbjorn1 *, M.C. Smastuen2, B. Nakstad3, M.H. Vatn4, G. Perminow5. 1Akershus University Hospital and University of Oslo, Lorenskog, Norway, 2Institute of Biostatistics, University of Oslo, Oslo, Norway, 3Dep of Child and Adolescent Medicine, Ahus and University of Oslo, Lorenskog, Norway, 4Epigen, Institute of Clinical Medicine, University of Oslo, Lorenskog, Norway, 5Department of Pediatrics, Oslo University Hospital, Ulleval, Oslo, Norway Introduction: Serological nuclear and antimicrobial antibodies are predictive markers of disease course and complications in ulcerative colitis (UC) and Crohn’s disease (CD). The stability of serological titers over time has been questioned. Aim: We wanted to compare antibody titers before and after treatment in newly diagnosed treatment naive pediatric patients with inflammatory bowel disease (IBD). Methods: Patients

to a labeled end of an amplified gene. T-RFLP is an established technique for analysing bacterial species in faecal samples. Methods: This was a quantitative analysis with a major focus on evaluating a biomarker based on intestinal microbiota. The subjects were 69 UC patients together with an 80 relatives as controls. Twenty-three patients had active UC (group I) and 46 had quiescent UC (group II). The latter included 17 with mild inflammation in the large intestine (group IIa), and 29 without inflammation (group IIb). The patients’ relatives were consanguineous (group III, n = 47), and non-consanguineous (group IV, n = 33). The Discriminant analysis of operationaltaxonomic-unit (OTU) on T-RFLP fingerprints was done. The Canonical Discriminant Function Coefficient (Df) for each OTU was calculated by using group I and group IV, in whom the difference of intestinal flora was thought to be greatest. The individual OTUs were multiplied by the Df value, and the sum was termed the Discriminant Score (Ds). The analysis was by SPSS (IBM Statistics 20.0). Results: The Ds decreased thus: group I > group IIa > group IIb > group III > group IV. As certain strains of bacteria are associated with the development of UC, while others not, this should show up in the OTU values in T-RFLP analysis. The analysis was set to factor this assumption, and the OUTs with 0 value 95% of all cases together with the OTUs of structure matrix value