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Background Isolated colonic (L2) Crohn’s disease (CD) in adults is thought to have unique clinical and genetic features compared with ileal (L1) CD and ulcerative colitis (UC). Similar studies in paediatrics are scarce. Our goal was to characterize the clinical features of paediatric patients with isolated colonic CD and compare them to patients with ileo-cecal CD and those with UC. Methods This was a multi-center retrospective study including 21 sites affiliated with the Porto IBD group and IBD interest group of ESPGHAN. Data of paediatric patients diagnosed between 2014–2017 with L1 or L2 CD, or with UC, was collected, including information on demographic, clinical and laboratory parameters at diagnosis, end of induction, 1 year and 3 years after diagnosis (or at last follow-up). Results Data was collected on 300 children (102 L1, 94 L2, 104 UC) with similar demographic features. At diagnosis, bloody stools were identified in 45% of L2 patients, compared with 15% and 95% of L1 and UC patients, respectively (P Conclusion Paediatric patients with isolated colonic CD exhibit several clinical features which differentiate them from ileo-cecal CD and UC. Prospective studies are required to understand the pathogenesis of this unique entity and define short- and long-term outcomes.

Background Calgranulin-C (S100A12) is a new faecal marker of inflammation that is potentially more specific for Inflammatory Bowel Disease (IBD) than calprotectin, since it is only released by activated granulocytes. In recent years it has been confirmed that the S100A12 has comparable sensitivity and specificity to fecal calprotectin (FC) in adult patients with IBD. The aim of our study was to evaluate concentration of faecal S100A12 and calprotectin (FC) to see which of the two tests best correlated to inflammation in IBD children. Methods Between September 2019 and March 2020, we prospectively enrolled all IBD pediatric patients, both Crohn’s Disease (CD) and Ulcerative Colitis (UC). Blood and faecal samples were collected in order to evaluate serological markers of inflammation, faecal S100A12A and FC. S100A12 and FC were determined by enzyme-linked immunosorbent assay (ELISA). Results One hundred seventeen consecutive children, 46 (39%) with CD and 71 (61%) with UC were enrolled in the study. The mean age was 14.6 years (range:5–18), 44% female. Twenty three children were in clinical relapse (20%). No significant differences in S100 A12A levels were found between the UC and the CD groups (mean ±ds 25 ±32mcg/ml vs 34 ±27 mcg/ml respectively, p=0.22).In the UC group we found a statistically significant correlation of both calprotectin and S100A12 with CRP (r=0.253, p=0.044 and r=0.252, p=0.040, respectively). In CD group we found that both calprotectin and S100A12 correlated with hemoglobin (r= -0.343, p=0,024; r=-0.401, p 0.008 respectively), hematocrit (r=-0.361, p=0,046; r=-0.434, p=0.015, respectively), fibrinogen (r=0.499, p< 0,001; r=0.325, p =0.038, respectively), and white blood cells count (r=0.309, p=0.044; r=0.394, p=0.021, respectively). Moreover, in CD group, FC correlated with CRP (r=0.431, p=0.004) and erythrocyte sedimentation rate (r=0.430, p=0.004). Finally, S100A12 correlated with platelet count both in CD and UC group (r=0.351, p=0.021and r=0.254, p=0.038, respectively) IBD children in clinical relapse had higher values ​​of S100A12 and FC than patients in remission (66±47 mcg/ml vs 43±42 mcg/ml, p=0.05 and 260±192 mg/Kg vs 166±169 mg/Kg, p=0.046, respectively) Conclusion Our preliminary data show that both faecal S100A12 and FC are useful non-invasive biomarkers which reflect inflammatory activity of IBD children. Our future aim is to evaluate the correlation of S100A12 and endoscopic finding in order to further clarify its role in the diagnosis and the management of pediatric IBD.

Background Multiple pathways link Vitamin D status with the risk of development and the clinical course of Inflammatory Bowel Disease (IBD). However, limited studies have been conducted on the relationship between vitamin D and disease activity in IBD, especially in pediatric population and the results have been inconsistent. Moreover Vitamin D metabolites may provide a more precise assessment of sufficiency and mineral metabolism than total 25-hydroxyvitamin-D (25(OH)D). The aim of our study was to evaluate the concentrations of total25(OH)D, 24,25-dihydroxyvitamin D (24,25(OH)2D) and calcitriol (1,25-(OH)2D) to correlate these values with the disease activity markers. Methods We prospectively enrolled all IBD pediatric patients. Total 25(OH)D, 24,25(OH)2D and1,25-(OH)2D levels were measured by enzyme-linked immunosorbent assay (ELISA). In each patient with IBD, the activity scores of disease and the main inflammation markers were correlated to Vitamin D metabolites. We prospectively enrolled all IBD pediatric patients. Total 25(OH)D, 24,25(OH)2D and1,25-(OH)2D levels were measured by enzyme-linked immunosorbent assay (ELISA). In each patient with IBD, the activity scores of disease and the main inflammation markers were correlated to Vitamin D metabolites. Results One hundred twenty three consecutive IBD children were enrolled, 43% with Crohn Disease (CD),55% Ulcerative colitis (UC), 2% indeterminate colitis. No difference in 25(OH)D,24,25(OH)2D and 1,25-(OH)2D levels were found between CD and UC patients. A significant indirect correlation was found between C reactive protein and 1,25-(OH)2D levels in patients with IBD (r=-0.275, p=0.046) and in CD group (r=-0.477, p=0.039). Moreover, in patients with IBD and CD we found a significant indirect correlation between erythrocyte sedimentation rate(ESR) and 25(OH)D (r=-0.212, p=0.024 and and r=-0.282, p=0.047 respectively). Instead, in the UC group we found only a direct correlation for both fibrinogen and ESR with 1,25-(OH)2Dlevels (r=0.407, p 0.028 and r=0.446, p=0.013). Conclusion Our results suggest that both the active form and the total Vitamin D levels are inversely associated with disease activity especially in CD children. Further studies are needed to clarify the role of Vitamin D deficiency as a consequence or a cause of inflammation.

We sought to correlate hepcidin levels in inflammatory bowel disease [IBD] children with disease activity, inflammatory markers, and iron load test [ILT] and to compare IBD patients with coeliac and healthy patients.Between December 2012 and June 2013, 145 subjects [50 IBD patients, 45 coeliac patients and 50 healthy controls] were included in the study. All patients underwent the following examinations: blood count, iron status, erythropoiesis parameters, serum hepcidin, C-reactive protein [CRP], and erythrocyte sedimentation rate [ESR]. In order to evaluate the efficacy of iron absorption, ILT was performed in IBD patients. Disease activity indexes and IBD duration, localisation, and therapy were also evaluated, and a faecal sample for calprotectin collected.Serum hepcidin was significantly higher in IBD patients with active disease compared with both coeliac and healthy patients [p = 0.005, p = 0.003 respectively]. In a multivariate logistic regression model, having a Paediatric Crohn's Disease Activity Index [PCDAI] / Paediatric Ulcerative Colitis Activity Index [PUCAI] ≥ 30 resulted in the only variable independently associated with a positive serum hepcidin (odds ratio [OR] = 6.87; 95% confidence interval [CI] 1.4-33, p = 0.01]]. Patients with iron malabsorption [IM] showed higher values of ESR, CRP, and hepcidin [p = 0.02, p = 0.001, and p = 0.06, respectively]. Eight out of 12 [66.7%] children with IM showed an active disease compared with 6/31 [19.3%] children with normal ILT [p = 0.01]. Hepcidin levels correlated negatively with ILT [r = -0.451, p = 0.002], and positively with ferritin and CRP [r = 0.442, p = 0.0001; r = 0.243, p = 0.009, respectively]Our study demonstrates that serum hepcidin is increased in IBD children with active disease and it is responsible for IM.

The effect of antisecretory treatment on extraesophageal symptoms of gastroesophageal reflux disease was evaluated. Seventy-eight children presenting with typical and extraesophageal symptoms of gastroesophageal reflux disease underwent a multichannel intraluminal impedance and pH monitoring (MII/pH). Children with a positive MII/pH were randomly treated with proton pump inhibitors (PPIs) or histamine H(2) -receptor antagonists (H(2) RAs) during 3 months. At the end of the treatment period, all patients were recalled. A second treatment period of 3 months was given to those patients who were not symptom-free after 3 months. Thirty-five of the forty-one (85.4%) children with a pathologic MII/pH presented with extraesophageal symptoms and were treated with PPIs (omeprazole; n:19) or H(2) RAs (ranitidine; n:16) for 12 weeks. After 3 months, 11/19 (57.9%) PPI-treated patients had a complete resolution of symptoms; 6/8 nonresponders were treated with PPI for another 3 months and became all symptom-free. The other two underwent a Nissen fundoplication. Only 5/16 (31.2 %) patients treated with H(2) RAs had a complete resolution of symptoms after 3 months; 1/11 was treated again with H(2) RAs during 3 months, and 10/11 were changed to PPIs. In 3/10, a partial resolution of symptoms was achieved, while in 7/10, a complete remission was obtained (P < 0.05). Antisecretory reflux treatment improves extraesophageal reflux symptoms. The efficacy of PPIs is superior to that of H(2) RAs in these children.

all prescribedmedications. Demographic, dietary and clinical information, PCDAI, Harvey Bradshaw (HB) and Lewis score (LS) were collected at 0, 12 and 52 weeks. CE’s were evaluated by an experienced reader blinded to patient clinical information and timing. Results: Sixteen patients were screened; 10 enrolled; and 9 completed the initial 12 week trial; receiving 85% of estimated caloric needs prior to, and 101%, on the SCD. HB significantly decreased from 3.3 +2.0 to 0.6 +1.3 (p=0.007) as did PCDAI (21.1 +5.9 to 7.8 +7.1; p=0.011). LS declined significantly from 2153+732 to 960+433 (p=0.012). Seven patients continued the SCD to 52weekswith HB (0.1 +0.4) and PCDAI (5.4 +5.5) remaining improved (p=0.016 and 0.027 compared to baseline) withmean LS at 1046 +372 and 2 patients showing sustained mucosal healing. Conclusions: Clinical and mucosal improvements were seen in childrenwith CD using the SCD over 12 and 52weeks. Additionally, CE can monitor mucosal improvement in treatment trials for pediatric CD. Further studies are critically needed to understand the mechanisms underlying SCD’s effectiveness in children with CD.

severe disease activity decreased from 31% to 6% and has been consistently below 10% over the last year. Mild disease activity also decreased from 23% to 16%. Overall remission increased from 46% to 78%. Conclusion: We demonstrated dramatic reduction of moderate to severe disease activity since joining the ICN collaboration due to a timely intervention based on readily available live data reporting. ICN is an excellent tool for improving the quality of care of our patients, managing their treatment and improving their outcomes.

Background: Genome wide association studies (GWAS) find a significative correlation between several single nucleotide polymorphisms (SNPs) involved in autophagy and the occurrence of Crohn’s disease (CD) risk both in children and in adult patients. However, few incomplete and discordant evidences about the correlation of these SPNs and a specific phenotype of CD have been described in pediatric patients. Our purpose is to investigate the relationship between the autophagy gene variants of ATG16L1 and IRGM1 and clinical features in our cohort of children affected by CD. Methods: Eighty consecutive children with CD (mean age: 14.8±4.6 years) were enrolled in our study. Genotyping for ATG16L1 (rs2241880) and IRGM1 (rs13361189; rs4958847) was performed in all patients. Phenotypic informations including disease localization and behaviour stratified according to the Paris classification were collected. Moreover, phenotype data regarding medical therapy, relapses, surgery recurrences and laboratoristic inflammation parameters were analysed. Results: CD patients with the homozygous variant for the ATG16L1 (var) allele showed a significant tendence to change the clinical behaviour switching to a stenosing or fistolizing phenotype during the course of disease compared with children carrying the homozygous protective allele of ATG16L1 (wt) and heterozygous patients (het) (p = 0.05). In addition, the presence of ATG16L1 var resulted to be associated with a major recurrence of clinical relapses and an earlier introduction of immunosuppressants (p = 0.006 and p = 0.04 respectively). However, ATG16L1 var seems not to be related to a positive family history and extraintestinal manifestations (p = 0.4 and p = 0.5) and resulted to be protective for perianal disease, which was more frequent in het and wt patients (p = 0.06). Patients carrying ATG16L1 var were more frequently males (p = 0.07) and presented a signifcant higher value of fecal calprotectin at diagnosis (p = 0.007). IRGM1 rs4958847 homozygous variant was correlated with a trend toward statistical significance regards to a positive family history (p = 0.078) and the presence of extraintestinal manifestations (p = 0.08). Conclusions: CD patients carrying ATG16L1 var seem to be characterized by a more aggressive disease course, including changes in clinical behaviour, a higher number of relapses and an earlier use of immunosuppressants. IRGM1 rs4958847 variant gene is correlated with a positive family history and with extraintestinal manifestations.