In an analysis of a large cohort of subjects with IBD, we found a significant association between symptoms of depression or anxiety and clinical recurrence. Patients with IBD should therefore be screened for clinically relevant levels of depression and anxiety and referred to psychologists or psychiatrists for further evaluation and treatment.
We conclude that it is not possible to diagnose Hp-related gastritis on the basis of the endoscopic appearance alone. The diagnosis should be based on other criteria, such as a rapid urease test, or a histological examination of gastric biopsies, or both.
Very-early-onset inflammatory bowel disease (VEO-IBD) is a heterogeneous phenotype associated with a spectrum of rare Mendelian disorders. Here, we perform whole-exomesequencing and genome-wide genotyping in 145 patients (median age-at-diagnosis of 3.5 years), in whom no Mendelian disorders were clinically suspected. In five patients we detect a primary immunodeficiency or enteropathy, with clinical consequences (XIAP, CYBA, SH2D1A, PCSK1). We also present a case study of a VEO-IBD patient with a mosaic de novo, pathogenic allele in CYBB. The mutation is present in~70% of phagocytes and sufficient to result in defective bacterial handling but not life-threatening infections. Finally, we show that VEO-IBD patients have, on average, higher IBD polygenic risk scores than population controls (99 patients and 18,780 controls; P < 4 × 10 −10 ), and replicate this finding in an independent cohort of VEO-IBD cases and controls (117 patients and 2,603 controls; P < 5 × 10 −10 ). This discovery indicates that a polygenic component operates in VEO-IBD pathogenesis.
The metabolism of the hydrogenated disaccharide maltitol was compared to that of sucrose in a group of eight normal subjects. On two separate days, with an interval of at least one week each subject ingested a load of 30 g of either substance. The evolution of the levels of plasma glucose, insulin, and free fatty acids was followed during the 6 hr following the oral load. Carbohydrate and lipid oxidation rates were assessed simultaneously by continuous indirect calorimetry during the 6 hr following the oral load. Plasma glucose and insulin peaks occurred 30 min after ingestion of the load for both sugars. The peak of the delta glucose concentration was significantly smaller after maltitol than after sucrose (21 +/- 4 vs 38 +/- 4 mg/100 ml, p less than 0.02), as was the peak of the delta insulin concentration (9.3 +/- 2.7 microU/ml after maltitol vs 25.5 +/- 5.0 microU/ml after sucrose, p less than 0.001). The peak of the stimulation of glucose oxidation occurred 60 min after the load of sucrose and 90 min after the load of maltitol. The delta glucose oxidation was significantly lower with maltitol than with sucrose during the first 90 min after the ingestion of the load. It was slightly higher (although not significantly) with maltitol than with sucrose starting from the 210th min. Maltitol resulted in a cumulated suprabasal glucose oxidation which amounted to 40% that obtained with sucrose after 180 min.
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