Evaluation of malnutrition development risk in hospitalized children.

Objectives: Many screening methods, such as the Screening Tool Risk on Nutritional Status and Growth (STRONGkids) and the Pediatric Yorkhill Malnutrition Score (PYMS), have been developed to detect malnutrition in pediatric patients. We aimed to explore the prevalence of malnutrition risk in hospitalized children via symptoms and identification of contributing factors, and to examine the efficacy of malnutrition screening tools for hospitalized children

Can Fecal Calprotectin Level Be Used as a Markers of Inflammation in the Diagnosis and Follow-Up of Cow's Milk Protein Allergy?

Purpose: Calprotectin is a cytosolic protein with immunomodulatory, antimicrobial, and antiproliferative actions. The concentration of calprotectin increases in infection, inflammation, and malignancy. We determined if calprotectin can be used as a marker for the diagnosis and follow-up of bowel inflammation in cow's milk protein allergy (CMPA). Methods: In total, 32 patients newly diagnosed with CMPA were included (24 IgE-mediated, 8 non-IgE-mediated). In all subjects, a complete blood count, total IgE, cow's milk-specific IgE, and fecal calprotectin (EC) were assessed before and after a cow's milk protein (CMP) elimination diet was started. The results were compared with those of 39 healthy children. Results: The mean EC value before the CMP elimination diet was 516 +/- 311 mu g/g in the 32 patients with CMPA and 296 +/- 94 mu g/g in the control group (P=0.011). The mean FC value after the diet in these patients was 254 +/- 169 mu g/g, which was significantly different from the mean value before the CMP elimination diet (P<0.001). When we compared EC levels before the CMP elimination diet in the IgE-mediated group with the control group, we found no significant statistical difference (P=0.142). The mean FC value before the CMP elimination diet was 886 278 pg/g in the non-IgE-mediated group and 296 +/- 94 pg/g in the control group; this difference was statistically significant (P<0.001). In the IgE-mediated and non-IgE-mediated groups, FC values after CMP elimination diet were 218 +/- 90 mu g/g and 359 +/- 288 mu g/g, respectively, and FC values before CMP elimination diet were 392 +/- 209 mu g/g and 886 +/- 278 mu g/g, respectively; these differences were statistically significant (P=0.001 and P=0.025, respectively). Conclusions: FC levels may be a useful marker for follow-up treatment and recurrence determination in CMPA

Association of Inflammatory Bowel Disease With Familial Mediterranean Fever in Turkish Children

Background and Aims: Inflammatory bowel disease (IBD) and familial Mediterranean fever (FMF) share common clinical and biological features. The prevalence of other inflammatory diseases, including IBD, is increased in FMF. We investigated the presence of IBD accompanying FMF in patients who were being followed up with a diagnosis of FMF and the relation of IBD with the MEFV gene mutation

The Incidence of Irritable Bowel Syndrome in Children Using the Rome III Criteria and the Effect of Trimebutine Treatment

Background/Aim

Clinical Features of Interleukin 10 Receptor Gene Mutations in Children With Very Early-Onset Inflammatory Bowel Disease

Objectives: In the present study, we studied a cohort of patients with very early onset inflammatory bowel disease (IBD) to determine the frequency of mutations in the interleukin 10 (IL10) receptor genes as a cause of early-onset IBD

Shear Wave Elastography in the Evaluation of Liver Fibrosis in Children

Background:Shear-wave elastography (SWE) is a novel noninvasive method that involves application of local mechanical compression on soft tissue using focused ultrasonography and acquiring strain images that show tissue response. In this study, our goal was to assess the performance of SWE in the staging of liver fibrosis in children with chronic liver disease.Methods:The study involved measuring SWE values in the right lobe of the liver in a patient group of 76 children with chronic liver disease and a control group of 50 healthy subjects. In the patient group, the shear elastic modulus values were correlated with biopsy results according to the Brunt scoring system (F0: portal fibrosis, F1: perisinusoidal or portal/periportal fibrosis, F2: both perisinusoidal and portal/periportal fibrosis, F3: bridging fibrosis, and F4: cirrhosis). Performance of SWE in estimating liver fibrosis in children was determined based on a receiver-operating characteristics (ROC) analysis.Results:Mean SWE values of the control group and F0 group were not statistically significantly different (P=0.106). The mean SWE values of the F1, F2, F3, and F4 groups were higher than that of the control group (all P<0.001). Based on kiloPascal measurement values, the area under the ROC curve was 95.2% (95% confidence interval [CI] 92.1-99.5), with a sensitivity for diagnosing liver fibrosis of 91.5%, a specificity of 94.0%, a positive predictive value of 93.1%, and a negative predictive value of 92.6%. Based on meter-per-second measurement values, the area under the ROC curve was 96.3% (95% CI 92.7-99.8), with a sensitivity for diagnosing liver fibrosis of 93.2%, a specificity of 94.0%, a positive predictive value of 93.2%, and a negative predictive value of 94.0%. Mean SWE values for patients with nonalcoholic steatohepatitis were higher than those in the remainder of the study group.Conclusions:Although liver fibrosis can be detected using SWE, differentiation of fibrosis stages could not be achieved. The presence of steatosis significantly increased the mean SWE values on elastography and so care should be taken when assessing children with nonalcoholic steatohepatitis

CD55 Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis

BACKGROUND Studies of monogenic gastrointestinal diseases have revealed molecular pathways critical to gut homeostasis and enabled the development of targeted therapies. METHODS We studied 11 patients with abdominal pain and diarrhea caused by early-onset protein-losing enteropathy with primary intestinal lymphangiectasia, edema due to hypoproteinemia, malabsorption, and less frequently, bowel inflammation, recurrent infections, and angiopathic thromboembolic disease; the disorder followed an autosomal recessive pattern of inheritance. Whole-exome sequencing was performed to identify gene variants. We evaluated the function of CD55 in patients' cells, which we confirmed by means of exogenous induction of expression of CD55. RESULTS We identified homozygous loss-of-function mutations in the gene encoding CD55 (decay-accelerating factor), which lead to loss of protein expression. Patients' T lymphocytes showed increased complement activation causing surface deposition of complement and the generation of soluble C5a. Costimulatory function and cytokine modulation by CD55 were defective. Genetic reconstitution of CD55 or treatment with a complement-inhibitory therapeutic antibody reversed abnormal complement activation. CONCLUSIONS CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55. (Funded by the National Institute of Allergy and Infectious Diseases and others.