Celiac disease (CD) may cause numerous nutrient deficiencies that a proper gluten-free diet (GFD) should compensate for. The study group consists of 40 children, aged 8.43 years (SD 3.5), on average, in whom CD was diagnosed on the basis of clinical symptoms, immunological and histopathological results. The patients’ height, weight, diet and biochemical tests were assessed three times: before diagnosis, after six months, and following one year of GFD. After one year, the patients’ weight and height increased but nutritional status (body mass index, BMI percentile) did not change significantly. The children’s diet before diagnosis was similar to that of the general Polish population: insufficient implementation of the dietary norm for energy, fiber, calcium, iodine, iron as well as folic acid, vitamins D, K, and E was observed. Over the year, the GFD of the children with CD did not change significantly for most of the above nutrients, or the changes were not significant for the overall assessment of the diet. Celiac patients following GFD may have a higher risk of iron, calcium and folate deficiencies. These results confirm the need for personalized nutritional education aimed at excluding gluten from the diet, as well as balancing the diet properly, in patients with CD.

IntroductionEosinophils contribute to the pathogenesis of inflammatory bowel disease (IBD) in the intestine. Eosinophilic cationic protein (ECP) is one of the most important eosinophilic specific mediators released during activation. The aim of the study was to evaluate the clinical value of serum ECP determination in children with active and inactive IBD and its correlation with disease activity.Material and methodsThere were 125 children with IBD (63 with Crohn's disease – CD, 44 with ulcerative colitis – UC, 18 indeterminate colitis – IC) enrolled in the study. Among them 83 children were in the active phase of the disease, while the remaining 42 were in remission. The control group consisted of 56 healthy children. The ECP was assessed three times in children with active IBD, at baseline and after 2 and 6 weeks of treatment and once in children with inactive IBD and controls using fluoroenzymeimmunoassays.ResultsWe found elevated ECP at baseline in the total active IBD group when compared to the inactive IBD and control groups, decreasing during treatment. Serum ECP was also elevated in the active UC and CD groups when compared to the inactive UC and CD groups, and correlated with clinical UC and CD activity (R = 0.57 and R = 0.52, p < 0.05, respectively) and duration of the clinical manifestation in UC (R = 0.62, p < 0.05) but not with the disease location in the gastrointestinal tract, or endoscopic and histopathological activity.ConclusionsEvaluation of serum ECP in children with IBD may be useful in disease activity assessment at onset and during the treatment.

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The aim of our study was to analyze the incidence and the clinical characteristic of celiac disease (CD) in pediatric population with type 1 diabetes mellitus (T1DM). Materials and methods: The data of 880 patients with T1DM, 429 girls, mean age 12.14 ±4.0 years was retrospectively retrieved from medical records. Patients with T1DM and CD were selected and a detailed analysis of CD prevalence and its clinical characteristic at the time of CD diagnosis was performed. The data were compared with the previous data from our center published a decade ago. Results: CD was suspected in 85/880 patients (9.65%) on the base of results of serological tests, but finally CD was diagnosed in 73/880 patients with T1DM (8.3%), in 53/429 girls (12.3%) and in 20/451 boys (4.4%). Most patients (71%) had CD diagnosed after T1DM onset. The majority of CD patients (72%) was asymptomatic. The CD diagnosis was not associated with inappropriate metabolic control of diabetes. The onset age of diabetes in children with CD was significantly lower than in those without CD (5.8 ±3.6 years vs. 7.56 ±4.0 years, p = 0.04). The prevalence of CD is significantly higher than a decade ago in our center (8.3% vs. 5.7%, p = 0.001). Conclusions: In light of increasing prevalence of mainly asymptomatic CD in patients with T1DM, CD screening is necessary. However positive serological tests, which are currently used in screening, and are the first step of diagnostics, in some patients allow only to suspect the CD and further diagnostic steps should be performed.

Congenital chloride diarrhea (CLD) is a rare, autosomal recessive disorder caused by mutations in the solute-linked carrier family 26 member 3 gene (SLC26A3) located in chromosome 7q31. The encoded protein belongs to the ion transporter family and is responsible for sodium-independent Cl À /HCO 3 À ion exchange. In this process, the exchanger protein located in the apical brush border of the intestinal epithelium in the ileum and large bowel subserves the absorption of chloride by epithelial cells and secretion of bicarbonate into the lumen of the bowel (1). Mutation disrupts this process and leads to secretory diarrhea with a high chloride content in the stool, hypochloremia, hyponatremia, and metabolic alkalosis. The first symptoms appear prenatally as polyhydramnios. Ultrasonography shows dilated intestinal loops. Premature birth is common (2). Without adequate treatment (replacement therapy with NaCl and KCl), severe electrolyte disturbances develop with episodes of dehydration. Chronic hypovolemia, followed by high aldosterone and elevated plasma renin activity, may lead to renal function impairment (2-4). Failure to thrive may occur (2).Celiac disease (CD) is characterized by immunemediated gluten intolerance resulting in enteropathy with atrophy of small bowel mucosa and impairment of food absorption. CD has a genetic background and is strongly associated with HLA DQ2, or DQ8. The prevalence of CD in Europe is estimated as 1 in 100 to 500. The most typical symptoms of its classical form in small children are chronic diarrhea and failure to thrive (5).