IntroductionConsumption of gluten proteins leads to an enteropathy characterised by lymphocytic infiltration of mucous membrane, crypts hypertrophy, and atrophy of villi. Enteropathy leads to disturbances in the immune system as well as secondary deficiency of vitamin E.AimAnalysis of the concentration of vitamin E in erythrocytes of patients with celiac disease.Material and methodsThree experimental groups were distinguished among 77 patients with histologically confirmed celiac disease (mean age: 17 years): those who strictly respected gluten-free diet (group I, n = 48), patients breaking dietary recommendations (group II, n = 22), and those with newly diagnosed disease (group III, n = 7). Additionally, a control group consisting of healthy individuals with negative serological markers of celiac disease was formed (group IV, n = 20). Vitamin E concentration was determined by high performance liquid chromatography with ultraviolet detector.ResultsSignificantly lower average concentration of vitamin E was demonstrated in erythrocytes in all examined groups of patients with celiac disease compared to the control group. Among the patients with celiac disease, the highest average concentration of vitamin E in erythrocytes was observed in the group who respected the gluten-free diet, a little lower in patients who violated dietary recommendations, and lowest among patients with newly diagnosed disease. These relationships, however, were not statistically significant.ConclusionsPatients with celiac disease are at risk of vitamin E deficiency irrespective of their diet. Vitamin supplementation should be considered in their case, especially immediately after diagnosis of the disease and in case of breaking a gluten-free diet regime.

Introduction: It is still unknown whether faecal calprotectin elevation may be caused by active untreated coeliac disease (CD) itself or whether it indicates the coexistence of CD and another disease associated with gastrointestinal inflammation. Aim: To assess faecal calprotectin concentration (FCC) and its correlation with the clinical form and histopathological picture of the small intestine in children with CD. Material and methods: Fifty-five children with newly recognised CD (mean age: 9.1 years) and 17 children with CD diagnosed at least year before and on a strict gluten-free diet (mean age: 12.3 years) were accepted for the study. Classical (n = 27), non-classical (n = 17), and asymptomatic form (n = 11) were distinguished in children with newly diagnosed CD based on the clinical picture. The histopathological small intestinal lesions were classified as Marsh 1 (n = 4), 3a (n = 5), 3b (n = 20), and 3c (n = 26). FCC was assessed using ELISA method with 50 µg/g as the upper limit of the normal. Results: FCC was abnormal for 21 patients with newly diagnosed CD (38.2%) and for six patients from the treated group (35.3%). Mean FCC for the analysed group of patients was 91.7 ±144.8 µg/g, in the group with newly diagnosed CD-100.9 ±154.4 µg/g, and in the treated group-61.8 ±106.2 µg/g (Z =-1.333; p = 0.183). In the group of patients with recently diagnosed CD a statistically significant relationship was not observed for FCC and both clinical picture (c 2 = 0.319, p = 0.852) and severity of small intestinal lesions according to the Marsh classification (rho = 0.136). Conclusions: Assessment of FCC seems to have no use as a marker for diagnostics and monitoring of CD irrespective of clinical form of the disease and severity of the inflammatory lesions within the small intestine.

In the present work we describe a 2-year-old boy whose battery ingestion was overlooked, and who had the battery endoscopically removed from the upper part of his oesophagus after several months. This is the only described case of such a long impaction of a lithium battery in the oesophagus, without development of severe complications. We stress the necessity to take into account ingestion of a dangerous foreign body by children demonstrating unspecific clinical signs.