The aim of this study was to observe the features of chronic gastritis in children with celiac disease (СD). Materials and methods. 176 children with chronic gastritis (CG) aged from 3 to 16 years were examined. Group I consisted 58 child ren with CG and newly diagnosed CD not adherent to the gluten-free diet (GFD), group II consisted 49 children with CG and CD, adherent to the GFD. In the group III of comparisons were 69 children with CG and excluded CD. The exa mination included serological, morphological methods to confirm or exclude CD. The histological examination of the biopsy specimens of the gastric mucosa, the determination of antiparietal antibodies by the method of iIFR and ELISA (antibodies to Castle’s intrinsic factor and Anti-H+/K+ ATPase antibodies) were carried out. Results. Helicobacter pylori infection was diagnosed in vast majority of patients in all groups. Autoantibodies to the gastric mucosa were found in every tenth patient in groups I and III, and did not occur in group II. In group II statistically significant the etiology of gastritis remained not determined. Endoscopically the gastric mucosa in groups I and II often remained intact. Accor ding to the morphological study in groups I and II, the pathological process was more often localized in the body of the stomach, and in group III in the antrum. Autoimmune gastritis is presented in groups without a statistically significant difference. Conclusion. Chronic gastritis is a frequent co-morbid pathology in СD, and it is also not uncommon in these patients. Data of endoscopy in children, regardless of diet, does not reflect the complete picture of CG. All children with CD, regardless of compliance with GFD, are recommended to take biopsy specimens of the gastric mucosa for histological examination in order to exclude CG, and in case of detecting atrophic changes in the gastric mucosa to define the antiparietal antibodies.
One of non-IgE-mediated disorders that pediatricians and allergologists have to deal with is food protein-induced enterocolitis syndrome (Food Protein Induced Enterocolitis Syndrome, FPIES). Cow milk and soy proteins are the most common cause of FPIES. Other foods that can cause FPIES include a wide range of solid food stuffs, such as grains, vegetables, fruits, and poultry. Food-borne enterocolitis is usually accompanied by acute recurring vomiting and diarrhea, lethargy, pallor, dehydration, and even hypovolemic shock. FPIES often occurs after the first introduction of complementary foods containing trigger products, usually not accompanied by fever or a significant increase in the level of C-reactive protein, and generally has a good prognosis. Depending on the severity of the disease, metabolic acidosis and meth-hemoglobinemia may develop. In chronic cases anemia, hypoalbuminemia and eosinophilia may occur. In acute cases laboratory evaluation may reveal thrombocytosis and neutrophilia, peaking 6 hours after a meal. Manifestations of FPIES usually disappear within 24-48 hours after elimination of the causative food. Radiological evaluation and other methods like endoscopy and gastric juice analysis can yield nonspecific results. Data on the incidence of FPIES is limited, and approximate assessment of affected children rate varies from 1.5 to 30 per 10,000. Further studies are needed to identify clinical subtypes and predisposing factors for the development of FPIES compared to immediate-type IgE-mediated gastroenteropathy.
In recent years, the number of obese women of childbearing age has increased significantly. The aim of this study was to reveal the influence of maternal obesity during pregnancy on the longterm health of the offspring. This study was performed in the outpatient clinic in St. Petersburg with 76 adolescents with chronic diseases aged from 6 to 17 years. The mean age of the examined was 12.67 ± 3.19 years; the ratio of girls to boys was 6 : 7. Children were divided into 2 groups: the main group included 26 adolescents whose mothers were obese before and during pregnancy. 50 teen agers from mothers with normal BMI during pregnancy presented comparison group. The main group and the comparison group did not differ in age and sex. The children were examined by a pediatrician. Data on the transferred diseases are obtained from an outpatient card. It has been established that maternal obesity may be considered a risk factor for miscarriage, having low birth weight babies or babies weighing more than 4 kg, as well as a risk factor for rickets, parathrophies and functional constipation in the first year of life. In adolescentes, obesity, euthyroid goiter, hypothalamic syndrome and other endocrinopathies are typical for children born from obese mothers. Several medical conditions related to obesity such as chronic pancreatitis, hiatal hernia, iron deficiency anemia and orthopaedic foot and ankle pathology are commonly seen in children of obese mothers. Maternal obesity is associated with diseases of children not only in the period of newborn, but also in adolescence.
Anthropometric evaluation is an essential feature of pediatric evaluation. Different countries use different approaches in pediatric growth assessment. The article presents a comparative analysis of the body length (BL) indicators of modern school-age children in St. Petersburg with regional standards (1991) and international standards (WHO Growth Reference 2007). Anthropometric evaluation was conducted among 6207 children aged 7 to 17 years; the median, standard deviation and centile distribution of the BL values of school-age children were determined. We found that the values of BL of modern school-age children are higher than that their peers had thirty years ago; in boys, the maximum difference is found during the pubertal growth spurt; Non-parametric and parametric indicators of BL in senior pupils of St. Petersburg are higher than in the standards of the World Health Organization; in junior schoolchildren no difference was found. The data we obtained create the prerequisites for the development of modern regional standards for growth assessment of children and school-age children in St. Petersburg and their practical use for pediatric examinations.
Congenital disorders of glycosylation (CDG) is a genetically heterogeneous and clinically polymorphic group of diseases caused by defects in various enzymes, the synthesis and processing of N-linked glycans or oligosaccharides into glycoproteins. Approximately half of all proteins expressed in cells are glycosylated to achieve their full functionality. Basically there are 2 variants of glycosylation: N-glycosylation and O-glycosylation. N-glycans are bound to the amide group of aspartine, whereas O-glycans are bonded to the hydroxyl group of serine or threonine. Synthesis of N-glycans occurs in 3 stages: the formation of nucleotide-linked sugars, assembly (in the cytosol and endoplasmic reticulum) and treatment (in the Golgi apparatus). Synthesis of O-glycans occurs mainly in the Golgi apparatus. The most frequently identified types of CDG are associated with a defect in the N-glycosylation pathway. CDGs are typically multisystem disorders with varying clinical manifestations such as hepatomegaly, cholestasis, liver failure, developmental delay, hypotonia, convulsions, facial dysmorphism and gastrointestinal disorders. Also histological findings showed liver fibrosis, malformation of the ducts, cirrhosis, and steatosis. CDGs typically present in the first months of life, and about 20% of patients do not survive to 5 years. The first line of CDG screening is based on the analysis of N-glycosylation of transf ferin. Exome sequencing or targeted gene panel is used for diagnosis. Several CDG subtypes are amenable to teraphy with mannose and galactose.
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