The possibility of a causal relationship between gluten intake and the development of symptoms in the absence of celiac disease (CD) and wheat allergy (WA) has recently gained new scientific interest and includes a condition known as non-celiac gluten sensitivity (NCGS). To date, NCGS has been widely described in adults, whereas there is little information about this pathology in pediatric practice. This article presents a clinical case of NCGS in a 6-year-old girl who was admitted to the gastroenterology department of the Republican Specialized Scientific and Practical Medical Center of Pediatrics (Republic of Uzbekistan) with complaints of abdominal pain, bloating, weight loss, liquid stools, headaches, and fatigue. The complaints appeared 5 months before hospitalization. Antibodies to tissue transglutaminase IgA were within reference ranges, specific IgE antibodies to wheat and gluten were not elevated. A biopsy from the distal duodenum revealed Marsh-Oberhuber 1 lesions. The patient was switched to a gluten-free diet (GFD) with suspected NCGS. At week 4 of the diet, an improvement was noted, but abdominal bloating persisted. An intolerance to components such as fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) was suspected. The use of the FODMAP diet significantly improved the condition. The reintroduction of gluten after 6 weeks resulted in a recurrence of symptoms, confirming the diagnosis of NCGS. Given that the number of gluten-related diseases is increasing, and not much is known about NCGS, we decided to present this case to raise awareness and questions regarding diagnosis, the need for specific monitoring, and treatment. Key words: FODMAP, gluten, children, non-celiac gluten sensitivity, celiac disease
Cystic fibrosis is a disease caused by mutations in a gene encoding CFTR-protein (Cystic Fibrosis Transmembrane conductance Regulator), located in the apical membrane of epithelial cells of the respiratory tract, intestines and pancreas. Defensins serve as important components of the innate human immune system, they play a key role in providing the first line of defense of a macroorganism against infection; they have high antimicrobial, antiviral, cytotoxic activity.Objective. To determine the values of fecal β-defensin-2 in children with cystic fibrosis and to reveal the dependence of its level on the exocrine function of the pancreas and the severity of the patient’s condition.Characteristics of children and research methods. The study included 57 children with cystic fibrosis, the average age was 20.93 ± 2.9 months. Cystic fibrosis was diagnosed on the basis of an increase in immunoreactive trypsin, sweat chlorides by Cook’s method (>60 meq / l). To assess the exocrine function of the pancreas the scientists determined the activity of fecal elastase. They evaluated the levels of fecal β-defensin-2 and calprotectin using a quantitative enzyme immunoassay.Results. The levels of fecal β-defensin-2 were increased (108.2 ± 11.3 ng / ml) in all children under examination. The researchers found no correlation between the levels of fecal β-defensin-2 and fecal elastase. The level of fecal calprotectin was significantly higher in the group of children with cystic fibrosis as compared to the control group. There was a significant correlation between the levels of fecal calprotectin and fecal β-defensin-2 (r=0.57; p <0.05), however, no correlations were found between the levels of fecal β-defensin-2 and fecal elastase. The group of children with a severe course of the disease demonstrated an increase in the level of fecal β-defensin-2, fecal calprotectin significantly more frequent.Conclusion. Children with cystic fibrosis demonstrated a significant increase in the concentration of β-defensin-2 as compared to the control group, which confirms the activation of the innate immune system of the intestinal mucosa. The researchers traced the relationship between high levels of fecal β-defensin-2 and the severity of the disease. The levels of fecal β-defensin-2 directly correlated with the concentration of fecal calprotectin and there was no correlation between the severity of pancreatic insufficiency and the concentration of fecal β-defensin-2.
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