The role of Candida sp. in etiopathogenesis of esophageal, gastric and duodenal mucosa inflammation in children.

The aim of the study was to demonstrate morphological traits of Candida-induced upper alimentary tract mucosa inflammation. The material for the study comprised 18 children aged 4 to 18 years treated at the I Department of Paediatrics and Gastroenterology, Institute Polish Mother Health Centre. In these children positive mycologic cultures were obtained from alimentary tract inflammed mucosa sections. Upper alimentary tract endoscopy was performed and macroscopic and microscopic evaluation was made. Children with excluded H. pylori infection, reflux disease, lambliosis and allergy were included into the investigated group. Savara-Muller’s classification was used for oesophageal mucosa inflammation evaluation, whereas gastric and duodenal mucosa inflammation were assessed according to Tytgat. Results: the most frequent macro lesions concerned simultaneously gastric and duodenal mucosa (44.46%). 27.77% of patients demonstrated oesophagitis, gastritis and duodenitis. In histopathological examination inflammatory lesions in oesophageal mucosa were observed in 38.88% (most frequently I degree). Chronic gastritis was found in all children, non-active in 11 and active in 7. Duodenal mucosa demonstrated traits of chronic active inflammation in 8 children and chronic in 5 of them. Conclusions: Candida fungi may be an etiopathogenetic factor of oesophageal, gastric and duodenal mucosa inflammation, Candida-induced mucosa inflammation is most frequently of chronic nature

Gut response to pasteurized donor human milk in a porcine model of the premature infant

This study investigated the tolerance and safety of pasteurized donor human milk (PDHM) given either alone or together with commercially-used supplements in a porcine model of premature infants. A porcine model, mimicking human neonates at 30-32 weeks of gestational age, was used. The 7-day experiment was performed on 20 piglets. After birth, the piglets were infused with porcine immunoglobulins via the umbilical artery and surgically fitted with a stomach port. The piglets were then randomized into five groups and fed either PDHM, different variants of fortified PDHM or 'raw' human milk (RHM). Preterm piglets fed PDHM showed signs of gastrointestinal intolerance. Four piglets across the various PDHM-fed groups died, none of them were from the group fed PDHM supplemented with long-chain polyunsaturated fatty acids (LC PUFA). In all groups fed PDHM, macroscopic features of enterocolitis were observed, however, these pathological gut changes were less manifested in piglets receiving PDHM supplemented with LC PUFA. The piglets fed RHM had no specific signs of gut damage. The poor tolerance to PDHM suggests changes in milk composition caused by the Holder pasteurization. The supplementation with LC PUFA probably improves tolerance to PDHM

A potential double role of anti-Lewis X antibodies in Helicobacter pylori-associated gastroduodenal diseases

In this study, we found Lewis X (Le(X)) determinants on 68% of Helicobacter pylori isolates from patients with chronic gastroduodenal diseases. Anti-Le(X) IgG were detected more frequently in the sera from dyspeptic children and adults (45 and 46%), with or without proved (culture) H. pylori infection, than in the sera from healthy individuals (14%, and 25%). In contrast, the prevalence of anti-Le(X) IgM was higher in the groups of healthy individuals than in the groups of dyspeptic patients. Moreover. anti-Le(X) monoclonal antibody of IgM class enhanced the uptake of Le(X)(+) but not Le(X)(-) H. pylori isolates by phagocytes. In the sera from some dyspeptic patients, we detected Le(X)-anti-Le(X) IgG immune complexes (Le(X) ICs). There was a great difference between children and adults as regards the presence of Le(X) ICs. The immune complexes were found in the sera from nine out of 29 (27%) H. pylori-infected and three out of eight (37%) uninfected adult dyspeptic patients. In comparison, Le(X)-anti-Le(X) IgG ICs were detected only for two out of 18 (11%) H. pylori-infected children. Le(X) ICs were not found in the sera from healthy individuals. Our results suggest that anti-Le(X) IgM may play a protective role in H. pylori infections. In contrast, anti-Le(X) IgG and particularly Le(X)-anti-Le(X) IgG ICs might contribute to the pathogenesis of chronic H. pylori infections