Eosinophilic esophagitis: Pathophysiology, diagnosis, and management.

Eosinophilic esophagitis (EoE) is a multifactorial esophageal inflammation, with a genetic predisposition, which combines a deficient esophageal mucosal barrier, an abnormal immune reaction to environmental allergens mediated by Th2 interleukins, immediate esophageal lesions and dysmotility, with secondary remodeling and fibrosis. Symptoms include reflux, abdominal pain, and food impaction, with a variation according to age. Fibroscopy shows major and minor endoscopic and histologic criteria, with a mucosal count≥15 eosinophils/high power field (Eo/hpf). A new entity has been defined, where gastroesophageal reflux disease (GERD) and EoE share responsibility: the PPIs-sensitive form of EoE (PPI-REE). Children with fibroscopy showing≥15 Eo/hpf need a second endoscopy following 8 weeks of PPI treatment. EoE has a strong association with other atopic disorders. Allergy testing (specific IgE blood test and skin prick tests [SPTs]) identifies patients at risk of anaphylaxis (14.8% of cases). The dietary therapy is based on a 4- to 12-week elimination test followed by endoscopy to check the disappearance of eosinophilic infiltration. The "dietary approaches are the amino acid-based formula, the allergy testing-based targeted diet, and the six-food elimination diet (empirical elimination of milk, wheat, soy, eggs, peanut/nuts, and fish/seafood). A recent first-line trial elimination of milk has been suggested, with wheat as a second elimination, if necessary. Dietary therapy allows remission and catch-up growth in 65% of cases. Swallowed topical steroids (budesonide in viscous gel or fluticasone propionate for nebulization) are an alternative, for which efficacy varies according to clinical and/or histological criteria and with relapses occurring at dosage tapering. Their use may be restricted by side effects, such as oral and/or esophageal candidiasis. The impact on long-term bone health and growth is unknown. Maintenance therapy is not standardized and is team-dependent, combining or not elimination diets and long-term steroids. The long-term risk of EoE is esophageal stenosis (25%) and endoscopic dilation may be repeated. Biotherapies have shown isolated histological improvement without significant clinical efficacy.

Characterization and properties of the human and bovine lactotransferrins extracted from the faeces of newborn infants.

Human lactotransferrin was characterized in the faecal extracts from breastfed babies. Quantitative determination of human copro-lactotransferrin from birth for a period of up to 3 weeks showed that the daily elimination decreased from 35 to 5 mg. The amount of copro-lactotransferrin corresponding to the endogenous secretion was calculated to be from 0.5 to 1 mg per day. When a cow's milk diet supplemented by partially or completely iron-saturated human or bovine lactotransferrin was fed to the babies, the amounts of copro-lactotransferrin excreted depended on the origin and on the iron saturation of the lactoransferrin. In particular, the amount of bovine copro-lactotransferrin in the faeces averaged 200 mg per day. The human and bovine copro-lactotransferrins were isolated by ion-exchange chromatography or by affinity chromatography and were still able to bind iron. The fingerprints of native human and bovine lactotransferrins hydrolysed in vitro by infant's gastric or duodenal secretions showed that both proteins were not extensively digested. This demonstrates that these lactotransferrins ingested by babies are not completely destroyed and keep their ability to bind iron, and thus may supplement the bacteriostatic effects of the endogenous lactotransferrin in the intestinal tract.