• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.4 no.2
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• pp.238-242
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• 2001

Food allergy is a disease caused by an abnormal immunological reaction to specific food proteins. Whole milk and soy beans are the most frequent causes of food allergy, some studies show that 2.2~2.8% of children aged between 1 and 2 year are allergic to milk. It can be classified to acute (urticaria, asthma, anaphylaxis) or chronic (diarrhea, atopic dermatitis) allergy according to clinical symptoms, or to IgE related or non IgE related allergy by an immunological aspect. Generally, allergies invading only the GI tract are mostly due to a non IgE related reaction. These hypersensitive, immunologic reactions of the GI tract, not related to specific IgE for food, present themselves in many ways such as food protein-induced enteropathy, food protein-induced enterocolitis syndrome (FPIES), celiac disease, food induced protocolitis, or allergic eosinophillic gastroenteritis. FPIES is one kind of non IgE related allergic reaction and is manifested as severe vomiting and diarrhea in infants between 1 week and 3 months. We report a case of FPIES in a 40-day old male infant presenting with 3 times of repeated events of watery diarrhea after cow's milk feeding.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.17 no.2
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• pp.74-79
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• 2014

Food protein-induced enterocolitis syndrome (FPIES) is an under-recognized non-IgE-mediated gastrointestinal food allergy. The diagnosis of FPIES is based on clinical history, sequential symptoms and the timing, after excluding other possible causes. It is definitively diagnosed by an oral food challenge test. Unfortunately, the diagnosis of FPIES is frequently delayed because of non-specific symptoms and insufficient definitive diagnostic biomarkers. FPIES is not well recognized by clinicians; the affected infants are often mismanaged as having viral gastroenteritis, food poisoning, sepsis, or a surgical disease. Familiarity with the clinical features of FPIES and awareness of the indexes of suspicion for FPIES are important to diagnose FPIES. Understanding the recently defined clinical terms and types of FPIES is mandatory to suspect and correctly diagnose FPIES. The aim of this review is to provide a case-driven presentation as a guide of how to recognize the clinical features of FPIES to improve diagnosis and management of patients with FPIES.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.10 no.2
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• pp.117-128
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• 2007

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE mediated hypersensitivity disorder, which is associated with mainly gastrointestinal symptoms and has a delayed onset. The vomiting and/or diarrheal symptoms of FPIES typically begin in the first month of life in association with a failure to thrive, metabolic acidosis, and shock. Therefore, the differential diagnosis of FPIES and neonatal or infantile sepsis-like illnesses or gastroenteritis is difficult. The early recognition of indexes of suspicion for FPIES may help in the diagnosis and treatment of this disorder. The diagnosis of FPIES is generally made through clinical practice and food-specific IgE test findings are typically negative in this condition. Therefore, oral cow's milk challenge (OCC) remains the valid diagnostic standard for FPIES. An investigation of positive OCC outcomes helps to find out a diagnostic algorithm of criteria of a positive challenge in FPIES. Moreover, it has not been clearly determined in infantile FPIES when $1^{st}$ follow up-oral food challenge (FU-OFC) should be performed, with what kind of food protein (e.g., cow's milk, soy), and how much protein should be administered. Hence, to prevent the risk of inappropriate FU-OFC or accidental exposure and achieve appropriate dietary management, it is necessary to identify tolerance rates to major foods under the careful follow up of infantile FPIES patients. On the other hand, small intestinal enteropathy with villous atrophy is observed in FPIES and this enteropathy seems to be in part induced by both of epithelial apoptosis and intercellular junctional complex breakdown. The purpose of this report is to introduce an update on diagnostic and therapeutic approaches in FPIES and suggest the possible histopathological evidences in this disorder.

• Clinical and Experimental Pediatrics
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• v.53 no.4
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• pp.525-531
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• 2010

Purpose : Expression levels of tumor necrosis factor (TNF)-${\alpha}$ expression on the mucosa of the small intestine is increased in patients with villous atrophy in food protein-induced enterocolitis syndrome (FPIES). TNF-${\alpha}$ has been reported to induce apoptotic cell death in the epithelial cells. We studied the TNF family and TNF-receptor family apoptosis on the duodenal mucosa to investigate their roles in the pathogenesis of FPIES. Methods : Fifteen infants diagnosed as having FPIES using standard oral challenge test and 5 controls were included. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining was performed to identify the apoptotic cell death bodies. Immunohistochemical staining of TNF-${\alpha}$, Fas ligand (FasL) for TNF family and TNF-related apoptosis-including ligand (TRAIL) receptor 1 (DR4), TRAIL receptor 2 (DR5), and Fas for TNF-receptor family were performed to determine the apoptotic mechanisms. Results : $TUNEL^+$ was significantly more highly expressed in the duodenal mucosa of FPIES patients than in controls ($P$-0.043). TNF-${\alpha}$ ($P$=0.0001) and DR4 ($P$=0.003) were significantly more highly expressed in FPIES patients than in controls. Expression levels of FasL, Fas, and DR5 were low in both groups and were not significantly different between the 2 groups. Conclusion : These results suggest that FPIES pathogenesis is induced by apoptosis, and that TNF-${\alpha}$ expression and DR4 pathway may have an important role in apoptosis.