Mediated Food Hypersensitivity Research Articles

Food protein-induced allergic proctocolitis in infants is associated with low serum levels of macrophage inflammatory protein-3a.

Food protein-induced allergic proctocolitis (FPIAP) is a nonimmunoglobulin (IgE)-mediated food hypersensitivity and the exact mechanisms that cause FPIAP are unknown. Chemokines play crucial roles in the development of allergic diseases. To examine serum levels of a group of chemokines in infants with FPIAP. In 67 infants with FPIAP and 65 healthy infants, we measured serum levels of mucosa-associated epithelial chemokine (MEC/CCL28), thymus-expressed chemokine (TECK/CCL25), CX3CL1 and macrophage inflammatory protein (MIP)-3a/CCL20. Infants with FPIAP had a lower median value of MIP3a/CCL20 than healthy infants [0.7 (0-222) vs. 4 (0-249) pg/mL, respectively] (p < 0.001). Infants with MIP3a/CCL20 levels ≤0.95 pg/mL have 13.93 times more risk of developing FPIAP than infants with MIP3a/CCL20 levels >0.95 pg/mL. Serum MEC/CCL28, TECK/CCL25, and CX3CL1 levels were similar between the infants with FPIAP and the control group. MIP3a/CCL20 serum levels were reduced in infants with FPIAP compared with healthy controls. Whether this finding has a role in pathogenesis remains to be determined.

Selective Reactions To Fish In Adult Patients With Food Protein-Induced Enterocolitis Syndrome (FPIES)

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE mediated food hypersensitivity. In the Mediterranean area, shellfish and fish are the most common foods implicated in adults. The objective of this study was to identify the types of fish most frequently trigger these reactions and to assess tolerance to other species.

M221 FOOD PROTEIN-INDUCED ENTEROCOLITIS SYNDROME MASQUERADING AS INTUSSUSCEPTION

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE mediated food hypersensitivity that typically affects infants. After ingestion of the culprit protein, a delayed onset of vomiting, lethargy, pallor, and bloody diarrhea can occur, which can be life-threatening. The differential diagnosis for acute vomiting in an infant is broad, making this diagnosis challenging. We present a patient in whom FPIES was initially thought to be intussusception, a common cause of childhood bowel obstruction where the intestines telescopes into itself, causing a delay in diagnosis and reoccurrence of symptoms.

Experience in food protein-induced enterocolitis syndrome in a paediatric allergy clinic

Food Protein-Induced Enterocolitis Syndrome (FPIES) is a gastrointestinal syndrome due to a non-IgE mediated food hypersensitivity.. The most common triggers are cow's milk and soy. Fish is one of the most frequently reported causes in Spain. The objective of this study is to describe the clinical characteristics of patients diagnosed with (FPIES) in a Paediatric Allergy Clinic. A retrospective descriptive study was carried out by reviewing medical records of patients diagnosed with FPIES in the Paediatric Allergy Unit of the Miguel Servet Children's Hospital from the years 2007 to 2017. A total of 135 patients were diagnosed during the study period, of whom 45% were male and 55% were female. The mean age at diagnosis was 11±1.5 months and the mean age of improvement was 2 years and 6 months±2.5 years (n=83). A personal history of atopy was observed in 31.9%. The main trigger foods were: white fish (41.4%), cow's milk (25.1%), and egg (15.5%). A conversion to IgE-mediated allergy was seen in 4.4% of patients. There was vomiting in 81.5% of the cases, with a mean of 1.75±1.1hours of latency, as well as diarrhoea in 41.5%, with a mean of 7.86±15.16hours of latency, and decline in 30.4% with a mean latency of 3.81±11.57hours. In our series, the most frequent trigger of the FPIES was fish. It was manifested mainly by late vomiting and a tolerance was reached mostly at 2 years 6 months.

Experience in food protein-induced enterocolitis syndrome in a paediatric allergy clinic

IntroductionFood protein-induced enterocolitis syndrome (FPIES) is a gastrointestinal syndrome due to a non-IgE mediated food hypersensitivity. The most common triggers are cow's milk and soy. Fish is one of the most frequently reported causes in Spain.The objective of this study is to describe the clinical characteristics of patients diagnosed with (FPIES) in a paediatric allergy clinic. Material and methodsA retrospective descriptive study was carried out by reviewing medical records of patients diagnosed with FPIES in the Paediatric Allergy Unit of the Miguel Servet Children's Hospital from the years 2007 to 2017. ResultsA total of 135 patients were diagnosed during the study period, of whom 45% were male and 55% were female. The mean age at diagnosis was 11±1.5 months and the mean age of improvement was 2 years and 6 months±2.5 years (n=83). A personal history of atopy was observed in 31.9%. The main trigger foods were: white fish (41.4%), cow's milk (25.1%), and egg (15.5%). A conversion to IgE-mediated allergy was seen in 4.4% of patients.There was vomiting in 81.5% of the cases, with a mean of 1.75±1.1h of latency, as well as diarrhoea in 41.5%, with a mean of 7.86±15.16h of latency, and decline in 30.4% with a mean latency of 3.81±11.57h. DiscussionIn our series, the most frequent trigger of the FPIES was fish. It was manifested mainly by late vomiting and a tolerance was reached mostly at 2 years 6 months.

EOSINOPHILIC ESOPHAGITIS TRIGGERED EXCLUSIVELY BY BIRCH AND MUGWORT CROSS-REACTIVE FOODS

Introduction Eosinophilic esophagitis (EoE) is characterized by non-IgE hypersensitivity to dietary antigens. Empiric six food elimination diet (SFED: milk, wheat, egg, soy, nuts, and seafood avoidance) leads to 50-74% remission, whereas elemental diet leads to >90% remission, suggesting additional dietary triggers in select patients. Exacerbation during pollen seasons has been demonstrated in a subset of EoE patients. However, a role of pollen cross-reactive foods in triggering EoE is not well established. Case Description We report a 32-year-old female with EoE who had disease remission on targeted elimination diet with birch/mugwort pollen cross-reactive foods alone. At age 22, the diagnosis of EoE was established by suggestive symptoms (dysphagia, epigastric/substernal chest pain) and esophageal biopsies demonstrating >40 eosinophils/high power field (hpf) after 8 weeks of proton pump inhibitor therapy. Empiric SFED did not lead to histological remission (>60 eosinophils/hpf). The patient reported worse EoE symptoms during tree pollen seasons and after ingesting raw birch and mugwort pollen-related foods, but denied oral allergy symptoms. Repeat skin prick tests on two occasions were negative to implicated pollens (wheal/flare (mm) to birch mix: 0/0, mugwort: 0/0). A steroid-sparing, targeted elimination diet of birch/mugwort pollen-related foods alone led to clinical and histological remission, with rare esophageal eosinophils (0-1 eosinophils/hpf). Discussion Pollen cross-reactive foods should be considered as targets for elimination diet therapy in the context of suggestive clinical history. In contrast to a prior report, assessment of pollen IgE-sensitization is not a reliable tool to guide clinical evaluation, consistent with EoE as a non-IgE mediated food hypersensitivity.

The role of intravenous access during oral food challenges in food protein-induced enterocolitis syndrome.

Food protein-induced enterocolitis syndrome (FPIES) is a non-immunoglobulin E mediated food hypersensitivity syndrome characterized by profuse vomiting and diarrhea, which leads to lethargy, dehydration, and hypotension. Given the potential severity of reactions, resolution of FPIES is confirmed via oral food challenge (OFC) during which intravenous (IV) access is recommended to facilitate IV fluids (IVF) and steroid therapy. Risk factors for IV treatment are not well characterized. The objectives of this study were to analyze predictors for IV treatment during OFC in patients with FPIES. A retrospective chart review was conducted of patients with The International Classification of Diseases, Ninth Revision codes 558.3 and 558.9, and with OFC who were seen in an allergy and immunology clinic from January 2000 to October 2015. OFC reaction severity was scored (1, mild; 2, moderate; 3, severe), and demographics, IV treatment frequency, and OFC outcomes were evaluated. The Fisher exact test and Wilcoxon rank sum test statistical analyses were performed. Of 184 patients, 28 met inclusion criteria, with 39 OFCs performed. The median age of onset of FPIES was 6 months. The median age at OFC was 2.6 years. This was 2.2 years (range, 0.3-8.5 years) from symptom onset. Of 39 OFCs, IV treatment, including IVF and/or steroids, was required in only 7.7%. Thirty-eight OFCs (97.4%) were of equal or lesser severity than historical reactions. The median severity of presenting reaction (3[IV+]:1[IV-]; p = 0.05) was greater in those who required IV treatment. OFCs with IV treatment were in younger patients (15 months [IV+]:32 months [IV-]; p = 0.039) who underwent OFCs earlier relative to the time of diagnosis (8 months [IV+]:28 months [IV-]); p = 0.018). Although FPIES can potentially elicit severe symptomatology, the patients most commonly experienced only vomiting and diarrhea, which often resolved with minimal treatment. Reactions generally did not worsen over time. Fewer than 10% of the patients challenged required IV treatment, all were young and with severe FPIES. It is reasonable to consider age and length of time from historical reactions when evaluating the necessity of IV placement in patients undergoing FPIES OFC.

Q&amp;A: Food additive intolerance

Q&A: Food additive intolerance 1) What is food additive intolerance and can you tell us what the most common symptoms are? Food additive intolerance is a non-IgE mediated food hypersensitivity. The hypersensitivity is induced by the food additives via a direct mast cell activation. Although the exact pathophysiology is unknown, various clinical signs are characteristic of food additive intolerance. These include cutaneous symtoms like redness of the skin, urticaria and angioedema as well as other organ related symptoms, such as dyspnea, hypotension or dizziness.

S1715 A New Preclinical Mouse Model for Antigen-Specific Non-IgE Mediated Food Hypersensitivity

S1715 A New Preclinical Mouse Model for Antigen-Specific Non-IgE Mediated Food Hypersensitivity

Helminths abrogate antigen-specific gut inflammation in a novel murine model of non-IgE mediated food hypersensitivity (97.13)

Abstract Non-IgE mediated (NIE) food hypersensitivities (FH) affect 2 million Americans. Helminths protect from IgE-mediated FH. Their effect on NIEFH has not been studied. We developed a murine model of NIEFH featuring severe antigen-specific enterocolitis with Th1/Th17 polarization. We used this unique model to test if helminths protect against NIEFH. METHODS: Rag1-/- mice, IL10-/- T cells and ovalbumin (OVA)-specific, TCR transgenic OT2 T cells were used to develop the NIEFH model. 6-wk-old Rag mice were reconstituted with IL10-/- and OT2 T cells. To determine if helminths protect, mice were infected with H. polygyrus before feeding low dose NSAID for 2 wks followed by OVA for 1 wk. RESULTS: On a 4-pt scale, histology score of duodenum, ileum and colon were 0.15±0.3, 0.85±0.8 &amp; 1.9±1.1 in helminth-infected mice (n=23) versus 3.8±0.5, 2.9±1.2 &amp; 3.0±0.8 in non-infected group (n=10) [p&amp;lt;0.02]. Laminar propria mononuclear cells (LPMC) from helminth-infected mice produced more IL10 in vitro than those from non-infected mice (1.4 vs 0.7 ng/ml, p&amp;lt;0.01). IL10 production was enhanced by OVA stimulation, but not by anti-CD3/28. LPMC from infected mice displayed less IL17 and IFNg when stimulated by anti-CD3/28 in vitro (p&amp;lt;0.01). CONCLUSION: Our study provides proof of concept that helminths protect against antigen-specific NIEFH. Abrogation of gut inflammation associates with suppressed IL17 &amp; IFNg, and elevated IL10 production probably from non-T cell source. NIH, Broad Foundation

Food protein-induced Enterocolitis Syndrome Caused by Fish

Introduction Food protein-induced enterocolitis syndrome (FPIES) occurs in infants. Typical symptoms include profuse vomiting and/or diarrhea several hours after ingestion of a given food. The disorder is a non-IgE mediated food hypersensitivity. The most frequently involved foods are milk and soy, but some cases of FPIES induced by solid foods have been described. We report 14 patients with FPIES due to fish protein. Material and methods History and physical examination, skin prick test (SPT) with fish allergens and Anisakis simplex, prick-by-prick test with implicated fish and determination of specific IgE antibodies against fish were performed. In eight children atopy patch test (APT) were also performed. In nine patients an open oral food challenge with the implicated fish was carried out. Results There were six boys and eight girls, aged from 9 to 12 months at diagnosis, with between two and six reactions to the offending fish proteins before the diagnosis was established. Four patients had a previous history of atopy. Presenting symptoms included diarrhea in two patients, profuse vomiting in six patients, and recurrent vomiting and subsequent diarrhea in three patients. In addition to these symptoms, associated septic appearance, apathy and lethargy were present in the remaining three patients. Onset of symptoms occurred a few minutes after fish ingestion in two patients and from 60 minutes to 6 hours in the 12 remaining patients. SPT to fish were negative in all patients. Serum food-specific IgE antibodies were negative in all patients except one. APT was positive in three patients. Open oral challenge (OC) was performed in nine infants and was positive in all. The patients were followed-up for between 1 and 7 years after diagnosis, and follow-up OC tests were performed after fish had been eliminated from the patients’ diet for 3-4 years. Four patients became clinically tolerant to the causal food. Three patients currently tolerate only one type of fish (swordfish). Conclusions We report 14 patients with FPIES caused by fish protein. The symptoms suggest a form of cell-mediated, non-IgE mediated food hypersensitivity. The gold standard for diagnosis is OC, although caution should be exercised in infants with several reactions or a recent diagnosis. After a period of elimination of the causal food from the diet, tolerance can develop.

Enhanced IL-4 but normal interferon-gamma production in children with isolated IgE mediated food hypersensitivity.

Atopic disorders such as atopic dermatitis and asthma have been characterised by an imbalance in interferon-gamma (INF-gamma) and IL-4. Whether similar imbalances are found in atopic disorders with different clinical manifestations, such as IgE mediated immediate food hypersensitivity, is not clear. We have examined the in vitro production of INF-gamma and IL-4 in peripheral blood mononuclear cells (PBMC) following phytohaemagglutinin stimulation from children with isolated immediate IgE mediated food hypersensitivity (egg, milk, "nut"), children with moderate and severe atopic dermatitis, and normal children. Children with immediate food reactions were excluded if they had a history or evidence of atopic dermatitis or asthma. PBMC from children with IgE mediated food hypersensitivity produced significantly more IL-4 (p = 0.013) but equivalent INF-gamma (p = 0.26) compared to PBMC from control children. In contrast, PBMC from children with atopic dermatitis produced significantly less INF-gamma (p < 0.001) and more IL-4 (p < 0.008) than PBMC from normal children. In addition, there was no difference in IL-4 (p = 0.74) but significantly less INF-gamma (p < 0.001) produced by PBMC from the children with atopic dermatitis than food hypersensitivity. We demonstrate that children with IgE mediated food hypersensitivity and no other manifestation of atopic disease have enhanced IL-4 production without the defect in INF-gamma production observed in childhood AD and asthma. We postulate that isolated IL-4 enhancement promotes the development of IgE mediated hypersensitivity disorders such as food allergy, whilst the combination of defective INF-gamma and enhanced IL-4 production promotes inflammatory atopic disorders such as AD and asthma.

Systemic Anaphylaxis to a Hidden Cross Reactive Food in a Surgical Resident With Latex Hypersensitivity

Background Health-care professionals are at an increased risk for severe latex hypersensitive reactions. Hidden cross-reactive foods can trigger systemic anaphylaxis. It is well recognized that latex-allergic individuals may also be allergic to certain foods due to crossreactive antigens. Objective: We describe a case of a 30-year-old surgical resident who developed a systemic anaphylactic reaction after ingesting snack crackers kept in close proximity to a bowl of guacamole. Results: The patient, who was highly sensitive to latex, was cautioned to avoid cross-reactive foods and to carry epipen and diphenhydramine with him at all times. Progressive anaphylaxis developed in spite of self-administration of epinephrine and prior counseling to avoid latex products, bananas, walnuts, avocados, and chestnuts. Conclusion: This case illustrates the severity of cross-reactive immunoglobulin E mediated food hypersensitivity in health-care workers who are strongly allergic to latex protein.

Role of IgE mediated food hypersensitivity in the pathogenesis of atopic dermatitis

Role of IgE mediated food hypersensitivity in the pathogenesis of atopic dermatitis