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Foods that account for 90% of allergic reactions in children are cow's milk protein, eggs, peanut, soy, tree nuts, fish, and wheat. Food allergy can manifest as urticaria/angioedema, anaphylaxis, atopic dermatitis, respiratory symptoms, or a gastrointestinal (GI) disorder. GI allergic manifestations can be classified as immunoglobulin E (IgE) mediated (immediate GI hypersensitivity and oral allergy syndrome); "mixed" GI allergy syndromes (involving some IgE components and some non-IgE or T-cell-mediated components) include eosinophilic esophagitis and eosinophilic gastroenteritis. Non-IgE-mediated or T-cell-mediated allergic GI disorders include dietary protein enteropathy, protein-induced enterocolitis, and proctitis. All these conditions share a common denominator: the response of the immune system to a specific protein leading to pathologic inflammatory changes in the GI tract. This immunological response can elicit symptoms such as diarrhea, vomiting, dysphagia, constipation, or GI blood loss, symptoms consistent with a GI disorder. The detection of food allergies can be accomplished by the use of radioallergosorbent (RAST) testing and skin prick tests in helping to assess the IgE-mediated disorders. Patch tests may help evaluate delayed hypersensitivity reactions. Treatment of GI allergic disorders ranges from strict dietary elimination of offending food(s), use of protein hydrolysates, and use of L-amino acid-based formula when protein hydrolysates fail. Treatment with topical (for eosinophilic esophagitis) or systemic steroids is used if all dietary measures are unsuccessful. Maternal breast feeding or the use from birth of hydrolysate formulas (extensive or partial hydrolysates) may be efficacious in the prevention of atopic disease in "high-risk" families (with at least 1 parent or sibling with a history of atopic disease).
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PMID:Gastrointestinal manifestations of food allergies in pediatric patients. 1620 93

Allergy is caused by an immune reaction that is out of all proportion to the antigenic stimuli. Classical allergy is a type I hypersensitivity reaction mediated by the interaction of mast cells (and eosinophils) coated with allergen-specific IgE and a cross-linking allergen. The physiological outcome is inflammation commonly displayed by urticaria, rhinitis, vomiting and diarrhoea, depending on the route of allergen entry. In extreme reactions anaphylactic shock can result that may lead to death. Chronic allergic responses most commonly present themselves as asthma and eczema. All these symptoms are the consequence of an imbalanced immune system making an unsuitable response to an environmental or food antigen. On bacterial colonisation of the colon after birth the appropriate microbiological stimuli is essential to redress the balance of the skewed T-helper 2 immune response present in the newborn. This normal interaction between baby and microbes is thought to be compromised in the Western world, with a reduction in bifidobacteria and an increase in clostridial species, particularly in bottle-fed infants. The use of probiotic therapy to prevent allergic disease has been demonstrated in two studies using a probiotic Lactobacillus rhamnosus GG in neonates. A long-term reduction in allergy has been shown in the test group, with lactobacillus reducing the incidence of atopic eczema. Management of allergy through probiotics has also been demonstrated in infants, using lactobacilli to control atopic eczema and cow's milk allergy. Unfortunately, these positive results have not been repeated in studies with older children and young adults.
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PMID:Probiotics and allergy. 1631 88

Cow milk protein intolerance (CMPI) affects 3% of infants under the age of 12 months and is often misdiagnosed as GERD or colic, risking dangerous exposure to antigens. Most infants out grow CMPI by 12 months; however, those with IgE-mediated reactions usually continue to be intolerant to cow's milk proteins and also develop other allergens including environmental allergens that cause asthmatic symptoms. Clinical manifestations of CMPI include diarrhea, bloody stools, vomiting, feeding refusal, eczema, atopic dermatitis, urticaria, angioedema, allergic rhinitis, coughing, wheezing, failure to thrive, and anaphylaxis. The research and literature showed that CMPI is easily missed in the primary care setting and needs to be considered as a cause of infant distress and clinical symptoms. This article focuses on correctly diagnosing CMPI and managing it in the primary care setting.
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PMID:The diagnosis and management of cow milk protein intolerance in the primary care setting. 1641 42

The efficacy of cyclosporin A (CsA) for the treatment of canine atopic dermatitis was evaluated based on the systematic review of prospective clinical trials published between 2001 and 2005. Ten studies with adequate design characteristics were included. These studies enrolled 799 dogs, 672 (84%) treated with CsA, 160 (20%) with placebo, 74 (9%) with oral glucocorticoids and 23 (3%) with antihistamines. Treatment duration varied from 2 weeks to 6 months. For safety analysis, data were available from 660 dogs. Lesion scores were improved from baseline in the range of 30-52%, 53-84% and 52-69% after 4, 6 and 16 weeks, respectively. The percentage of dogs with only mild pruritus rose from 0-13% at inclusion to 32-59% and 46-90% after 4 and 12 weeks, respectively. In most studies, the frequency of CsA administration could be reduced to every other day in 40% to 50% of patients after 4 weeks and to twice weekly in 20-26% of the dogs after 12-16 weeks. Meta-analysis confirmed highly significant effects of CsA compared to placebo, but none between oral CsA and glucocorticoids. The initial disease severity, age or body weight of subjects did not influence treatment success. Improvement by more than 50% over baseline of lesion scores was predictive of a better response during treatment maintenance. Vomiting and soft stools/diarrhoea were the most frequent adverse events seen at least once during the studies. These occurred in 25% and 15% of subjects, respectively. The frequency of each other type of adverse events was lower than 2.1%. In summary, the administration of CsA for the treatment of canine AD was found to be as effective as that of glucocorticoids, and adverse effects were minimal.
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PMID:A systematic review and meta-analysis of the efficacy and safety of cyclosporin for the treatment of atopic dermatitis in dogs. 1641 15

Adverse reactions to foods are frequent in everyday life. They are divided into toxic and immunologic food reactions. The awareness of toxic food reactions among adverse reactions to food is essential for correct diagnosis. Enzymatic food intolerance, adverse reactions to food or food additives, pharmacologic food intolerance, psychosomatic factors, food allergy with classic symptoms (anaphylaxis, urticaria-angioedema), atopic dermatitis, contact dermatitis (protein), upper and lower respiratory symptoms like rhinitis or asthma, and gastrointestinal disorders (oral allergy syndrome, colic, nausea, vomiting, diarrhea, abdominal pain) are discussed. Target organs throughout the body-ear, eye, pharynx, skin, lung, joints, and muscles-can be involved. The gold standard in diagnosis is a double-blind, placebo-controlled food challenge test. The diagnostic tools available for most food-related disorders are the skin-prick test and radioallergosorbent test. The treatment of food-induced urticaria consists of elimination of the offending food or substance from the diet, use of antihistamines, and immunotherapy.
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PMID:Adverse reactions to food and clinical expressions of food allergy. 1668 80

Food allergies in children present with a wide spectrum of clinical manifestations, including anaphylaxis, urticaria, angioedema, atopic dermatitis and gastrointestinal symptoms (such as vomiting, diarrhoea and failure to thrive). Symptoms usually begin in the first 2 years of life, often after the first known exposure to the food. Immediate reactions (occurring between several minutes and 2 hours after ingestion) are likely to be IgE-mediated and can usually be detected by skin prick testing (SPT) or measuring food-specific serum IgE antibody levels. Over 90% of IgE-mediated food allergies in childhood are caused by eight foods: cows milk, hens egg, soy, peanuts, tree nuts (and seeds), wheat, fish and shellfish. Anaphylaxis is a severe and potentially life-threatening form of IgE-mediated food allergy that requires prescription of self-injectable adrenaline. Delayed-onset reactions (occurring within several hours to days after ingestion) are often difficult to diagnose. They are usually SPT negative, and elimination or challenge protocols are required to make a definitive diagnosis. These forms of food allergy are not usually associated with anaphylaxis. The mainstay of diagnosis and management of food allergies is correct identification and avoidance of the offending antigen. Children often develop tolerance to cows milk, egg, soy and wheat by school age, whereas allergies to nuts and shellfish are more likely to be lifelong.
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PMID:4. Food allergy in childhood. 1701 10

Eosinophilic esophagitis (EE) is a clinical-pathological disorder which is being increasingly diagnosed. It is etiologically associated with hypersensitivity to airborne allergens and/or dietary components. However, immediate hypersensitivity to foods has rarely been proven as the etiologic cause of the disorder. Two patients are presented with a history of rhinoconjunctivitis, allergic asthma, atopic dermatitis and food allergies which are currently under control and who show specific IgE to pulses and chicken respectively. These patients developed acute dysphagia and vomiting immediately after ingesting these foods and following appropriate examination were diagnosed as suffering from EE. The study also showed signs of blood hypereosinophilia while the esophageal manometry revealed a motor disorder characterized by aperistalsis and non-propulsive simultaneous waves affecting the lower two-thirds of the organ composed of smooth muscle. Topical treatment with fluticasone propionate was administered over a period of 3 months, in addition to a diet abstaining from the aforementioned foods and this led to remission of dysphagia and normalization of the endoscopic, histological and manometric studies of the esophagus. This situation remained stable for a considerable length of time after steroid treatment was discontinued, which showed that exposure to foods seemed to be the cause of the esophageal disorder. Similarly, allergies to inhalants and other digestive symptoms which appear upon immediate ingestion of the foods involved would not justify the sudden onset of dysphagia. We offer a pathophysiological explanation for the mechanisms of the disease based on the activation of eosinophils and mast cells by IgE and their ability to disturb the dynamic behavior of the neural and muscle components of the esophageal wall.
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PMID:Food allergies and eosinophilic esophagitis--two case studies. 1706 99

Cow's milk protein allergy (CMPA) is best treated by complete elimination of cow's milk from the diet. For infants with CMPA who cannot be breast-fed, formulas based on extensively hydrolyzed proteins or on amino acids are the preferred substitutes for cow's milk-based formulas. In this study, we compared the tolerance and growth of infants with CMPA who were fed a new extensively hydrolyzed formula containing lactose (eHF) with those who were fed an amino acid formula (AAF). This was a prospective, multi-center, randomized, reference-controlled study. Seventy-seven infants <12 months old with suspected CMPA were enrolled. In 66 of these, CMPA was confirmed by oral challenge in a double-blind, placebo-controlled food challenge (DBPCFC) or by a medical history of severe allergic reaction to cow's milk and a positive skin prick test. These infants were then tested for their reaction to eHF and AAF in a DBPCFC. All infants tolerated both formulas and were randomized to receive either eHF (n = 34) or AAF (n = 32) for 180 days. Growth (weight, length, and head circumference) and tolerance [skin, gastro-intestinal, and respiratory tract symptoms of allergy] were evaluated after 30, 60, 90, and 180 days. There were no significant differences between the two groups in any of the growth measurements. Length and head circumference were similar to Euro-growth standards, but weight was slightly lower. Gastro-intestinal and respiratory tract symptoms of allergy were also similar in the two groups. However, whereas SCORAD scores for atopic dermatitis remained constant throughout the study in infants-fed eHF, there was a slight decrease in those fed AAF. Infants-fed eHF had significantly fewer incidents of vomiting than infants-fed AAF and a significantly higher frequency of soft stools. The new eHF is safe and well tolerated in infants diagnosed with CMPA.
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PMID:Safety and efficacy of a new extensively hydrolyzed formula for infants with cow's milk protein allergy. 1816 60

A joint study group on cow's milk allergy was convened by the Emilia-Romagna Working Group for Paediatric Allergy and by the Emilia-Romagna Working Group for Paediatric Gastroenterology to focus best practice for diagnosis, management and follow-up of cow's milk allergy in children and to offer a common approach for allergologists, gastroenterologists, general paediatricians and primary care physicians.The report prepared by the study group was discussed by members of Working Groups who met three times in Italy. This guide is the result of a consensus reached in the following areas. Cow's milk allergy should be suspected in children who have immediate symptoms such as acute urticaria/angioedema, wheezing, rhinitis, dry cough, vomiting, laryngeal edema, acute asthma with severe respiratory distress, anaphylaxis. Late reactions due to cow's milk allergy are atopic dermatitis, chronic diarrhoea, blood in the stools, iron deficiency anaemia, gastroesophageal reflux disease, constipation, chronic vomiting, colic, poor growth (food refusal), enterocolitis syndrome, protein-losing enteropathy with hypoalbuminemia, eosinophilic oesophagogastroenteropathy. An overview of acceptable means for diagnosis is included. According to symptoms and infant diet, three different algorithms for diagnosis and follow-up have been suggested.
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PMID:Cow's milk protein allergy in children: a practical guide. 2020 81

The foodborne pathogen Staphylococcus aureus produces the virulent staphylococcal enterotoxin A (SEA), a single-chain protein that consists of 233 amino acid residues with a molecular weight of 27 078 Da. SEA is a superantigen that is reported to contribute to animal (mastitis) and human (emesis, diarrhea, atopic dermatitis, arthritis, and toxic shock) syndromes. Changes of the native structural integrity may inactivate the toxin by preventing molecular interaction with cell membrane receptor sites of their host cells. In the present study, we evaluated the ability of one commercial and two freshly prepared apple juices and a commercial apple polyphenol preparation (Apple Poly) to inhibit the biological activity of SEA. Dilutions of freshly prepared apple juices and Apple Poly inhibited the biological activity of SEA without any significant cytotoxic effect on the spleen cells. Additional studies with antibody-coated immunomagnetic beads bearing specific antibodies against the toxin revealed that SEA added to apple juice appears to be largely irreversibly bound to the juice constituents. The results suggest that food-compatible and safe anti-toxin phenolic compounds can be used to inactivate SEA in vitro and possibly also in vivo, even after induction of T-cell proliferation by long-term exposure to SEA. The significance of the results for microbial food safety and human health is discussed.
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PMID:Inhibition of biological activity of staphylococcal enterotoxin A (SEA) by apple juice and apple polyphenols. 2040 9


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