Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
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We report on a baby food, cereal flour P (CFP), which, although guaranteed free of cow's milk protein, caused failure to thrive and diarrhea, vomiting, and coughing fits in a 22-month-old child. The purpose of this study was to identify the allergen involved. The investigation used prick tests, RAST, and the RAST inhibition method. Specific IgE was elevated to 100 kU/l for cow's milk and to 15.3 kU/l for alpha-lactalbumin (2.5 kU/l for casein, 0.7 kU/l for beta-lactoglobulin). Antibovine IgG IgEs were associated. RAST inhibition experiments demonstrated the presence of alpha-lactalbumin in "food-quality" lactose used in this flour, at a dose of 1-5 micrograms/g of CFP. The daily intake of alpha-lactalbumin was found to be less than 70 micrograms. This exquisite clinical sensitization was attributed to the intestinal hyperpermeability (IH) which favors the access of milk allergen to the blood, leading to an ever-growing state of hypersensitivity. It could have been due to egg- and mustard-associated allergies as well as to giardiasis and intestinal candidosis. This work underlines the risk of masked food allergens and the need of thoroughly informative labeling.
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PMID:Identification of a masked allergen, alpha-lactalbumin, in baby-food cereal flour guaranteed free of cow's milk protein. 890 5

The increase in the consumption of tropical nuts in the Northern Hemisphere during the last years, has evolved in a simultaneous enhancement of allergic IgE mediated (Hypersensitivity type 1) reported cases produced by this kind of food. The Brazil nut is the seed of the Bertholletia excelsa tree (Family Lecythidaceae) and, as in other seeds, proteins represent one of its major components making up 15-17% of its fresh weight and 50% of defatted flour. Of these, storage proteins are the most important ones, and the 12 S globulin legumin-like protein and the 2 S albumin have been described as the most representative. The 2 S protein, due to its high sulfur-rich amino acid content (3% cysteine and 18% methionine), is being studied, cloned and expressed in some important agronomic seeds (soybean, bean, oilseed rape) in order to enrich the nutritional quality of them. The case of a patient with serious clinical allergic symptoms (vomiting, diarrhoea and loss of consciousness) caused by oral contact with the Brazil nut, is presented. The patient gave a positive Skin Prick Test response to Brazil nut, kiwi and hazelnut extracts, and negative to regionally specific aeroallergens and other food extracts. The patient serum showed a high level of specific IgE by RAST to Brazil nut (> 17.5 PRU/ml, Class 4), and significative levels to hazelnut, and mustard. In vitro immunological studies (SDS-Immunoblotting and IEF-Immunoblotting) revealed IgE-binding proteins present in the extract. It was shown that not only the heavy (Mr 9) and light (Mr 4) subunits of the known allergenic 2 S albumin but also the alpha-subunits (Mr approximately 33.5 and 32) and at least one of the beta-subunits (Mr approximately 21) of the 12 S Brazil nut globulin, hitherto never involved in allergic problems, showed a strong IgE-binding capacity.
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PMID:Allergens from Brazil nut: immunochemical characterization. 920 50

Clinical manifestations of cow's milk allergy rarely occur in the first days after birth. We report on a newborn presenting with hemorrhagic meconium in the first hour of life followed by bloody diarrhea in the next few days. At day 14, an elevated total IgE, specific IgE to cow's milk and an eosinophilia in peripheral blood were found. Symptoms disappeared when the milk feed was changed to an extensively hydrolyzed casein-formula. Two challenges with cow's milk formula (on day 30 and at 7 months of age) were followed by recurrence of vomiting, watery diarrhea and failure to thrive. At the age of 17 months cow's milk was tolerated well. Although other pathogenetic mechanisms cannot completely be ruled out, there is strong evidence that cow's milk allergy--induced by intra-uterine sensitization--explains the symptoms in our patient. In conclusion, cow's milk allergy can occur even in the first days of life, and our clinical observation supports the concept of intra-uterine sensitization to allergens.
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PMID:A case of cow's milk allergy in the neonatal period--evidence for intrauterine sensitization? 953 57

Persistent diarrhea, vomiting, and dehydration are symptoms often seen in patients suffering from food allergy after chronic antigen exposure; however, the precise mechanisms involved have not been well defined. In an effort to clarify the mechanisms of the chronic intestinal changes attributable to genuine IgE-mediated anaphylactic reactions induced by orally administered antigen, a mouse model was established by s.c. implantation of a murine hybridoma capable of producing monoclonal anti-trinitrophenyl IgE antibody, and the morphologic and immunologic changes occurring in the intestine upon chronic antigen exposure were investigated. In the early stage after ingestion of the antigen, diarrhea and noticeable infiltration of mast cells as well as eosinophils into the lamina propria were observed. A substantial increase in serum histamine levels as well as an increase in leukotriene C4 synthesis in the jejunal mucosa were observed 1 h after antigen challenge. Also, the synthesis of leukotriene B4 was significantly elevated for up to 9 h after antigen challenge. The expression of both intercellular adhesion molecule-1 (ICAM-1) on mucosal vascular endothelial cells and IAd on epithelial cells was markedly enhanced, and noticeable infiltration of eosinophils and lymphocytes was also confirmed in the mouse model after chronic antigen exposure. These findings suggest that oral antigen exposure induces anaphylactic reactions in the intestine mediated by mast cells and eosinophils in response to the IgE-antigen complex in the early phase, and also induces lymphocyte migration after chronic antigen exposure.
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PMID:Chronic oral antigen exposure induces lymphocyte migration in anaphylactic mouse intestine. 980 64

Assessment of activation of immune mechanisms is valuable in the early diagnosis of cow's milk allergy (CMA). The purpose of this study was to evaluate peripheral blood lymphocyte subclasses in children suspected of having CMA and healthy infants in order to detect an early marker for food allergy. Altogether 47 breast-fed infants, aged from 0.4 to 10 months were followed-up prospectively from birth because of atopic heredity. Twenty-three of the infants were healthy and 24 infants had a strong suspicion of and later challenge-proven cow's milk allergy. Leucocyte subsets were determined from peripheral blood mononuclear cells by flow cytometry. In response to a clinical cow's milk challenge, seven infants developed urticaria, 11 infants had eczema, three patients had loose stools, diarrhoea or vomiting and three infants had eczema and diarrhoea, loose stools or vomiting. The total percentage of B cells and also the proportion of B cells bearing a low-affinity IgE receptor as a marker for activation were significantly higher, whereas the percentage of CD8+ T cells was significantly lower in infants with challenge-proven CMA than in healthy controls. These results imply that infants with active CMA have a defect in regulation of B-cell function. Further, they suggest that imbalance of the ratio of suppressor and helper T cells might be an important factor in the etiopathogenesis of CMA. Our results show that large numbers of activated CD19+ B cells and low numbers of CD8+ T cells could be considered as early markers for food allergy since they are already detectable in peripheral blood during the earliest symptoms of CMA.
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PMID:Large number of CD19+/CD23+ B cells and small number of CD8+ T cells as early markers for cow's milk allergy (CMA). 981 28

There have been reports of increased prevalence of certain food allergies in patients with Type I latex allergy (LA). A detailed food allergy history was obtained from 137 patients with LA. Latex allergy was defined by positive history of IgE mediated reactions to contact with latex and positive skin prick test to latex and/or positive in vitro test (AlaSTAT and/or Pharmacia CAP). Food allergy was diagnosed by a convincing history of possible IgE mediated symptoms occurring within 60 minutes of ingestion. We identified 49 potential allergic reactions to foods in 29 (21.1%) patients. Foods responsible for these reactions include banana 9 (18.3%), avocado 8 (16.3%), shellfish 6 (12.2%), fish 4 (8.1%), kiwi 6 (12.2%), tomato 3 (6.1%), watermelon, peach, carrot 2 (4.1%) each, and apple, chestnut, cherry, coconut, apricot, strawberry, loquat, one (2.0%) each. Reactions to foods included local mouth irritation, angioedema, urticaria, asthma, nausea, vomiting, diarrhea, rhinitis, or anaphylaxis. Our study confirms the earlier reports of increased prevalence of food allergies in patients with LA. We also report increased prevalence of shellfish and fish allergy not previously reported. The nature of cross reacting epitopes or independent sensitization between latex and these foods is not clear.
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PMID:Prevalence of food allergy in 137 latex-allergic patients. 1020 85

Confirmed adverse reactions to foods may be caused by toxic, enzymatic, pharmacological, "pseudoallergic" or allergic mechanisms. True food allergies are mostly IgE-mediated and directed against one or only a few food proteins. They appear typically as eczema and gastrointestinal symptoms (vomiting, diarrhoea, abdominal cramps) among infants and as oral allergy syndrome, urticaria/angioedema, rhinoconjunctivitis or anaphylaxis among adults. The majority of food allergies among adults is caused by cross-reactivity of IgE against inhalative allergens also reacting with food proteins. This must be considered in investigations by skin-prick testing and/or specific IgE measurement, since the sensitivity of these tests for inhalative allergens is higher than for food proteins. The most frequent differential diagnoses of true allergies are pseudoallergic reactions to food additives or pharmacological reactions to biogenic amines. The diagnosis of these reactions can usually be based on the history and course under a corresponding diet. In clinical practice additional investigations by double-blind placebo-controlled food challenges are rarely required. A positive challenge test demonstrates only the cause-and-effect relationship of the foods and the patient's symptoms but does not demonstrate the underlying mechanism. The therapy of food intolerance is a corresponding diet. This requires a careful diagnosis and identification of the causative foods.
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PMID:[Food intolerance and food allergy]. 1041 28

Adverse reactions to foods involving abnormal immune reactions to food antigens occur in 2-7% of the North American population; the numbers are perhaps higher in children. Both IgE-mediated and non-IgE-mediated allergic responses occur. IgE-mediated allergic responses to foods are the most dramatic and perhaps the most easily diagnosed type of food allergy. Non-IgE-mediated food hypersensitivity is more chronic, less acute, less obvious in its clinical presentation, and often more difficult to diagnose. It usually presents in infants between one week and three months of age with vomiting and diarrhea, although irritability, poor feeding, and failure to thrive are not uncommon. A thorough history and physical examination are often key in establishing a diagnosis of food protein hypersensitivity. In non-IgE-mediated disease, skin tests and immunological studies are not helpful. Eliminating the food allergen is the only means of dealing with a food allergy in most patients. About 85% of infants who have formula protein intolerance will outgrow their symptoms somewhere between 1 month and 3 years of age, older children and adults are somewhat less likely to lose their sensitivity, although approximately one-third will after 1-2 years of dietary restriction.
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PMID:Food hypersensitivity in children. 1056 87

Many of the adverse events induced by rifampin have been considered allergic in origin. The flu-like syndrome and other hypersensitivity reactions seem to be caused by immune complexes, although their pathogenetic mechanisms are not fully elucidated. Many cases have been reported of the flu-like syndrome, thrombocytopenia, hemolytic anemia, and renal failure caused by rifampin. In almost all of the patients in whom they were sought, nonreaginic antirifampin antibodies were detected. On the other hand, anaphylactic reactions seem to be IgE-mediated. We have analyzed the 18 reported cases of anaphylactic reactions severe enough to cause marked hypotension. The interval between the onset of treatment and the anaphylactic reaction was highly variable. Most patients presented with prodromes, mainly rash, before the development of anaphylactic symptoms, and, in most cases, the reaction occurred after reexposure to rifampin. Clinical findings include a variety of symptoms, such as fever, exanthem, dyspnea, abdominal pain, and vomiting. Seven of the 9 patients in whom HIV status was known were seropositive, including the only 2 patients who died. We believe that, in case of a non-life-threatening adverse reaction caused by immune complexes, rifampin could be readministered, if necessary, at a more frequent and reduced dose, perhaps with the addition of corticosteroids. In case of anaphylactic reactions the drug should be avoided, although desensitization procedures may be useful. Certain laboratory findings may serve as a clue to predict anaphylactic reactions in patients who have experienced minor adverse events to rifampin. However, the diagnostic value of such findings is not well established and, therefore, patients with previous adverse reactions should be carefully monitored if reexposure to rifampin is essential.
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PMID:Hypersensitivity reactions to rifampin. Pathogenetic mechanisms, clinical manifestations, management strategies, and review of the anaphylactic-like reactions. 1057 18

Food Protein-Induced Enterocolitis Syndrome (FPIES) is a symptom complex of severe vomiting and diarrhea caused by non-IgE-mediated allergy to cow's milk and/or soy in infants. Symptoms typically begin in the first month of life in association with failure to thrive and may progress to acidemia and methemoglobinemia. Symptoms resolve after the causal protein (usually sensitivity to both cow's milk and soy) is removed from the diet. Symptoms recur approximately 2 hours after reintroduction of the protein along with a coincident elevation of the peripheral blood polymorphonuclear leukocyte count. The sensitivity is usually outgrown by 3 years of age. The purpose of this review is to delineate the characteristic clinical features, diagnosis and management of FPIES. Furthermore, infantile FPIES will be discussed in relation to clinical syndromes that share features with it ("atypical FPIES") and other food-allergic disorders affecting the gastrointestinal tract.
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PMID:Food protein-induced enterocolitis syndrome: clinical perspectives. 1063 98


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