Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 is the most common food allergy in infants and young children. It is estimated that up to 50% of pediatric cow's milk allergy is non-IgE-mediated. Allergic proctocolitis is a benign disorder manifesting with blood-streaked stools in otherwise healthy-appearing infants who are breast- or formula-fed. Symptoms resolve within 48-72 h following elimination of dietary cow's milk protein. Most infants tolerate cow's milk by their first birthday. Food protein-induced enterocolitis syndrome presents in young formula-fed infants with chronic emesis, diarrhea, and failure to thrive. Reintroduction of cow's milk protein following a period of avoidance results in profuse, repetitive emesis within 2-3 h following ingestion; 20% of acute exposures may be associated with hypovolemic shock. Treatment of acute reactions is with vigorous hydration. Most children become tolerant with age; attempts of re-introduction of milk must be done under physician supervision and with secure i.v. access. Allergic eosinophilic gastroenteritis affects infants as well as older children and adolescents. Abdominal pain, emesis, diarrhea, failure to thrive, or weight loss are the most common symptoms. A subset of patients may develop protein-losing enteropathy. Fifty percent of affected children are atopic and have evidence of food-specific IgE antibody but skin prick tests and serum food-IgE levels correlate with response to elimination diet poorly. Elemental diet based on the amino-acid formula leads to resolutions of gastrointestinal eosinophilic inflammation typically within 6 wk.
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PMID:Educational clinical case series for pediatric allergy and immunology: allergic proctocolitis, food protein-induced enterocolitis syndrome and allergic eosinophilic gastroenteritis with protein-losing gastroenteropathy as manifestations of non-IgE-mediated cow's milk allergy. 1758 15

Immediate-type allergies (type I) allergies to environmental allergens such as plant pollen, pet dander, food, honeybees' and wasps' venom affect around a third of the total population in developed countries. The diseases comprise a broad spectrum from rather mild diseases such as hay fever and skin reactions like urticaria to severe ones such as bronchial asthma, vomiting and diarrhea and finally anaphylactic shock. Type I allergies are caused by an errant immune response leading to the production of allergen-specific IgE. The usual algorithm for the diagnosis of type I allergies begins with obtaining a detailed patient history and continues with the confirmation by skin tests and/or in vitro measurement of IgE. Allergen biochips are a promising new technology for the in vitro measurement of specific IgE in type-I allergic patients. In contrast to conventional in vitro tools, they consist of multiple allergen components spotted onto a microarray. This allows to perform multiple analyses in a single measurement analysing patient-specific sensitisation patterns, the so called "component resolved diagnosis". This review considers prospects and difficulties with this new technology and also reviews patents related to this field.
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PMID:The potential of allergen biochips. 1907 8

We report two cases of anaphylactic reactions to peach with negative result of ImmunoCAP to peach. Case 1 is a 35-year-old man, who felt an itch in his oral cavity immediately after ingesting a whole fresh peach. He rapidly developed generalized urticaria, dyspnea, vomiting, and loss of consciousness. He recovered after treatment at a local hospital, thereafter he was referred to our hospital because ImmunoCAP conducted for screening allergens revealed a negative test result to peach and the cause of anaphylaxis remained unclear. He had a history of pollinosis. He reported that he previously felt an itch on his oral cavity after ingesting melon, watermelon, apple, and strawberry. Serum total IgE was 436 IU/ml. CAP-RAST revealed negative results to peach, strawberry and kiwi. Skin prick tests (SPTs) with raw peach pulp, canned peach pulp, strawberry and kiwi were positive. Case 2 is a 30-year-old woman who felt an itch on her oral cavity accompanied by blepharedema, rhinorrhea, generalized urticaria, nausea, abdominal pain and diarrhea after eating peach. She had a history of pollinosis. She reported that she previously developed urticaria after ingesting an apple. Serum total IgE was 85 IU/ml. ImmunoCAP revealed negative results to peach and apple. SPTs with canned yellow peach, strawberry and apple were positive. Consequently, the two patients were diagnosed with anaphylaxis due to peach, and allergic symptoms have never recurred since they avoided ingesting peach. Furthermore, in two patients ImmunoCAP to rPru p 1, rPru p 3, and rPru p 4 were negative. However, in IgE-immunoblotting of peach, serum IgE antibodies of two patients were bound to approximately 10 kDa proteins. Meanwhile, the cross-reactivity between Rosaceae fruits, such as peach, apple, apricot, and plum, has been reported. These results suggest that in patients, who are suspected of having peach anaphylaxis and show a negative ImmunoCAP result to peach, the additional testing, such as SPT with peach, should be performed for diagnosis.
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PMID:[Anaphylaxis due to peach with negative ImmunoCAP result to peach allergens, including rPru p 1, rPru p 3, AND rPru p 4: a report of two cases]. 1932 77

In the past two decades, peanut allergy prevalence has increased in the West but has been perceived as having remained low in Asia. To review the clinical presentation of Asian children with peanut hypersensitivity and measure their IgE responses to major peanut allergens. We enrolled 31 children presenting with various allergies and a positive skin prick test to peanut from the Children's hospital outpatient allergy clinic in Singapore. A detailed questionnaire was completed by parents. The children's serum IgE specific to native Ara h 1, native Ara h 2, and recombinant Ara h 3 were detected using ELISA. Of the 31 patients, 19 had previously documented reactions to peanuts, while 12 had no previous clinical reaction. Most, 89.5% (17/19) of first reactions featured skin changes (urticaria, erythema, angioedema), but only 36.8% (7/19) involved skin symptoms alone. Respiratory symptoms and GI symptoms occurred in 42.1% and 26.3% of patients respectively and did not occur as the sole manifestation of reaction. The most common GI manifestation was emesis, present in 26.3% (5/19) of subjects. Two children experienced impaired consciousness with systemic, anaphylactic events. Although most sought treatment for their first peanut reaction only one patient received epinephrine. Half of our patients reported a subsequent accidental ingestion after the diagnosis of peanut allergy, with a median time from diagnosis to first accidental ingestion of 4 months and a reported increased severity of reaction in approximately half of the repeat exposures. Eighty-seven percent of children had specific IgE directed against at least one of the major peanut allergens. Among all patients, 87.1% had IgE specific to both Ara h 1 and Ara h 2 and 54.8% to rAra h 3. Asian children with peanut sensitization have clinically similar presentations and respond to the same major allergenic proteins as their Western counterparts. The perceived differences between the populations in this context do not stem from divergent clinical or immunological responses.
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PMID:Serological and clinical characteristics of children with peanut sensitization in an Asian community. 1970 75

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated food allergy characterized by severe vomiting, diarrhea, and often failure to thrive in infants. Symptoms typically resolve after the triggering food-derived protein is removed from the diet and recur within few hours after the re-exposure to the causal protein. The diagnosis is based on clinical symptoms and a positive food challenge. In this study, we report a case of FPIES to rice in an 8-month-old boy. We performed a double-blind placebo-controlled food challenge (DBPCFC) to rice and we measured the intracellular T cell expression of interleukin-4 (IL-4); IL-10, and interferon gamma (IFN-gamma) pre-and post-challenge during an acute FPIES reaction and when tolerance to rice had been achieved. For the first time we describe an increase in T cell IL-4 and decrease in IFN-gamma expression after a positive challenge with rice (i.e. rice triggered a FPIES attack) and an increase in T cell IL-10 expression after rice challenge 6 months later after a negative challenge (i.e., the child had acquired tolerance to rice) in an 8 month old with documented FPIES to rice. A Th2 activation associated with high IL-4 levels may contribute to the pathophysiology of the disease. On the other hand, T cell-derived IL-10 may play a role in the acquisition of immunotolerance by regulating the Th1 and Th2 responses.
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PMID:Cytokine expression in CD3+ cells in an infant with food protein-induced enterocolitis syndrome (FPIES): case report. 2001 55

We report a case of food protein-induced enterocolitis syndrome (FPIES) with milk whose signs of milk intolerance began in the 1st days of life, consisting in minor and nonspecific symptoms. The 3 foods in question were cow's milk, soja, and wheat. The diagnosis of FPIES was suspected at the age of 9 months, after 3 hospitalizations for vomiting, sometimes associated with lethargy and hypotension, which occurred around 2h after cow's milk ingestion. Symptoms were not associated with positive specific IgE and cutaneous tests. Signs then occurred with soja and wheat. Because of the late diagnosis, 3 anaphylactic shock episodes occurred. FPIES is an uncommon cell-mediated food allergy reaction. This syndrome is characterized by gastrointestinal symptoms, especially severe vomiting, sometimes associated with anaphylactic shock. Usually signs occur 2h after ingestion. These reactions begin early, in the 1st months of life, and regress by the age of 3 years in 38-100% of cases depending on the responsible food. They are usually induced by cow's milk and soy proteins. Diagnosis is difficult and delayed because of nonspecific symptoms. Oral food challenge is the only examination that confirms the diagnosis. Treatment involves the exclusion of the specific food involved. Severe reactions require treatment of shock and adjunction of corticosteroids.
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PMID:[A new case of food protein-induced enterocolitis syndrome]. 2034 36

Peanut allergy currently affects around 1% of the UK and US paediatric population and represents a major healthcare concern because it is outgrown in less than 20% of cases and is a major cause of anaphylaxis. Its main symptoms, triggered by peanut ingestion, are cutaneous (urticaria, erythema, angioedema), gastrointestinal (abdominal pain, vomiting, diarrhoea), respiratory (wheezing, dyspnoea) and cardiovascular (hypotension, arrhythmia, shock). The usual onset of symptoms occurs soon after peanut ingestion (minutes to hours); however some patients have biphasic reactions, with exacerbations occurring up to 8 hours later. Peanut allergy diagnostic is based mainly upon the medical history (preferably including a diet diary and elimination diets), skin testing, peanut-specific IgE measurement and ideally a peanut oral challenge. Peanut allergy management includes monitorisation and education for avoiding peanut-containing foods and for recognising and treating anaphylactic episodes (self-injectable adrenalin and rapid-acting antihistamines). In the past, anti-IgE antibodies were shown to decrease the risk of anaphylaxis by reducing the allergic patients' reactivity to peanuts. Recent investigations, driven by the need to develop efficient treatment and prevention strategies for peanut allergy, suggest that oral immunotherapy with peanuts, although exposing the patients to significant risk, may represent a promising therapeutic approach. Furthermore, contrary to the general view that peanut avoidance in infants could prevent peanut allergy, a recent study shows that the opposite may be true as early consumption of peanuts in infancy is associated with a low prevalence of peanut allergy.
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PMID:[Peanut allergy]. 2069 62

A 6-year-old boy was referred for evaluation because he had several vomiting episodes, from the age of 2 years, following short-neck clam ingestion. He tested negative for short-neck clam-specific IgE just before visiting our hospital, and he was not allergic to other foods or shellfish. The patient had low levels of short-neck clam-specific IgE (1.04 UA/ml), and the skin prick test was positive for short-neck clam (4 mm). The lymphocyte stimulation test was positive (5305 counts per min (cpm), stimulation index (SI) =1211%) and the patch test was positive for short-neck clam ingestion. An oral challenge test with boiled short-neck clam induced abdominal pain and vomiting 2 h after ingestion, and the patient presented with increased peripheral leukocytes after 6 h. He was therefore diagnosed with food protein-induced enterocolitis syndrome (FPIES) due to short-neck clam ingestion. To our knowledge, this is the first case report of FPIES induced by the intake of shellfish.
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PMID:[Case of food protein-induced enterocolitis syndrome caused by short-neck clam ingestion]. 2121 29

A 13-year-old girl who had had pollinosis since the age of eight began to experience itching of the ears and vomiting after eating fresh fruits such as peach, apple and watermelon. This occurred at 10 years of age. The girl displayed positive reactions to six kinds of pollens, eleven kinds of fruits, numerous vegetables and to recombinant: rBet v2 present in specific IgE antibodies. She also reacted positively to several pollens, fruits and rBet v2 in the skin prick test. In the component-resolved diagnosis (CRD) using microarray technology, she also tested positive for profilin, a pan-allergen among plants. It is reported that profilin cross-reacts between pollen, fruits, vegetables and latex. From these results, we concluded that the allergic reactions to multiple kinds of foodstuff and pollens observed in this subject were due to cross-reactivity induced by profilin. Our results demonstrate that CRD by microarray is a reliable test in the diagnosis of PFAS.
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PMID:Sensitization profiles of a case of pollen-food allergy syndrome. 2125 19


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