Cases reported "Anaphylaxis"

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1/16. A study on severe food reactions in sweden--is soy protein an underestimated cause of food anaphylaxis?

    BACKGROUND AND methods: Because of a fatal case of soy anaphylaxis occurring in sweden in 1992, a study was started the following year in which all physicians were asked to report fatal and life-threatening reactions caused by food. The results of the first 3 years of the study are reported here, including results from another ongoing study on deaths from asthma during the same period. RESULTS: In 1993-6, 61 cases of severe reactions to food were reported, five of them fatal. Peanut, soy, and tree nuts seemed to have caused 45 of the 61 reactions, and four of them were fatal. If two cases occurring less than a year before our study started are included, we are aware of two deaths caused by peanuts and four deaths caused by soy. All four youngsters who died from soy anaphylaxis with asthma were severely allergic to peanuts but had no previously known allergy to soy. In most cases, there was a rather symptom-free period for 30-90 min between early mild symptoms and severe and rapidly deteriorating asthma. CONCLUSIONS: Soy has probably been underestimated as a cause of food anaphylaxis. Those at risk seem to be young people with asthma and peanut allergy so severe that they notice symptoms after indirect contact.
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2/16. Anaphylactic reaction to young garlic.

    BACKGROUND: garlic is well known to cause contact dermatitis and asthma. However, it is a very rare cause of food allergy. We present the case of a 23-year-old woman with previous history of allergy to pollen and dried fruit, and food-dependent, exercise-induced anaphylaxis for which no specific food could be identified as responsible, who experienced an anaphylactic reaction after eating young garlic. methods: skin prick tests and specific IgE immunoassay with several pollens and foods were performed, as well as the prick-prick test with young garlic and SDS-PAGE followed by immunoblotting IgE to young garlic and other liliaceae species, mustard, sesame, parsley, celery, hazelnut, almond, and pollen of birch and mugwort. RESULTS: skin prick tests and specific IgE were mainly positive for grass, plane tree, and mugwort pollen; peanut; hazelnut; walnut; almond; and mustard. Prick-prick tests with young garlic and garlic were positive. Total IgE was 113 U/ml. SDS-PAGE immunoblotting showed IgE-binding bands at 12 kDa to young garlic, garlic, onion, and leek extracts. Similar bands could also be detected with mugwort pollen and hazelnut extract. CONCLUSIONS: We describe IgE-mediated reaction to young garlic in a patient sensitized to pollen and dried fruit.
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3/16. pollen mixtures used as health food may be a harmful source of allergens.

    We describe herein one case of systemic anaphylaxis due to the ingestion of an undefined mixture of pollens, sold as a dietary supplement. The patient, who suffered from rhinoconjunctivitis due to grass pollen (with sensitization to several trees), had a severe episode of anaphylaxis immediately after eating this health food. The episode required emergency care. We attempted to study the pollen mixture responsible, but no pollen granules could be identified. We prepared a solid phase with the pollen mixture, and we observed a RAST positivity with the patient's serum and pools of sera containing specific IgE to trees. Furthermore, a RAST-inhibition assay of the patient's serum showed highly positive results with grasses, birch, alder and Compositae. Therefore, we concluded that the pollen mixture contained determinants capable of cross-reacting with the patient's IgE. This case report is evidence of the possible risks due to the use of undefined herbal products by allergic patients.
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4/16. anaphylaxis to raw potato.

    BACKGROUND: Potato allergy has been described rarely, generally in relation to the Oral Allergy syndrome (OAS). Adults with seasonal allergic rhinitis have been reported in whom peeling of raw potatoes causes oculonasal symptoms, wheezing, and contact urticaria. skin testing with fresh fruits and vegetables has been recommended in cases of OAS, although the sensitivity of commercial potato extract is reportedly equal to that of fresh potato. CASE REPORT: This report describes a 4-year-old with raw potato-induced anaphylaxis. He rapidly developed urticaria, angioedema, respiratory distress, vomiting and diarrhea after biting into a raw potato that was being used for painting in preschool. review of systems is significant for viral-induced wheezing, but no symptoms suggestive of seasonal allergic rhinitis were evident. His mother has a history of seasonal allergic rhinitis and contact urticaria with raw potato. skin testing to commercial potato extract was negative and skin testing to fresh potato by the prick prick method was markedly positive. skin testing to birch tree was negative. An open challenge to a small amount of cooked potato was negative. Food challenge to raw potato was not considered indicated in this case of immediate anaphylaxis to a single food. CONCLUSIONS: This patient had clinical and skin test reactivity to raw and uncooked potato in the absence of OAS. The patient will be followed for the development of seasonal allergic rhinitis.
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5/16. anaphylaxis after ingestion of sharon fruit.

    BACKGROUND: The sharon fruit is the edible fruit of the persimmon tree (diospyros kaki) which belongs to the ebenaceae family. There are few references of allergic reaction to this fruit. We introduce a case of a 33-years old man with a anaphylactic reaction immediately after ingestion of sharon fruit. methods: skin prick test (SPT) were performed by prick by prick with sharon fruit, legumes, vegetables, and fresh fruit. The test was considered positive when the average diameter of the wheal was > 3 mm. serum-specific IgE was identified with use of the EIA, and SDS-PAGE immunoblotting. RESULTS: The skin by prick test with sharon fruit was positive in our case, and negative in five controls patients. Specific IgE in patient serum, assayed by EIA was positive for sharon fruit, but the results of immunoblotting were non-specific. CONCLUSION: We have introduced a cause of anaphylaxis by sharon fruit that suggest an IgE mediated hypersensitivity reaction.
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6/16. Anaphylactic reactions after therapeutic injection of mistletoe (viscum album L.).

    mistletoe (viscum album) is a plant that is semiparasitic of several trees: apple, oak, pine trees, etc. Because of the probable cytolytic action of one of the leaf's most abundant composites, in some countries mistletoe is used as a complementary medicine. Although only a few adverse reactions have been noted (cephalea, fever), cases of anaphylactic shock have been described. We present three cases of severe reaction after injection of mistletoe extract. Two of the patients had cancer. The third, whose brother had cancer, used the plant for preventive purposes. We discuss the danger of possible severe reactions due to the use of products employed in so-called alternative therapies.
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7/16. serum tryptase analysis in a woman with amniotic fluid embolism. A case report.

    BACKGROUND: Recent studies have noted a striking similarity between amniotic fluid embolism (AFE) and anaphylaxis. serum tryptase levels may therefore serve as a marker of mast cell degranulation in AFE cases. CASE: A 40-year-old woman, gravida 6, para 4, experienced the acute onset of facial erythema, eclampsia-type seizures, severe hypoxia, cardiac arrest and disseminated intravascular coagulation while in early active labor. The patient was declared dead 37 minutes after the onset of resuscitative efforts. At autopsy, fetal squames were found within the pulmonary tree, uterine blood vessels and brain. A peripheral venous blood specimen, obtained approximately one and a half hours postmortem, revealed a tryptase level of 4.7 ng/mL (normal, < 1). CONCLUSION: An elevated serum tryptase level, in conjunction with our patient's clinical history, adds further supporting evidence to the concept of AFE as an anaphylactoid syndrome of pregnancy.
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8/16. Immediate systemic hypersensitivity reaction associated with topical application of Australian tea tree oil.

    Australian tea tree oil has been used as a veterinary antiseptic for many years and, more recently, has been extended into human use. There have been many reports of allergic contact dermatitis and toxicity reactions, but it has never been implicated in immediate systemic hypersensitivity reactions. A 38-year-old man experienced immediate flushing, pruritus, throat constriction, and lightheadedness after topical application of tea tree oil. Our purpose was to determine whether this represented an immunoglobulin e (IgE)--mediated reaction. skin-prick and intradermal testing was performed, as well as enzyme-linked immunosorbent assays for specific IgG and IgE against tea tree oil. The patient had a positive wheal and flare reaction on intradermal testing with tea tree oil. All five patient controls were negative on skin testing. No specific IgG or IgE was detected. We present the first reported case of an immediate systemic hypersensitivity reaction occurring after topical application of Australian tea tree oil, confirmed by positive wheal and flare reaction on skin testing.
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9/16. Bugged.

    This was a great save. The crew could easily have missed the presentation of anaphylaxis and let the window for treatment with epinephrine slip away. This patient was in anaphylactic shock. There were no signs that supported a traumatic injury, and that, combined with diaphoresis, urticaria and tachycardic central pulse, contributed to the suspicion of anaphylaxis. anaphylaxis is classified as distributive shock. This type of shock is caused by profound systemic vasodilation, and the heart is unable to increase output enough to maintain blood pressure. Other causes of distributive shock include sepsis and spinal cord injury. It is rare to have both hypotension and wheezing in such cases. In an anaphylactic reaction, an allergen, such as a food protein, medication, insect venom or latex, is introduced into the body. The mast cells of the immune system have a protein on their surface called IgE antibodies (immunoglobulin e). The mast cells are filled with histamines [table: see text] and leukotrienes, which are chemical mediators. These are released when the allergen reacts with the IgE antibodies. When these mediators are released, they cause smooth-muscle constriction in the respiratory and gastrointestinal tracts, resulting in wheezing, stridor, nausea, vomiting and diarrhea. They also cause vascular dilation, leading to edema and urticaria. Most patients will present with either profound vascular effect (shock) or wheezing; this is a rather rare presentation of a patient having both. The medication best suited to counteract the effects of these medicators is epinephrine. epinephrine is an alpha- and beta-agonist, acting to constrict the vasculature and dilate the smooth muscles in the bronchial tree. Antihistamines can alleviate symptoms of anaphylaxis, but should only be used in addition to epinephrine, not as a substitute. In life-threatening reactions, epinephrine must be given quickly and in a form that the body can distribute. Use of the subcutaneous route with a solution mixed at 1:1,000 dilution is appropriate in most patients, but if the patient is in profound shock and not perfusing the skin (pale, cold, clammy skin), then a more diluted concentration must be given i.v. at a slow rate (1 cc every minute of the 1:1,000 dilution) until the patient recovers. If i.v. access is delayed or not available, give the 1:1,000 dilution intramuscularly, in the tongue or down the endotracheal tube. Refer to your local protocols for dosage, but the usual dose of epinephrine is 0.3-0.5 mg, or 0.01 mg/kg in a child. There are more than 40 million people in the U.S. with allergic histories that place them at risk for developing anaphylaxis. Each year over 5,000 deaths are attributed to anaphylaxis. The risk of death from anaphylaxis increases with a more rapid onset of signs and symptoms. Up to 25% of patients will experience a biphasic reaction. This means there is a recurrence of symptoms several hours after the initial reaction, and it is prudent to observe patients for a period of time following their initial treatment.
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10/16. Cross-reactivity between coconut and hazelnut proteins in a patient with coconut anaphylaxis.

    BACKGROUND: The medical literature reports few cases of severe allergic reactions to coconut. We encountered a patient with anaphylaxis to coconut and oral symptoms to tree nuts. OBJECTIVE: To identify cross-reactive antibodies between coconut and other tree nuts. methods: We performed commercial radioallergosorbent tests to coconut and various tree nuts using the patient's serum. skin prick testing was performed to fresh coconut and commercial extracts of coconut, almond, brazil nut, cashew, pecan, walnut, and hazelnut. proteins from fresh coconut, commercial coconut extract, and tree nuts were extracted. Immunoblot and inhibition assays were performed to evaluate for cross-reacting IgE antibodies between similar-sized allergens in coconut and hazelnut. RESULTS: Positive skin test results occurred to the coconut and multiple tree nut extracts. in vitro serum specific IgE was present for coconut, hazelnut, brazil nut, and cashew. Immunoblots demonstrated IgE binding to 35- and 50-kDa protein bands in the coconut and hazelnut extracts. Inhibition assays using coconut demonstrated complete inhibition of hazelnut specific IgE, but inhibition assays using hazelnut showed only partial inhibition of coconut specific IgE. CONCLUSIONS: Our study demonstrates the presence of cross-reactive allergens between hazelnut (a tree nut) and coconut (a distantly related palm family member). Because there are many potentially cross-reactive allergens among the tree nuts, we recommend patients with coconut hypersensitivity be investigated for further tree nut allergies.
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