moonman.gif (5533 bytes) Anaphylaxis & Asthma

Anaphylactic shock is a severe and potentially life-threatening allergic reaction which occurs when an allergen enters the bloodstream and circulates, causing a general reaction. Symptoms begin with a rapid heart rate, flushing, swelling of the throat, nausea, coughing, and chest tightness. Severe wheezing (asthma), cramping, and a rapid drop in blood pressure follow may lead to cardiac arrest. Hives and vomiting are also common features. The treatment for anaphylaxis is injected epinephrine (adrenalin), followed by antihistamines and steroids.

Stephen J. Gislason MD

The most explosive, immediate, and obvious reactions are mediated by basophil and mast cell degranulation. Typical patterns of immediate reactions include angioedema, asthma, urticaria, flushing, pruritus, rhinitis - rhinorrhea, tachycardia, hypotension, vomiting, diarrhea, and abdominal pain. Anaphylaxis is the most dangerous Type 1 reaction. The major features are bronchoconstriction, edema, with increased capillary permeability and rapid movement of water from blood to tissue spaces leading to hypovolemic shock.

Sampson et al reported on 13 children and adolescents with fatal and near-fatal food anaphylaxis. All 13 had asthma with previous serious reactions to food - peanuts (4), nuts (6), cows milk (2), and egg (1). The six patients who died had itching or tingling in the mouth, tightness of the throat, irritability, abdominal pain or vomiting within 3 to 30 minutes of eating the food. None of the fatalities had self-injected epinephrine. All of the survivors received epinephrine within 30 minutes of the onset of symptoms.

Anaphylaxis was rapidly progressive and uniphasic in 7 patients and biphasic in 3 who had early oral and abdominal symptoms followed by a 1-2 hour remission, followed by increasing respiratory symptoms, hypotension, and death. Three children who survived had a protracted course requiring ventilatory support and treatment with vasopressors for 3 to 21 days after the onset. This report emphasizes the potential severity of food reactions and the importance of prompt administration of epinephrine.

Occasionally, anaphylaxis will only occur with reactive food intake followed by vigorous exertion. A case of wheat-dependent exercise-induced anaphylaxis was investigated by Japanese researchers. The patient, a 42 year-old man, would developed generalized urticaria and loss of consciousness playing tennis following a meal of wheat bread and tea. His symptoms were reproduced and studied. Sodium bicarbonate pre-treatment prevented the anaphylaxis. Another case-report described wheat allergy as a trigger for exercise-induce anaphylaxis in an 18 year old girl; one hour after lunch she exercised and developed urticaria, abdominal pain, diarrhea, dyspnea. Two further episodes occasioned a challenged study which confirmed the wheat reactivity and showed that sodium cromoglycate blocked the reaction.

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Abstracts

 

Life-threatening, recurrent anaphylaxis caused by allergy to gliadin and exercise.
Author Varjonen E; Vainio E; Kalimo K
Address Department of Dermatology, University Hospital of Helsinki, Finland.
Source Clin Exp Allergy, 1997 Feb, 27:2, 162-6
Abstract Exercise-induced urticaria or anaphylaxis is regarded as a distinct form of physical allergy. In some patients the symptoms occur only after ingestion of various food products in connection with exercise. We have come across patients with cereal dependent exercise-induced anaphylaxis. OBJECTIVES: The purpose of the present study was to analyse the allergens in cereals responsible for the severe anaphylactic symptoms and to verify the test methods suitable for screening the patients with cereal dependent exercise-induced anaphylaxis. METHODS: The patients underwent skin-prick tests (SPT) with common inhalant and food allergens as well as with various cereal extracts. IgE-immunoblotting was used to identify the allergenic fractions. RESULTS: Five patients found positive in SPT with NaCl wheat suspension had IgE antibodies to wheat, rye, barley and oats, especially directed against the ethanolsoluble protein fractions in immunoblotting. No IgE antibodies were detected against other cereals. The patients had been unaware of any cereal allergy since anaphylaxis occurred only in association with exercise postprandially. The patients were directed to follow a gluten-free diet and have been free from symptoms, being able to continue their outdoor physical activities. CONCLUSION: Wheat gliadin and the corresponding ethanol-soluble proteins of taxonomically closely related cereals were found to be the allergens in cereal-dependent exercise-induced anaphylaxis. Skin-prick testing with NaCl wheat suspension was a simple and practical test to screen patients with this kind of occult, possibly life-threatening, allergy to cereals.
Title Epinephrine absorption in children with a history of anaphylaxis.
Author Simons FE; Roberts JR; Gu X; Simons KJ
Address Department of Pediatrics and Child Health, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Source J Allergy Clin Immunol, 1998 Jan, 101:1 Pt 1, 33-7
 
Abstract  Prompt injection of epinephrine is the cornerstone of systemic anaphylaxis treatment. The rate of epinephrine absorption has not been reported previously in allergic children. OBJECTIVE: Our objective was to study the clinical pharmacology of epinephrine in this population. METHODS: We performed a prospective, randomized, blinded, parallel-group study in 17 children with a history of anaphylaxis to food, Hymenoptera venom, or other substances. We injected 0.01 ml/kg epinephrine solution (maximum 0.3 ml [0.3 mg]) subcutaneously, or 0.3 mg epinephrine intramuscularly from an autoinjector. Plasma epinephrine concentrations, heart rate, blood pressure, and adverse effects were monitored. RESULTS: In nine children who received epinephrine subcutaneously, the mean maximum plasma epinephrine concentration (+/- SEM) was 1802 +/- 214 pg/ml, achieved at a mean time of 34 +/- 14 minutes (range, 5 to 120 minutes). Only two of the nine children achieved maximum plasma concentrations by 5 minutes. In eight children who received epinephrine intramuscularly, the mean maximum plasma concentration was 2136 +/- 351 pg/ml, achieved at a mean time of 8 +/- 2 minutes, which was significantly faster than the mean time at which maximum plasma concentrations were achieved after subcutaneous epinephrine injection (p < 0.05). Six of the eight children achieved maximum plasma concentrations by 5 minutes. The terminal elimination half-life was 43 +/- 15 minutes. No serious adverse effects were noted in any child. CONCLUSIONS: In children, recommendations for subcutaneous epinephrine injection are based on anecdotal experience, and should be reevaluated in view of our finding of delayed epinephrine absorption when this route is used. This delay might have important clinical implications during an episode of systemic anaphylaxis. The intramuscular route of injection is preferable.