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PubMedDate not supplied

[Anaphylaxis.].

Anaphylaxis is a life threatening medical emergency in which the possibility for patient morbidity and mortality is high. It is the most serious of allergic disorders. An understanding of the pathophysiology of anaphylaxis and recognition of symptoms is paramount for its diagnosis. The term anaphylaxis refers to a generalized allergic reaction that results from a type I immunologic reaction. IgE activation of mast cells and basophils results in the release of preformed mediatiors including histamine, prostaglandins, and leukotrienes. These mediators induce vascular permeability, vascular smooth muscle relaxation and constriction of bronchial smooth muscles. Anaphylactoid reactions are clinically and pathologically similar but are not IgE mediated. This pathophysiologic sequence of events leads to the clinical manifestations of anaphylaxis including urticaria, angioedema, pruritus, and bronchospasms, eventually leading to hypotension and death if left untreated. This article discusses current demographics, causes and pathophysiology of anaphylaxis and provides guidelines for the treatment of anaphylaxis. The importance of prompt and correct treatment with adrenaline as well as thorough medical evaluation is also reviewed.

English Abstract↗
PubMedDate not supplied

Risk of anaphylaxis in a hospital population in relation to the use of various drugs: an international study.

PURPOSE: To evaluate the risk of anaphylaxis following exposure to medications given during hospitalization. METHODS: Cases with anaphylaxis and controls, matched according to length of hospital stay, were enrolled from hospitals in Hungary, Spain, India and Sweden. Exposures were recorded from the hospital record. The incidence of anaphylaxis was calculated among those exposed to various drugs, with denominators estimated from exposure rates in the controls and number of hospitalizations. RESULTS: Among 184 cases and 1003 controls, the incidence of anaphylaxis was in the range of 5-15 cases per 100,000 exposed patients for most analgesics and antibiotics administered orally or parenterally; for parenteral penicillin, it was 32. Incidence estimates were somewhat higher for blood, dextran, pentoxifylline and both ionic and nonionic contrast media, ranging from 35 to 95 cases. The highest estimates were for streptokinase and plasma, at 378 and 284. With no exposed controls, the incidence could not be calculated for anti-snake venom, but it was clearly higher than for other exposures. CONCLUSIONS: Although anaphylaxis is known to occur following exposure to a large number of drugs, the incidence is not well documented. We have demonstrated a relatively low risk for dipyrone, diclofenac, paracetamol, ampicillin, cloxacillin and cephalosporins. An intermediate risk was shown for parenteral penicillin, dextran, contrast media, blood and pentoxifylline. The highest incidence was observed for plasma, streptokinase and anti-snake venom (the latter used only in India).

Anaphylaxis↗
PubMed1997

Effect of cytochalasin D on systemic and local anaphylaxis in a murine model.

We investigated the effect of cytochalasin D on anaphylaxis. Cytochalasin D dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in rats. Especially, cytochalasin D inhibited compound 48/80-induced systemic anaphylaxis 100% with a dose of 1 microg g-1 body weight (BW). Cytochalasin D significantly inhibited serum histamine levels induced by compound 48/80. Cytochalasin D (10(-1) microg g-1 BW) also inhibited local anaphylaxis activated by anti-dinitrophenyl (DNP) IgE to 79.6+/-1.8%. Cytochalasin D dose-dependently inhibited histamine release from the rat peritoneal mast cells activated by compound 48/80 or anti-DNP IgE. The level of cAMP in rat peritoneal mast cells, when cytochalasin D was added, transiently and significantly increased about fourfold compared with that of basal cells. Our studies provide evidence that cytochalasin D will be beneficial in the treatment of anaphylaxis.

Anaphylaxis↗
PubMed2000

Inhibitory effect of mast cell-dependent anaphylaxis by Gleditsia sinensis.

We investigated the effect of aqueous extract of Gleditsia sinensis thorns (Leguminosae) (GSAE) on the mast cell-dependent anaphylaxis. GSAE (0.005 to 1 g/kg) dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in rats. GSAE (0.1 and 1 g/kg) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. When GSAE was pretreated at the same concentrations with systemic anaphylaxis, the plasma histamine levels were reduced in a dose-dependent manner. GSAE (0.001 to 1 mg/ml) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cyclic AMP in RPMC, When CSAE (1 mg/ml) was added, transiently and significantly increased about fourfold compared with that of basal cells. Moreover, GSAE (0.01 and 0.1 mg/ml) had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis factor-alpha production from RPMC. These results suggest a possible use of GSAE in managing mast cell-dependent anaphylaxis.

Anaphylaxis↗
PubMed1994

How is anaphylaxis recognized?

Prompt recognition of anaphylaxis may be lifesaving. Although its presentation has been described, there are no criteria for making a rapid diagnosis. A systematic review of the literature was performed to develop objective clinical criteria aimed at improving the recognition of anaphylaxis. A MEDLINE search of the word anaphylaxis over a 1-year period identified all of the reports describing the initial manifestations. Of 160 reviewed articles, 116 contained a clinical description of anaphylaxis. Eighty-nine (77%) of these 116 articles were case reports. Hypotension (84 reports [72%]) and urticaria and/or angioedema (70 reports [60%]) were the most frequently described signs. Of the identified allergens, 73% were diagnostic or therapeutic agents. In 72 of the 80 articles in which a reaction time could be identified, the reaction occurred within 60 minutes. As a result of this analysis, we conclude that anaphylaxis recognition may be improved by the identification of one of the following criteria, which describe the presentation in 82% of the analyzed reports: (1) exposure to an allergen within 1 hour produces one or more systemic signs (hypotension, upper or lower respiratory tract compromise, or increased gastrointestinal tract motility), or (2) urticaria or angioedema accompanies at least one of these systemic signs.

Allergens↗
PubMedDate not supplied

Investigating the TNP-OVA and direct popliteal lymph node assays for the detection of immunostimulation by drugs associated with anaphylaxis in humans.

Using current animal models, it is not possible to identify low-molecular-weight compounds (LMWCs) that are likely to be associated with anaphylaxis. It is generally accepted that the ultimate effector mechanism involves drug-induced IgE antibody. The objective of the present study was to determine if diclofenac, zomepirac and glafenine, which are associated with anaphylaxis in humans, have immunostimulating potential in the murine TNP-OVA (trinitrophenyl-ovalbumin) popliteal lymph node assay (PLNA), and more specifically to determine if the immunostimulation caused by these LMWCs results in IgE antibody production. These LMWCs were chosen because both zomepirac and glafenine were removed from the market due to high association with anaphylaxis, and diclofenac, which remains on the market, is frequently associated with anaphylaxis. In addition to conducting a TNP-OVA PLNA, the immunostimulating potential of these compounds was examined in the direct PLNA. When co-administered with TNP-OVA, all three LMWCs caused dose-dependent (0.25, 0.50, 1.00 and 1.25 mg) increases in popliteal lymph node (PLN) weight and cellularity that were observed beginning with the 0.25-mg dose. In addition, beginning with the 0.25-mg dose, all three compounds caused dose-dependent increases in TNP-OVA specific IgM and IgG(1) antibody-forming cells (AFCs). Diclofenac induced an isotype switch and caused a dose-dependent increase in the number of IgE AFCs with no detectable IgG(2a) AFCs and minimal high-dose-only IgG(2b) AFCs. Zomepirac induced IgE, IgG(2a) and IgG(2b) AFCs following the injection of 0.50 mg only, and glafenine induced IgE, IgG(2a) and IgG(2b) AFCs following the injection of 0.50-1.00 mg. In the direct PLNA, diclofenac caused dose-dependent increases in PLN weight and cellularity that were observed beginning with dose of 0.50 mg, whereas zomepirac failed to increase any PLN parameter and glafenine only increased the PLN weight. These results suggest that diclofenac, zomepirac and glafenine are immunostimulating LMWCs in the TNP-OVA PLNA with the potential to induce IgE antibody against a co-administered hapten-conjugate. Furthermore, these results suggest that the TNP-OVA PLNA offered significant advantages over the direct PLNA. Although it is not realistic to suggest that a single assay, based on a low number of test compounds, can identify all LMWCs with the potential to cause anaphylaxis in humans, these observations do demonstrate the potential utility of the PLNAs in examining LMWC-induced immunomodulation and support further development and investigation of the assays.

Adjuvants, Immunologic↗
PubMed1986

Aggregate anaphylaxis and carboxypeptidase N.

Bradykinin (BK) is widely believed to play a role in the pathogenesis of anaphylaxis. To help clarify any such roles, we examined for effects of inhibitors of kininase II (angiotensin converting enzyme, ACE) and "kininase I" (carboxypeptidase N, CPN), on the early course of egg albumin-induced aggregate anaphylaxis in anesthetized guinea pigs. In this model, pulmonary and systemic arterial blood pressure (BP) rise (unless pulmonary fibrillation occurs), lung wgt increases by approximately 60% and pulmonary microvessels are occluded by cell-rich thrombi, all within 5 min of i.v. antigen. The 30 min mortality rate is approximately 2%. ACE inhibitors (BPP9a, Captopril and MK 422; doses up to 140 mumol/kg) do not make anaphylaxis more nor less severe in terms discernible by changes in BP, lung wgt, EKG or intravascular coagulation. In marked contrast, an inhibitor of CPN (2-mercaptomethyl-3-guanidinoethylthiopropionic acid, 2-MGP; 8-16 mumol/kg) increases the 30 min mortality rate to 94% and lung wgt to 180% of control. The animals die in ventricular fibrillation. Given the enormous BK potentiating effects of BPP9a, Captopril and MK 422, it seems likely that little if any BK is formed in the early min of anaphylaxis. 2-MGP does not potentiate BP effects of BK but markedly potentiates effects of C3a anaphylatoxin. Thus, our data support the views that BK is neither a primary nor secondary mediator of aggregate anaphylaxis, and the adverse effects of 2-MGP are best explained in terms of preservation of anaphylatoxins and not in terms of preservation of kinins.

3-Mercaptopropionic Acid↗
PubMed1991

PAF induces rat plasma extravasation and releases eicosanoids during anaphylaxis.

The effects of anaphylaxis on vascular protein extravasation in selected tissues and on the release of prostaglandins in the peritoneal cavity were studied in sensitized rats. Extravasation of Evans blue dye was used as a measure of vascular permeability. Specific antigen challenge increased by 279, 297, 328, 250, and 192% the protein extravasation in the trachea, upper and lower bronchi, pancreas, and duodenum, respectively, but did not modify significantly the vascular permeability of the lung parenchyma, heart, liver, and kidney. Extravasation of Evans blue dye also was increased by 43-fold in the peritoneal cavity. Pretreatment of the animals with indomethacin (10 mg/kg) did not modify significantly the protein extravasation of the trachea, upper and lower bronchi, pancreas, and duodenum induced by anaphylaxis. Pretreatment with a mixture of mepyramine (3 mg/kg) and methysergide (2.5 mg/kg) reduced by 62, 66, and 40% the protein extravasation in the trachea, upper bronchi, and peritoneal cavity, respectively, in similar conditions. The PAF antagonist BN-52021 (5 mg/kg) very strongly reduced the protein extravasation elicited by anaphylaxis in the trachea, upper and lower bronchi, pancreas, and duodenum by 72, 87, 82, 67, and 85%, respectively, and by 53% in the peritoneal cavity. Anaphylaxis also increased the concentrations of thromboxane B2 and leukotriene B4 in the peritoneal exudates, but prostaglandin E2 levels were not affected. Pretreatment with BN-52021 reduced by 29 and 75% the level of thromboxane B2 and leukotriene B4 in the exudates. These results suggest that PAF, histamine, and serotonin mediate the protein extravasation associated with anaphylaxis, whereas prostaglandins are likely to play a minor role in this reaction.

Anaphylaxis↗
PubMed2005

Usefulness of serum mast cell-specific chymase levels for postmortem diagnosis of anaphylaxis.

Chymase, a serine protease, is stored mainly in secretory granules of human mast cells. Serum chymase concentration was examined in 8 autopsy cases with anaphylaxis as well as in 104 control cases without anaphylaxis. It was detected in all 8 cases with anaphylaxis (range 3-380 ng/ml, mean 89.8 ng/ml), while it was detected in only 2 of the 104 controls and was below a detectable level (<3 ng/ml) in the other 102. Serum tryptase levels are known to be a diagnostic indicator of anaphylaxis, therefore the relationship between serum chymase and tryptase levels was investigated in the 8 cases of anaphylactic death; a significant positive correlation was found (r=0.826, p=0.011). Furthermore, chymase was shown to be quite stable in serum. These results showed that measurement of serum chymase levels might be an additional tool for postmortem diagnosis of anaphylaxis.

Aged↗
PubMed2003

Hypotension associated with systemic aggregated anaphylaxis is not attenuated by a selective endothelin-A receptor antagonist, BQ 610, in rabbits in vivo.

PURPOSE: The present study was done to investigate the role of endothelin-1 (ET-1) in hypotension and bronchospasm provoked by anaphylaxis in rabbits in vivo. METHODS: Forty-five rabbits sensitized to horse serum were randomly allocated to five groups: Group 1 (n = 10) received 0.5 nmol x kg(-1) of ET-1; Group 2 (n = 10) received 0.5 nmol x kg(-1) of ET-1 and 200 nmol x kg(-1) of a selective ETA receptor antagonist, BQ 610, without anaphylaxis; Group 3 (n = 5) received 200nmol x kg(-1) of BQ 610 alone without anaphylaxis, Group 4 (n = 10) received normal saline alone before being antigen challenged to induce anaphylaxis; Group 5 (n = 10) received 200 nmol x kg(-1) of BQ 610 before antigen challenge. RESULTS: Mean arterial pressure (MAP) values were significantly different between Groups 1 and 2. Heart rate (HR), central venous pressure (CVP), dynamic pulmonary compliance (C(dyn)), and pulmonary airway resistance (R(L)) did not differ significantly between Groups 1 and 2. MAP values were significantly decreased compared with baseline in both Groups 4 and 5; however, the values were not significantly different between two groups. CVP values were significantly different between Groups 4 and 5 only at the 15-min time point following antigen challenge. HR, R(L), and C(dyn) values were not significantly different between Groups 4 and 5, nor were the survival rates. CONCLUSION: BQ 610 does not improve hypotension or survival rates in systemic aggregated anaphylactic rabbits in vivo, implying that circulating ET-1 may not play an important role in anaphylaxis, although direct proof of production of circulating ET-1 or activation of ETA receptors is lacking in this study.

Anaphylaxis↗
PubMed1985

Failure of sulfites to produce clinical responses in patients with systemic mastocytosis or recurrent anaphylaxis: results of a single-blind study.

Although sulfite sensitivity can precipitate asthma in a subpopulation of subjects with asthma, its role in precipitating anaphylaxis or as a nonspecific mast cell degranulator in systemic mastocytosis has not been examined. To evaluate critically the importance of sulfites in these diseases, eight patients with systemic mastocytosis and 25 patients with unexplained, recurrent anaphylaxis were challenged in a single-blind fashion; sodium bisulfite in capsules was administered in increasing doses of 1, 5, 10, 25, 50, 100, and 200 mg every 30 minutes. On separate occasions a liquid suspension of 200 mg of sodium bisulfite was administered to one patient with systemic mastocytosis and nine patients with anaphylaxis. Vital signs, pulmonary function tests, plasma histamine levels, and clinical reactions were monitored. There were no observable responses in either the mastocytosis group or in 23 of 25 patients in the anaphylaxis group. Two patients in the anaphylaxis group with initial positive challenges had similar symptoms on subsequent placebo challenge. One subject with asthma and with a history suggestive of sulfite sensitivity responded to oral challenge with 5 mg of sodium bisulfite and 100 micrograms of sodium bisulfite intradermally with a dramatic reduction in FEV, requiring treatment with bronchodilators. A comparison of baseline plasma histamine levels with those obtained after the sulfite challenge procedure in each category demonstrated a significant rise (p less than 0.05) in the systemic mastocytosis group. The overall level of significance determined by applying paired sample t tests to the histamine data from all subjects was p less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Biphasic and protracted anaphylaxis.

We performed a prospective study of anaphylaxis in 25 consecutive patients. Three distinct clinical patterns were observed: uniphasic, biphasic, and protracted anaphylaxis. Thirteen patients (52%) experienced a single episode. Biphasic anaphylaxis occurred in five patients (20%), two episodes of hypotension or laryngeal edema separated by asymptomatic intervals of 1 to 8 hours. Initial therapy included large doses of glucocorticoids in three of the five patients. Seven patients (28%) suffered hypotension, lower respiratory obstruction, or laryngeal obstruction that persisted 5 to 32 hours despite vigorous therapy that included systemic glucocorticoids. Recurrent or prolonged reactions were 2.8-fold more likely if the onset was 30 or more minutes after exposure to the stimulus or if the offending agent had been administered by mouth (p less than 0.03). Fatal reactions occurred in one patient who was taking propranolol and in one who was adrenal insufficient. The results of this study demonstrate that biphasic and protracted anaphylaxis are common, despite glucocorticoid therapy. Potentially life-endangering recurrences occurred in five (28%) of the 18 patients who responded to initial therapy. These observations indicate that patients should be followed carefully after apparent remission of anaphylaxis.

Adolescent↗
PubMed1992

Changes in cell-mediated immune responses after experimentally-induced anaphylaxis in dogs.

Experimentally-induced type 1 hypersensitivities were induced in normal dogs to either ovalbumin or Ascaris antigen. In vitro and in vivo cell-mediated immune responses were measured before sensitization and again at 1 and 6 days after induction of anaphylaxis by intravenous challenge with antigen. Histamine-modulated lymphocyte functions, such as histamine-induced suppression, histamine co-mitogen induced blastogenesis and the in vivo cutaneous responses to intradermally injected mitogens decreased post anaphylaxis. Spontaneous suppression of the autologous mixed-lymphocyte reaction increased post anaphylaxis. Lymphocyte blastogenic response to Concanavalin A (Con A) decreased at 6 (but not at 1) days post anaphylaxis probably due to a mediator other than histamine. Blastogenesis of 24 h preincubated cells by suboptimal concentration of Con A, declined post anaphylaxis, but Con A-induced suppression was not significantly altered. Dogs with atopic dermatitis have some altered cell-mediated immune responses. Altered histamine-induced and spontaneous suppression, histamine suppression of mitogenesis and decreased contact sensitivity observed in this experimental type 1 hypersensitivity mimicked that of atopic dogs. Increased cutaneous response to mitogens observed in atopic dogs was not reproduced in the type 1 hypersensitive dogs. These findings suggest some of the altered cell-mediated immune functions observed in dogs with atopic dermatitis result from type 1 hypersensitivity. The other abnormalities may be intrinsic to the atopic state.

Anaphylaxis↗
PubMed2004

Appropriate use of epinephrine in anaphylaxis.

We are submitting a case-based presentation illustrating medical errors in the use of epinephrine for the treatment of anaphylaxis. Readers will learn from mistakes made by other emergency caregivers in treating anaphylaxis. The article will specifically review the recommended use of epinephrine in the management of anaphylaxis. Four patients are presented who were seen in consultation by our outpatient allergy service. In all 4 cases, the history was suggestive of an episode of anaphylaxis in which emergency care providers mismanaged treatment. In 2 cases, the patients required ICU care after improperly receiving intravenous epinephrine. In the remaining 2 cases, epinephrine use was either omitted or significantly delayed in its administration. Our presentation includes a review of consensus statements regarding the treatment of anaphylaxis with particular regard to the use of epinephrine. We hope that this information will help prevent similar errors from harming other patients.

Adrenergic Agonists↗
PubMed2006

Differential accumulation of pulmonary and cardiac mast cell-subsets and eosinophils between fatal anaphylaxis and asthma death: a postmortem comparative study.

The distribution profile of infiltrated mast cell-subpopulations and eosinophils in the lung and heart sections of the patients who died of severe allergic hyperresponsiveness, was investigated. Four study groups were designed comprising 9 cases who died in systemic anaphylaxis (Group I), 10 asthmatic individuals whose death were assigned to acute and severe bronchial asthma (Group II), 10 asthmatic cases who died from non-immunological diseases (Group III). Twenty consecutive autopsies of non-allergic subjects who died of unnatural causes (Group IV) served as control group in this study. Utilizing antibodies against human tryptase and chymase and a double immunohistochemical staining method, we distinguished successfully all three subsets of mast cells (MC), MC-TC (containing both tryptase and chymase), MC-T (containing only tryptase) and MC-C (containing only chymase) types, subdivided on the basis of the protease compositions of their secretory granules. In order to immunostaining eosinophils, we used antibody to major basic protein as a marker. We also measured postmortem blood tryptase, specific and total serum IgE. The intriguing finding of this study was the marked differences of cellular composition in the lung between fatal anaphylaxis and asthma death. Significant augmentation of MCs infiltrated in lung and heart sections of anaphylaxis patients and drastic infiltration of bronchial eosinophils in asthmatic death and consequent release of their related inflammatory mediators might explain the differential expression of the associated symptoms in these two groups. The anaphylactic deaths did show neither emphysema nor significant mucous bronchial secretions whereas all asthmatic deaths did. The degree of pulmonary congestion and edema was also more severe in anaphylaxis. This corresponded with the histological findings and the location and number of mast cell-subsets and eosinophils in the different compartments of the lungs. We have demonstrated that the third type of mast cell MC-C is only found in the lungs in anaphylactic deaths. The practical consequence of our study will be that it is now possible to confirm a suspicion of anaphylaxis death not only by measurements of serum mast cell tryptase, but also by immunohistochemical methods.

Adolescent↗
PubMed1994

Biphasic systemic anaphylaxis: an inpatient and outpatient study.

We attempted to ascertain the incidence of systemic biphasic anaphylactic reactions in both outpatients and inpatients. Madigan Army Medical Center is a large teaching facility. The Allergy Clinic staff sees approximately 20,000 patients per year, and an average of 27,000 allergy immunotherapy injections are administered each year. During the years 1988 to 1991 we collected data from a total of 35 patients who had experienced, during the 30-minute waiting period in the clinic, symptoms and signs consistent with anaphylaxis. A total of 44 anaphylactic reactions were noted, with only two (5%) involving a biphasic systemic pattern. All patients were observed and treated within the clinic until symptoms and signs had resolved. None of the patients were treated with or were presently using glucocorticosteroids during the time of their reactions. Of the reactions noted, 25 (57%) involved only cutaneous manifestations of anaphylaxis, three (7%) involved the laryngeal/upper airway area, eight (18%) involved bronchospasm alone, three (7%) involved the rhinoconjunctivae, and five (11%) involved more than one site or type. None of the patients experienced any symptoms or signs of cardiovascular compromise or collapse after allergy extract injections. During the years 1986 to 1992 a total of 59 patients were admitted to the medical ward or intensive care unit with the diagnosis of systemic anaphylaxis. Of 59 patients, four (7%) experienced a recurrent (biphasic) anaphylactic reaction without reexposure to the initial inciting agent. The remaining 55 patients (93%) did not experience any further systemic anaphylaxis after initial hospital admission and treatment. Two of the patients with biphasic anaphylaxis were first seen with hypotension and generalized urticaria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Use of epinephrine for anaphylaxis by emergency medical technicians in a wilderness setting.

STUDY OBJECTIVE: To describe a case series of emergency medical technician-basic (EMT-B)-administered epinephrine for anaphylaxis in a wilderness setting. DESIGN: Case series of patients in anaphylaxis who received epinephrine subcutaneously from EMT-Bs. SETTING: National park rural/wilderness emergency medical service system covering 863,000 acres and serving approximately 2 million annual visitors. PARTICIPANTS: Prehospital care providers were National Park Service rangers with EMT-B training. Patients in the series were visitors to Sequoia and Kings Canyon National Parks with anaphylaxis resulting from insect stings. INTERVENTION: Subcutaneous administration of epinephrine by EMT-Bs trained in recognition, understanding, and treatment of anaphylaxis. RESULTS: Eight patients with anaphylaxis resulting from Hymenoptera stings, from June 1992 through September 1993, received EMT-B-administered epinephrine. All patients improved clinically after treatment with epinephrine within 25 minutes. No major side effects occurred. CONCLUSION: Our data suggest that EMT-B-administered epinephrine is safe when used by EMT-Bs in the rural/wilderness setting, with appropriate physician supervision. Further study in large trials will be required to demonstrate safety and efficacy.

Adolescent↗
PubMed2003

Fast omega-gliadin is a major allergen in wheat-dependent exercise-induced anaphylaxis.

BACKGROUND: Wheat-dependent exercise-induced anaphylaxis is an anaphylaxy induced by physical exercise after ingestion of wheat. An immediate-type hypersensitivity to water/salt-insoluble fraction of wheat proteins (gluten) has been considered to underlie in this disease. OBJECTIVE: The aim of the study is to determine the major allergen in Japanese patients with wheat-dependent exercise-induced anaphylaxis by using a panel of purified wheat gliadins and glutenins. METHODS: Water/salt-insoluble wheat proteins, alpha-gliadin, beta-gliadin, gamma-gliadin, fast omega-gliadin, slow omega-gliadin, high molecular weight glutenin and low molecular weight glutenin, were purified, and five patients with wheat-dependent exercise-induced anaphylaxis, whose diagnose had been determined by positive-challenge test, were evaluated for skin prick test, dot-blotting test and CAP-RAST inhibition test by using these purified wheat proteins. RESULTS: The fast omega-gliadin was the most potent allergen among these water/salt-insoluble proteins when evaluated by skin prick test and dot-blotting test. Fast and slow omega-gliadin, and gamma-gliadin caused dose-dependent inhibition of the serum IgE-binding to solid-phase gluten in the patients. The incubation with fast omega-gliadin of the patient's serum caused dose-dependent inhibition in the IgE-binding to gamma-gliadin as well as slow omega-gliadin, indicating a cross-reactivity of these proteins in IgE-binding. CONCLUSION: We concluded that fast omega-gliadin is a major allergen among these water/salt-insoluble proteins for wheat-dependent exercise-induced anaphylaxis in Japanese patients, and IgE against fast omega-gliadin cross-reacts to gamma-gliadin and slow omega-gliadin.

Adolescent↗