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Anaphylaxis: can we tell who is at risk of a fatal reaction?

PURPOSE OF REVIEW: Anaphylaxis is frightening and patients commonly fear their next reaction will be fatal. This review looks at the characteristics of fatal reactions to find if a fatal recurrence is predictable. RECENT FINDINGS: Most publications on fatal anaphylaxis are case reports that do not help predict risks. Most epidemiological studies focus on non-fatal reactions. The UK fatal anaphylaxis register demonstrates that over two-thirds of those dying from sting reactions and over four-fifths dying from drug anaphylaxis had no previous indication of their allergy, whereas those dying from food allergy had usually had previous reactions but these were typically not severe. Recent reports of anaphylaxis epidemiology based on diagnostic coding or attendance for treatment may be biased by differences in health service resource utilization according to the cause and course of the reaction. SUMMARY: Most fatal anaphylactic reactions are unpredictable. The appropriate management after recovery from a severe reaction may be protective against a fatal recurrence. An accurate identification of the cause and effective avoidance is a crucial part of this management, together with effective treatment of asthma for those with food allergy, immunotherapy for sting allergy, the avoidance of drugs that potentiate anaphylaxis, and effective training in self-treatment.

Age Factors↗

Oxygen consumption, assessed with the oxygen absorption spectrophotometer, decreases independently of venoconstriction during hepatic anaphylaxis in perfused rat liver.

Anaphylactic shock is accompanied by a decrease in oxygen consumption. However, it is not well known whether oxygen consumption decreases during local anaphylactic reaction in liver. We determined the effects of anaphylaxis and norepinephrine on oxygen consumption in isolated rat livers perfused portally and recirculatingly at constant flow with blood (hematocrit, 12%). Oxygen consumption was continuously measured by monitoring the portal-hepatic venous oxygen saturation differences using the absorption spectrophotometer, the probes of which were built in perfusion lines. Hepatic anaphylaxis was induced by an injection of ovalbumin (0.01 or 0.1 mg) into the perfusate of the isolated liver of the rat sensitized with subcutaneous ovalbumin (1 mg). Hepatic venoconstriction and liver weight loss were similarly observed in response to norepinephrine (0.01-10 micromol L(-1)) and anaphylaxis. However, hepatic anaphylaxis reduced oxygen consumption, whereas norepinephrine increased it. There was a possibility that anaphylactic venoconstriction could reduce the perfused surface area, resulting in decreased oxygen consumption. However, pretreatment with a vasodilator of sodium nitroprusside substantially attenuated venoconstriction but not the decrease in oxygen consumption during anaphylaxis. Thus, we conclude that local hepatic anaphylaxis decreases oxygen consumption independently of venoconstriction in isolated blood-perfused rat livers.

Anaphylaxis↗

Inhibitory effects of Agaricus blazei on mast cell-mediated anaphylaxis-like reactions.

Agaricus blazei is a medicinal mushroom native to Brazil. It used to be a source of anti-tumor and immunmoactive compounds and considered a health food in many countries. However, its specific effect against mast cell-mediated anaphylactic reactions is still unknown. In the present study, we investigated the effect of Agaricus blazei water extract (ABWE) on mast cell-mediated anaphylaxis-like reactions. We examined whether ABWE could inhibit systemic anaphylaxis-like reaction, ear swelling response, passive cutaneous anaphylaxis, and mast cell activation. ABWE inhibited compound 48/80-induced systemic anaphylaxis-like reaction, ear swelling response, and passive cutaneous anaphylaxis-like reaction in mice. ABWE also inhibited anti-dinitrophenyl (DNP) IgE-mediated passive cutaneous anaphylaxis. ABWE dose-dependently inhibited compound 48/80-induced or anti-DNP IgE-mediated histamine release from rat peritoneal mast cells (RPMC). Moreover, pretreatment with ABWE reduced compound 48/80-induced calcium uptake into RPMC. When ABWE was added, the level of intracellular cAMP in RPMC showed a significant increase compared with that of control cells. In addition, ABWE significantly inhibited compound 48/80-induced cAMP reduction in RPMC. These results propose that ABWE may be beneficial in the treatment of mast cell-mediated anaphylactic reactions.

Agaricus↗

Drug absorption from the gastrointestinal tract and immunity: the mechanism of the decreased absorption of salicylic acid during systemic anaphylaxis. I.

Previous studies have demonstrated the decrease of intestinal salicylic acid absorption in ovalbumin-immunized rats during systemic anaphylaxis. In the present study, the mechanism whereby systemic anaphylaxis interferes with the intestinal absorption of salicylic acid was studied. The pH of the luminal solution was not affected by the intravenous challenge with ovalbumin. A significant increase of the intraluminal protein was observed in rats under systemic anaphylaxis. However, there was no significant difference between ovalbumin-treated rats and saline-treated ones on the binding of salicylic acid with intraluminal macromolecular substances. Enhanced mucus release in the perfusate was also observed in sensitized rats but the extent of decrease in absorption of salicylic acid did not correlate with the increase in amount of the intraluminal mucus in the same animals. In addition, no significant effect was observed on the uptake by the intestinal everted sac of rats with systemic anaphylaxis. These findings suggested that mucus as well as protein is not responsible for the decrease of absorption of salicylic acid induced by systemic anaphylaxis. From these observations, it would appear that the circulatory changes in the gastrointestinal tract may play an important role in the decreased absorption of salicylic acid during systemic anaphylaxis.

Anaphylaxis↗

The causes of anaphylaxis and its management in adults.

Anaphylaxis is a potentially life-threatening condition which nurses may encounter while practising in any sphere of nursing. This article reviews the management of adults presenting with severe anaphylaxis in a general hospital setting. It summarizes data obtained from studies on the incidence of anaphylaxis, explains their significance, and defines the terms used when describing the pathophysiology of the condition. This is followed by an examination of the pathophysiology surrounding anaphylaxis with a summary of common causative agents. An overview of the management of patients with anaphylaxis is presented, together with a summary of the literature relating to the legal and ethical issues that nurses may face when encountering patients presenting with or experiencing anaphylaxis.

Adult↗

Serious shortcomings in the management of children with anaphylaxis in Scottish schools.

BACKGROUND: The United Kingdom incidence of anaphylaxis has increased very sharply over the last decade, with the highest rates of hospital admissions occurring in school-aged children. This raises concerns about the extent to which schools are aware of approaches to the prevention and treatment of anaphylaxis. METHODS AND FINDINGS: We undertook a national postal survey of 250 Scottish schools enquiring about approaches to managing children considered to be at risk of anaphylaxis. We obtained responses from 148 (60%) schools, 90 (61%) of which reported having at least one at risk child. Most (80%) schools with children considered to be at risk reported having personalised care plans and invariably reported having at least one member of staff trained in the emergency treatment of anaphylaxis. Access to adrenaline was available on-site in 97% of these schools. However, significantly fewer schools without children considered to be at risk reported having a trained member of staff (48%, p < 0.001), with access to adrenaline being very poor (12%, p < 0.001). Overall, 59% of respondents did not feel confident in their school's ability to respond in an emergency situation. CONCLUSIONS: Most schools with children considered to be at risk of anaphylaxis report using personal care plans and having a member of staff trained in the use of, and with access to, adrenaline. The picture is, however, less encouraging in schools without known at risk children, both in relation to staff training and access to adrenaline. The majority of schools with at risk children have poorly developed strategies for preventing food-triggered anaphylaxis reactions. There is a need for detailed national guidelines for all schools, which the Scottish Executive must now ensure are developed and implemented.

Adolescent↗

Anaphylaxis in children: a 5-year experience.

OBJECTIVES: To identify the causative agents, presenting signs and symptoms, and course of disease in children diagnosed with anaphylaxis. Design. Five-year retrospective chart review. SETTING: Urban children's hospital pediatric emergency department, operating suite, and inpatient units. PARTICIPANTS: Fifty-five cases of anaphylaxis in 50 patients 1 to 19 years of age. INTERVENTIONS: None. RESULTS: The most common inciting agents in this population were latex (27%), food (25%), drugs (16%), and venoms (15%). Thirty-two cases (58%) occurred outside of the hospital, including 3 of 11 severe cases. Nineteen (35%) had histories of prior allergy to the causative agent. Most agent exposures were intravenous (38%), oral (27%), or dermal (20%). The most common systems involved were respiratory (93%), skin (93%), cardiovascular (26%), and neurologic (26%). Features distinguishing the 11 patients requiring intensive care included latex agents (45%), nonenteral route of exposure (91%), and presence of cardiovascular symptoms (45%). Of the 17 patients with known past anaphylaxis, only 5 had epinephrine self-administration devices available, and 3 had used them. CONCLUSIONS: (1) Most patients with anaphylaxis present with skin or respiratory symptoms. (2) Severely ill children more commonly have nonenteral and/or latex exposures that occur in the hospital. (3) Most children with anaphylaxis have no stated histories of prior reaction to the causative agent. (4) Those patients who have had past episodes of anaphylaxis infrequently have epinephrine self-administration devices available for use.

Adolescent↗

Fatal and near fatal idiopathic anaphylaxis.

OBJECTIVE: To document that idiopathic anaphylaxis may have a fatal or near fatal outcome. DESIGN: Review of selected cases seen personally by authors during the past 16 years. SETTING: University faculty practice and private practices. PATIENTS: All cases of idiopathic anaphylaxis seen by the authors are not presented, but 10 cases were selected to demonstrate two fatalities and eight cases of near fatalities. RESULTS: Two fatal cases had expired before emergency service therapy. Eight near fatal cases responded to acute therapy and subsequently were controlled. Remission of idiopathic anaphylaxis was then induced. Idiopathic anaphylaxis may be fatal or potentially fatal and must be treated to prevent a fatal outcome. CONCLUSIONS: The documentation of fatalities and near fatalities should help patients and their physicians accept intense management of idiopathic anaphylaxis that will result in control and induction of a remission in idiopathic anaphylaxis.

Adolescent↗

Anti-IL-4 antibody inhibits antigen specific IgE response but fails to prevent chicken gamma globulin-induced active systemic anaphylaxis: evidence for the involvement of IgG antibodies.

It has recently been reported that interleukin-4 (IL-4) is required for the production of IgE, and anti-IL-4 monoclonal antibody (mAb) inhibits in vivo IgE responses. These suggest that blocking of IL-4 activity may be useful for the prevention or treatment of immediate hypersensitivity disorders. In this study we investigated whether anti-IL-4 has a regulatory role in chicken-gamma globulin (CGG)-induced active systemic anaphylaxis. Multiple injections of anti-IL-4 (up to 40 mg/mouse) failed to protect the mice from fatal anaphylaxis. Anti-IL-4 strongly suppressed CGG-specific IgE response (> 90%) without any suppressive effect on CGG-specific IgG (IgG1, IgG2a, IgG2b, and IgG3) responses. Because these data suggest the possibility that fatal anaphylaxis could be induced by IgG antibodies, we examined the possibility using anti-CGG polyclonal and the subclasses of IgG monoclonal antibodies. Passive sensitization of mice with polyclonal antibodies elicited severe and fatal anaphylactic shock; about 50% of the mice died. The activity of antibodies was not diminished by heat treatment (56 degrees C, 2h), suggesting that the anaphylaxis was not mediated by IgE. Shock was also elicited by each subclass of IgG mAb; of these, IgG1 was the most effective. Combination of the IgG subclasses elicited more exaggerated shock; about 30% of mice died. These data indicate that IgG antibodies are themselves sufficient to induce systemic anaphylaxis. Therefore, the failure of anti-IL-4 to prevent active anaphylaxis is probably due to the inability of anti-IL-4 to suppress the production of IgG antibodies.

Anaphylaxis↗

Outcome of prophylactic therapy for idiopathic anaphylaxis.

OBJECTIVE: To determine the efficacy of a prophylactic regimen (prednisone, H1 blockade, and sympathomimetic amine therapy) in patients with idiopathic anaphylaxis. DESIGN: Clinical trial before and after treatment. SETTING: Referral-based allergy clinic at a major medical center. PATIENTS: Fifty-three patients with a history compatible with idiopathic anaphylaxis for at least 6 months before presentation to the allergy service and with subsequent management by the service for at least 6 months. INTERVENTIONS: Patients with frequent life-threatening symptoms were treated with a prophylactic regimen. Patients with infrequent episodes of idiopathic anaphylaxis were only treated acutely for each episode of anaphylaxis. MEASUREMENTS AND MAIN RESULTS: The results favored prophylactic treatment with prednisone for patients who were classified as generalized-frequent in the clinical outcome measures of frequency (per patient per year) of episodes (mean before treatment, 7.31 +/- 6.46; after treatment, 3.61 +/- 4.73; P less than 0.02) and emergency room visits (mean before treatment, 1.94 +/- 3.42; after treatment, 0.21 +/- 0.44; P less than 0.005) and for patients classified as angioedema-frequent in the frequency of episodes (mean before treatment, 14.93 +/- 15.89; after treatment, 2.58 +/- 2.18; P less than 0.003) and emergency room visits (mean before treatment, 0.76 +/- 1.01; after treatment, 0.07 +/- 0.11; P less than 0.025). No statistically significant difference was found for patients classified as generalized-infrequent in the frequency of episodes (mean before treatment, 2.01 +/- 1.30; after treatment, 1.36 +/- 1.79) or of the emergency room visits (mean before treatment, 0.56 +/- 0.71; after treatment, 0.32 +/- 0.75) or for patients classified as angioedema-infrequent in the frequency of episodes (mean before treatment, 1.94 +/- 1.55; after treatment, 2.03 +/- 2.16) or of emergency room visits (mean before treatment, 0.27 +/- 0.44; after treatment, 0.37 +/- 0.59). CONCLUSIONS: Prophylactic treatment with prednisone and H1 antihistamines with or without sympathomimetic amines improves clinical outcome in patients who are classified as idiopathic anaphylaxis-angioedema frequent and idiopathic anaphylaxis-generalized frequent.

Adolescent↗

Clinical and functional differences among patients with idiopathic anaphylaxis.

BACKGROUND: There are no studies assesing whether patients with idiopathic anaphylaxis are a heterogenous population OBJECTIVE: A study has been carried out to assess whether clinical and functional differences (mast cell releasability) exist between two sub-types of Idiopathic Anaphylaxis (Generalized Idiopathic Anaphylaxis -IA-G- and Idiopathic Anaphylaxis with Angioedema -IA-A-). METHODS: Patients were selected from the Idiopathic Anaphylaxis (IA) patient population of Hospital General de Albacete (Albacete, Spain) and this data were collected between 1990 and 1995. This series is composed of 81 patients. In the interest of seeing whether an IA classification is warranted between IA-G and IA-A, a logistic regression model was constructed in order to know if differences exist between IA-G and IA-A. To evaluate mast cell releaseability in different groups (IA-G, IA-A, atopic patients, urticaria and healthy subjects) we analysed the log 10 wheal area produced by four consecutive concentrations of codeine (from 90 to 3,3 mg/ ml). In those patients with IA-G, the variable urticaria was controlled, but not in those with IA-A. A parallel line assay was used to study the differences arising among all groups. When the conditions of parallelism and linearity were not fulfilled, a Hotelling's T2 test was performed. RESULTS: In the logistic regression equation total IgE, with an O.R. of 1.006 (95% C.I. 1.001-1.01) favoured the presence of IA-G; whereas the presence of urticaria did not favour the presence of IA-G, with an O.R. of 0.159 (95% C.I. 0.04-0.507). IA-G and IA-A patients showed a higher cutaneous reaction to codeine than atopic patients (p=0.005 and p=0.001 respectively). However, IA-G patients had a lower reaction to codeine than those patients with urticaria (p=0.048). No differences were observed among patients with IA-A and patients with urticaria, as was the case between IA-A and IA-G patients with respect to cutaneous response to codeine. CONCLUSION: Apparently, IA-G patients appear to be closely related to the presence of atopy, while IA-A patients are closely related to the presence of urticaria. Along with other unknown factors, an enhanced mast cell releaseability may explain these episodes of Idiopathic Anaphylaxis among atopic patients.

Adult↗

Anaphylaxis and epinephrine prescribing patterns in a military hospital: underutilization of the intramuscular route.

Epinephrine is the only definitive treatment of anaphylaxis, and recent evidence suggests that the intramuscular route has superior pharmacokinetics to subcutaneous administration. There is little data regarding what route is commonly used in clinical practice. The objective of this article is to determine the rate of epinephrine use in cases of anaphylaxis and route of administration utilized. A retrospective review was made of 220 medical records with the primary diagnosis of urticaria, angioedema, or anaphylaxis over a 28-month period at a military medical center. Twenty-four cases of anaphylaxis identified in the records. Demographics, along with signs and symptoms of those experiencing anaphylaxis, were similar to other published reports. Epinephrine was given in only 50% of cases and largely by the subcutaneous route. No intramuscular epinephrine was administered. H1 blockers and steroids were the most commonly administered treatments. H2 blockers were given at the same rate as epinephrine. An autoinjector was prescribed in 29% of cases with instruction on its use documented in 13%. An allergy referral was made in 29% of cases. Greater educational efforts and collaboration are needed between the allergy community and other providers regarding the importance of administering epinephrine intramuscularly, prescribing autoinjectors, and referring to an allergist in cases of anaphylaxis.

Adolescent↗

Are general practitioners alert to anaphylaxis diagnosis and treatment?

INTRODUCTION: Anaphylaxis is a potentially lethal condition. Prevention of mortality depends on the correct diagnosis and on early epinephrine injection by the patients affected. OBJECTIVE: Evaluate practical knowledge of diagnostic and therapeutic aspects of anaphylaxis in general practitioners. MATERIAL AND METHODS: 100 GPs were inquired through the use of an anonymous and voluntary questionnaire with 5 multiple-choice questions (just one correct answer): 3 about diagnostic aspects and two about therapeutic aspects of anaphylaxis. There was also one other question where it was asked the commercial name of the only device for epinephrine auto-injection available in Portugal. Eight minutes were given to fulfil the questionnaire. 92 complete questionnaires were eligible for evaluation. RESULTS: In the three diagnostic questions we observed a percent of correct answers ranging from 36 to 46%. In the two questions regarding anaphylaxis therapy only 18 to 22% of the GPs gave the correct answers. Only 14% of the GPs were able to indicate the correct commercial name of the epinephrine auto-administration kit. CONCLUSIONS: The results of this study stress the need to promote, within the GP community, continuous medical education programmes regarding adequate diagnosis and treatment of anaphylaxis. Wrong concepts related to anaphylaxis treatment are frequently observed and this is a serious problem since GPs are the front-line doctors in the management of out-patient anaphylactic reactions and therefore it is absolutely mandatory that they can be able not only to accurately diagnose and treat an acute anaphylactic episode but also to make a correct retrospective diagnosis and to advise on the use of epinephrine auto-injectors.

Adult↗

[The so-called "idiopathic" anaphylaxis: allergic and pseudo-allergic reactions].

The anaphylaxis that is called idiopathic (A.I.) forms less than 1% of the publications that are concerned with anaphylaxis. The clinical picture associates all the symptoms of anaphylaxis, with particular frequency of Quincke's laryngeal oedema. A vital risk is supposed. No abnormal biological factor can be found. There is an associated, variable pathology in 20% of subjects, 58% are atopic. A.I. effects women more--69%. Quincke's hereditary angioneurotic oedema, the carcinoid syndrome, and the capillary hyperpermeability syndrome, paroxysm with monoclonal gammopathy, systemic mastocytosis must be eliminated as well as false anaphylaxis. The authors review the exceptional causes that may not be considered: drug anaphylaxis, to foods, hymenoptera, effort anaphylaxis, to hydatic antigens, to toboggans, to progesterone. Pathogenic hypotheses incriminate sensitization to unknown allergens, functional anomalies of mastocytes, heterogeneity of IgE. Addition of allergic and non-allergic factors is possible. Release of mediators other than histamine is one hypothesis proposed, to account for the inefficiency of anti H1. Prevention requires avoidance of aspirin, non-steroid anti-inflammatory drugs and beta blockers. Basic treatment is always corticosteroids, with anti H1 and sympathomimetic amines where the A.I. is severe.

Adrenal Cortex Hormones↗

Incidence of anaphylaxis in the emergency department: a 1-year study in a university hospital.

The aim of this study was to estimate the incidence of anaphylaxis in an emergency department, identify rate and risk factors of recurrent anaphylaxis, and describe its clinical features and management. A retrospective study of patients who attended the emergency department at Thammasat University Hospital was conducted during 2003-2004 with anaphylactically related ICD-9 and ICD-10 terms. There were 64 patients who experienced 65 anaphylactic episodes during the 1-year period. The anaphylaxis occurrence rate was 223 per 100,000 patients per year. The most common manifestations were cutaneous symptoms and signs, followed by respiratory expression. Food allergy was the most common cause of anaphylaxis. Eighty-five percent of admitted cases had monophasic anaphylaxis. Patients with and without biphasic reactions did not differ significantly in terms of epinephrine and steroid usage. In conclusion, anaphylaxis is not rare. Epinephrine and steroid usage did not prevent biphasic reactions.

Adult↗

Divalent hapten-induced intestinal anaphylaxis in the mouse: uptake and characterization of a bystander protein.

We examined the mucosal barrier function during anaphylaxis induced by the hapten N,N'-di-2,4,dinitrophenyl-lysine (di-DNP-lysine) in BDF1 female mice immunized with dinitrophenylated Ascaris suum extract. Immunized mice were gavaged with 10 mg or 50 mg of ovalbumin (OVA) with or without N,N'-di-2,4,-DNP-lysine (di-DNP-lysine). Animals that received di-DNP-lysine underwent anaphylaxis and were observed to have significantly greater serum concentrations of immunoreactive OVA (iOVA) than control mice. The severity of anaphylaxis, which varied with the dose of di-DNP-lysine administered, influenced the uptake of OVA; greater amounts of iOVA were detected in serum of mice undergoing more severe anaphylaxis. On gel permeation of serum from both groups of mice, immunoreactive OVA was found to have a molecular size similar to native OVA. Di-DNP-lysine is a synthetic hapten that reliably induced anaphylaxis in sensitized animals challenged by gavage. Anaphylaxis resulted in the uptake into the circulation of greater quantities of an unrelated protein antigen present in the intestinal lumen. The protein antigen that was taken up into the circulation appeared to be intact and thus may have an influence on the development of the immune response, or lack thereof, to this bystander antigen.

Anaphylaxis↗

Clinical summary and course of idiopathic anaphylaxis in 73 patients.

Seventy-three patients with anaphylaxis of unknown cause were studied. Repeated histories and physical examinations were performed by the Northwestern University (Chicago) allergy service in an attempt to find a cause for the anaphylaxis. Documentation of abnormal physical findings during an episode of anaphylaxis was necessary in each patient. Prior to our initial consultation, these 73 patients had required 115 emergency room visits and 37 hospitalizations. No deaths have occurred in 224 patient years of follow-up from initial presentation. Thirty-eight (52%) patients have infrequent reactions (defined as one episode only or mild episodes less than six times per year) requiring acute treatment alone. Thirty-five (48%) patients have severe or frequent life-threatening reactions (defined as episodes that include syncope, documented hypotension, and airway compromise as major manifestations) requiring maintenance antihistamines and prednisone. Laboratory studies were not helpful in finding a cause of anaphylaxis in any of the 73 patients. Associated atopic conditions were present in 45 patients. Twenty-three patients had chronic idiopathic angioedema, urticaria, or both prior to developing idiopathic anaphylaxis. Sixteen patients only treated acutely for each episode of anaphylaxis and seven patients previously receiving maintenance medication are now asymptomatic without medication for longer than one year.

Adolescent↗

Anti-IL-4 monoclonal antibody prevents antibiotics-induced active fatal anaphylaxis.

We previously reported that anti-IL-4 mAb (11B11) failed to prevent protein-induced fatal murine anaphylaxis. To investigate the effect of anti-IL-4 on hapten-induced anaphylaxis, a model of murine anaphylaxis induced by antibiotics, penicillin V (Pen V) and cephalothin (CET), was developed, and the effect of anti-IL-4 on the anaphylaxis was observed. Pen V and CET induced 100 and 70 to 90% fatal reactions, respectively, when C57BL/6 mice were sensitized i.p. with 500 microg of antibiotic-OVA conjugate with 2 x 10(9) Bordetella pertussis and 1.0 mg of alum and challenged i.v. with 100 microg of antibiotic-BSA conjugate 14 days later. Serum taken from mice sensitized to Pen V passively sensitized normal mice to develop systemic anaphylaxis, and this ability of the serum was abrogated by heating at 56 degrees C for 2 h or depletion of IgE, but not IgG, Abs. Thus, the antibiotic-induced fatal reaction was an IgE-dependent anaphylactic reaction. Administration of anti-IL-4 at the beginning of sensitization completely prevented the fatal anaphylactic reactions to both Pen V and CET. This effect of anti-IL-4 was associated with its suppressive activity on antibiotic-specific serum IgE, but not IgG, levels. More importantly, anti-IL-4 therapy in previously sensitized mice was also effective in preventing the fatal reactions and rapidly reduced the established IgE levels. This study provides a new animal model of hapten-induced anaphylaxis and indicates that blocking of IL-4 activity may be beneficial in allergic diseases caused by a variety of haptens in which IgE Abs play a major role.

Anaphylaxis↗