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At least 19 recordsLinked to original sources
PubMed1985

[Anaphylaxis to muscle relaxants. Predictive value of intradermal tests and study of crossed anaphylaxis].

37 patients were studied, all of whom presented with anaphylaxis to a muscle relaxant. The diagnosis was made after simultaneous intradermal testing (IDT), human basophil degranulation tests (HBDT) and Prausnitz-Küstner tests (PK) of passive cutaneous anaphylaxis. Three tests were positive in 6 patients, both IDT and PK in 9, and both IDT and HBDT in 8. In 14 patients, the IDT, repeated twice, were positive both times. A search for crossed anaphylaxis to the other muscle relaxants was carried out in all the patients during a second series of tests, a few months to years after the first one. The drugs tested, at dilutions of the pharmaceutical preparation of 10(-3) or more, were: suxamethonium, gallamine, alcuronium, pancuronium, vecuronium, d-tubocurarine. The reliability of IDT in the diagnosis of anaphylaxis is discussed in terms of the small reactive concentration, the producibility of the tests, the one HBDT that did become positive later, and in one case the occurrence of shock by crossed anaphylaxis. Skin reactivity seemed to remain constant with time, so allowing the use of IDT as a diagnostic tool, in cases of old anaphylactoid shocks, occurring during general anaesthetics. The frequency of crossed anaphylaxis was assessed to be about 84%. The sensitivity to one or other drugs varied with each patient. Pancuronium and vecuronium appeared to be the least likely drugs to cause crossed anaphylaxis. The predictive use of these tests is discussed. It is also suggested that muscle relaxants with only one quaternary ammonium group should be used, this chemical characteristic probably reducing the risks of sensitization.

Adolescent↗
PubMed1997

Systemic anaphylaxis in the mouse can be mediated largely through IgG1 and Fc gammaRIII. Assessment of the cardiopulmonary changes, mast cell degranulation, and death associated with active or IgE- or IgG1-dependent passive anaphylaxis.

We attempted to elicit active anaphylaxis to ovalbumin, or passive IgE- or IgG1-dependent anaphylaxis, in mice lacking either the Fc epsilonRI alpha chain or the FcR gamma chain common to Fc epsilonRI and Fc gammaRI/III, or in mice lacking mast cells (KitW/ KitW-v mice), and compared the responses to those in the corresponding wild-type mice. We found that the FcR gamma chain is required for the death, as well as for most of the pathophysiological changes, associated with active anaphylaxis or IgE- or IgG1-dependent passive anaphylaxis. Moreover, some of the physiological changes associated with either active, or IgG1-dependent passive, anaphylactic responses were significantly greater in Fc epsilonRI alpha chain -/- mice than in the corresponding normal mice. Finally, while both KitW/KitW-v and congenic +/+ mice exhibited fatal active anaphylaxis, mast cell-deficient mice exhibited weaker physiological responses than the corresponding wild-type mice in both active and IgG1-dependent passive systemic anaphylaxis. Our findings strongly suggest that while IgE antibodies and Fc epsilonRI may influence the intensity and/or kinetics of some of the pathophysiological changes associated with active anaphylaxis in the mouse, the mortality associated with this response can be mediated largely by IgG1 antibodies and Fc gammaRIII.

Anaphylaxis↗
PubMed1983

Investigation of leukotriene involvement in the vasopermeability response associated with guinea pig tracheal anaphylaxis: comparison with cutaneous anaphylaxis.

A direct comparison of the role of leukotrienes in mediating the increase in microvascular permeability associated with guinea pig tracheal and cutaneous anaphylaxis was obtained by simultaneous administration of inflammatory stimuli to both trachea and ear. The SRS-A antagonist, FPL 55712, reduced the increase in tracheal extravascular albumin content evoked by LTC4, LTD4, and LTE4 but failed to significantly reduce the tracheal microvascular permeability response associated with local anaphylaxis. Moreover, the inhibitory effect of the histamine H1-receptor antagonist, mepyramine, was not augmented by the additional presence of FPL 55712. In contrast to tracheal anaphylaxis, a distinct leukotriene component was indicated in cutaneous anaphylaxis since the mepyramine-FPL 55712 combination produced a greater inhibition than mepyramine alone. These results suggest that the degree of leukotriene involvement in anaphylaxis may vary between tissues.

Anaphylaxis↗
PubMed1989

Passive air-pouch anaphylaxis in rats. I. Induction of anaphylaxis.

Induction of an experimental passive anaphylaxis of the air-pouch type, passive air-pouch anaphylaxis, was carried out in an attempt to induce a reproducible anaphylaxis model suitable for quantitative studies. Rats were injected subcutaneously with 10 ml of air into the dorsal skin to make an air-pouch and with 2 ml of antiserum at an appropriate dilution for passive sensitization, and then 5 ml of air was removed. The challenge with 5 ml of antigen solution into the air-pouch 48 h later provoked mast cell degranulation and increased vascular permeability induced by released histamine. Treatment with monovalent hapten prior to the antigen challenge almost completely inhibited histamine release and plasma exudation to levels similar to those in the nonsensitized group. In this model, mast cell-dependent late-phase allergic reaction, such as leukocyte migration or the increase of plasma exudation following mast cell degeneration, was not observed.

Air↗
PubMed1979

The effects of H1 and H2 receptor antagonism on the response of monkey skin to intradermal histamine, reverse-type anaphylaxis, and passive cutaneous anaphylaxis.

The effects of H1 and H2 receptor anatagonists on models of allergic reactions in monkey skin have been studied. Intradermal histamine is markedly inhibited by H1 receptor antagonists but not by H2 receptor antagonists in the doses used. However, the combination of both receptor antagonists gives greater inhibition than that seen with H1 receptor blockade alone. Reverse-type anaphylaxis is also markedly inhibited by H1 but not H2 receptor antagonists. Passive cutaneous anaphylaxis (PCA) is likewise inhibited by H1 receptor antagonism, but not by H2 receptor antagonism. The combination of the two inhibitors leads to a complete inhibition of this PCA response. The data suggest that the addition of an H2 receptor antagonist may potentiate the effect of H1 blockade alone.

Anaphylaxis↗
PubMed1982

Protective effects of the glucocorticoid, budesonide, on lung anaphylaxis in actively sensitized guinea-pigs: inhibition of IgE-but not of IgG-mediated anaphylaxis.

1 The effect of glucocorticoid pretreatment on antigen-induced bronchoconstriction was studied in guinea-pigs actively sensitized to two different ovalbumin regiments (one producing IgE- and IgG-like antibodies and the other exclusively IgG-like antibodies). 2 Budesonide (50 mg/kg) and hydrocortisone (50 mg/kg) given as one intraperitoneal injection 15-20 h before and anaphylactic tests or as two consecutive intraperitoneal injections 5 and 6 days before, led to a decreased bronchial capacity. In this respect glucocorticoid pretreatment was effective only in guinea-pigs sensitized to produce both IgE-like and IgG-like antibodies. 3 Budesonide pretreatment also reduced the capacity of anaphylactically-challenged chopped lung tissue to release histamine in guinea-pigs sensitized to produce both IgE- and IgG-like antibodies. 4 Budesonide pretreatment did not change the levels of circulating IgG1a and IgE-like homocytotropic antibodies as measured by passive cutaneous anaphylaxis; nor did it affect histamine or methacholine-induced bronchoconstriction in vivo or the capacity of histamine or methacholine to contract the guinea-pig isolated trachea preparation of the isoprenaline-induced relaxation of this preparation. 5 The selective inhibitory effects of budesonide and hydrocortisone on IgE-mediated but not IgG-mediated anaphylaxis and the relevance to human atopic disease are discussed.

Anaphylaxis↗
PubMed1987

Pharmacological studies on the release of slow reacting substance of anaphylaxis during anti-immunoglobulin E antibody mediated passive peritoneal anaphylaxis in rats.

The release of slow reacting substance of anaphylaxis (SRS-A) by anti-immunoglobulin E(IgE; epsilon)-antibody mediated passive peritoneal anaphylaxis (PPA) in rats was investigated immunopharmacologically. A significant amount of SRS-A was released by anti-epsilon-antibody in the peritoneal cavity of rats passively sensitized with IgE. The amount of SRS-A released by anti-epsilon-antibody was about one third less than that released in an anti-gamma-antibody and IgG2a system. The release of SRS-A was initiated at 2 min and reached its maximum 5 to 10 min after the injection of anti-epsilon-antibody. Disodium cromoglycate, tranilast and ketotifen inhibited the release of both SRS-A and histamine caused by anti-epsilon-antibody mediated PPA. Glucocorticoids (hydrocortisone, prednisolone and dexamethasone) also inhibited the release of both mediators. rho-Bromophenacyl bromide inhibited the release of both mediators. AA-861, a potent 5-lipoxygenase inhibitor, inhibited the release of SRS-A but not histamine. Indomethacin slightly enhanced the release of SRS-A and inhibited the release of histamine. Cytarabine resulted in leucopenia and inhibited the release of histamine but not SRS-A during PPA. Dextran sulfate reduced the number of glass adherent peritoneal cells and inhibited the release of SRS-A but not histamine. These results suggest the suitability of anti-epsilon-antibody mediated rat PPA for investigating the effect of anti-allergic agents on the release of SRS-A.

Anaphylaxis↗
PubMedDate not supplied

Using test dose challenges to restore essential therapy in patients with idiopathic anaphylaxis and pharmacophobia: report of a patient with idiopathic anaphylaxis and statin phobia.

Idiopathic anaphylaxis (IA) is a well-documented condition in which anaphylaxis occurs in the absence of an identifiable precipitant. However, many patients with IA find it difficult to accept this diagnosis and continue to search for an external cause. It is not uncommon for these highly anxious patients to discontinue essential medications that they feel are responsible for the reaction despite reassurance from their physicians to the contrary. In extreme cases, these patients may develop an actual phobia to preexisting medications and avoid them despite adverse consequences to their health. To illustrate this concept, we report a case involving a female patient with familial hypercholesterolemia who experienced a single episode of IA and developed a "statin phobia," falsely implicating her medication (lovastatin) for the reaction. After 5 years of failed therapy with other antihyperlipidemic agents, the patient finally agreed to undergo test dosing to a similar statin agent atorvastatin. On successful completion of the test, she resumed therapy with atorvastatin and her low-density lipoprotein (LDL) levels were reduced by 50% over 5 months. We conclude that patients with a confirmed diagnosis of IA who manifest phobic responses to beneficial medications should be reassured of the diagnosis promptly by their physician. When reassurance fails and the medication is essential to the patient's health, test dose challenges may be conducted to reintroduce the drug to the patient's regimen.

Anaphylaxis↗
PubMed2002

Rat monoclonal anti-murine IgE antibody removes IgE molecules already bound to mast cells or basophilic leukemia cells, resulting in the inhibition of systemic anaphylaxis and passive cutaneous anaphylaxis.

IgE plays a central role in allergic reactions. Some anti-IgE antibodies (HMK-12, 6HD5) inhibit the binding of IgE to the FcepsilonRI of mast cells/basophilic leukemia cells (PT-18, RBL/2H3), but less inhibition is seen with the anti-allotypic JKS-6 and the anti-idiotypic Eb-1. Anti-IgE HMK-12 can detach bound IgE molecules from the FcepsilonRI. When mast cells or basophils were incubated with monoclonal anti-DNP-IgE SPE-7, washed and treated with anti-IgE HMK-12, anti-IgE/IgE complexes were found in the supernatant. Similar results were obtained with the Fab fragment of HMK-12. Mice injected with anti-DNP-IgE SPE-7 and later with DNP-BSA had the typical systemic anaphylactic shock. However, if they were injected with the anti-IgE antibody (HMK-12) before the challenge, they did not get an anaphylactic shock. In the sera of mice injected with monoclonal IgE SPE-7 and anti-IgE antibody (HMK-12), IgE/anti-IgE complexes were detected. No passive cutaneous anaphylaxis occurred if the rats were injected with anti-IgE antibodies before the challenge. In summary, anti-IgE antibodies can remove IgE antibodies from the FcepsilonRI; anti-IgE/IgE complexes can be detected in vitro and in vivo, and anti-IgE antibodies can inhibit IgE-mediated systemic or local anaphylactic reactions.

Anaphylaxis↗
PubMed1995

Undifferentiated somatoform idiopathic anaphylaxis: nonorganic symptoms mimicking idiopathic anaphylaxis.

BACKGROUND: Northwestern University's Division of Allergy and Immunology has had experience with the diagnosis and treatment of more than 350 patients with idiopathic anaphylaxis (IA). In 1992 we reported a group of patients with IA whose presentations mimicked IA, but IA and other organic causes were later excluded. Psychologic factors were suspected as the underlying problem. These patients were classified as IA-variant. Management of these cases was extremely difficult. There was significant morbidity and high and unnecessary costs. OBJECTIVE: We aim to distinguish the nature of this disease and to highlight the evaluation and treatment of this group of patients. METHODS: Their cases are reviewed and reported. RESULTS: Common features included (1) presenting symptoms mimicking IA, (2) no objective findings that correlated with 1, (3) no response to the therapeutic regimen for IA, (4) meeting the Diagnostic and Statistical Manual of Mental Disorders criteria for undifferentiated somatoform disorder, and (5) significant wasted health care expenditure. CONCLUSIONS: This group of patients were better defined as having undifferentiated somatoform-IA. An algorithm was proposed to expedite the diagnosis of the disease so that with early recognition of the disease, unwarranted repetitive consultations, tests, and inappropriate therapy can be avoided.

Adult↗
PubMed1983

Life-threatening inhalant allergy: typical anaphylaxis induced by inhalational allergen challenge in patients with idiopathic recurrent anaphylaxis.

Eight patients, referred to an allergy service because of anaphylactic syndromes, were investigated for the usual causes (drugs, foods, insect stings etc.) without satisfactory results. All were atopic by history and/or allergy skin testing. Inhalation challenges, using nebulized common inhalant allergens to which the patients were positive by skin tests, were performed to test whether such inhaled allergens could be causing the anaphylactic episodes. Four of the eight patients developed anaphylactic episodes similar to the spontaneous attacks. Two of the other four patients developed precipitous asthma with some suggestion of non-pulmonary anaphylactic features. It is suggested that inhaled allergens may be a common cause of recurrent anaphylaxis where other recognized causes have been excluded.

Adolescent↗
PubMed1978

Release of mediators of anaphylaxis: inhibition of prostaglandin synthesis and the modification of release of slow reacting substance of anaphylaxis and histamine.

1 When isolated perfused lungs from sensitized guinea-pigs were challenged with antigen, histamine, slow reacting substance of anaphylaxis (SRS-A) and prostaglandin-like substances were released into the effluent. 2 Treatment of the lungs before and during challenge with indomethacin (0.5--10 microgram/ml), sodium aspirin (1--10 microgram/ml), sodium meclofenamate (0.1--1 microgram/ml) or ketoprofen (0.5--5 microgram/ml) inhibited the release of prostaglandins while increasing the output of histamine and SRS-A between three- and five-fold. 3 Diethylcarbamazine (0.2--1 mg/ml) reduced the release of SRS-A and histamine but increased the amount of prostaglandin-like substances produced. 4 Eicosatetraynoic acid (10 microgram/ml) inhibited formation of prostaglandins but did not modify release of histamine and SRS-A. 5 The results with non-steroid anti-inflammatory drugs and diethylcarbamazine suggest that prostaglandins, or some other product of the cyclo-oxygenase system, depress the anaphylactic release of SRS-A and histamine.

5,8,11,14-Eicosatetraynoic Acid↗