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At least 19 recordsLinked to original sources

Serial use of aprotinin and incidence of allergic reactions.

Allergic reactions to aprotinin, a polypeptide, have been reported on several occasions. A survey of 136 courses of aprotinin, given to patients with gastric cancer as a protease inhibitor, has shown an incidence of less than 1% of acute anaphylaxis and a similar incidence of minor allergic responses. Two cases of acute allergic responses are described. Fifteen patients received repeated courses of aprotinin at 6-weekly intervals and no allergic phenomena were detected. Provided patients are challenged intra-dermally or with eye drops before each course, it is considered that aprotinin is safe to use in repeated fashion.

Aprotinin↗

Management of immediate allergic reactions.

Allergic and pseudoallergic reactions can be associated with all drug classes used in dental practice. A thorough medical history is essential to avoid challenging a patient with an agent for which they have proven intolerance. Despite this precaution, the dentist must be prepared to manage an immediate reaction, should it occur. In all cases, management should begin with standard ABC assessment and oxygen supplementation. The administration of either diphenhydramine or epinephrine is predicated on the severity of the reaction. Suggestions regarding dosages and routes of administration are summarized in Table 4. The duration of action for epinephrine is relatively brief (10 to 30 minutes), and dosages may need to be repeated if symptoms recur. Following stabilization, patients who have experienced anaphylactoid reactions should be transported by EMS to the closest emergency room for definitive management. A treatment algorithm summarizing management of allergic reactions is presented in Figure 1.

Adrenergic Agonists↗

Successful re-treatment with cis-dichlorodiammineplatinum(II) after apparent allergic reactions.

Allergic or anaphylactic-like reactions have been reported with cis-dichlorodiammineplatinum(II) (CDDP) administration. We have seen two reactions among 50 patients treated in a phase II trial of CDDP. Both patients were successfully rechallenged after diphenhydramine pretreatment, and therapy was continued. In vivo and in vitro studies performed in one patient included negative skin tests, negative histamine release assay, negative lymphocyte stimulation studies, and normal total serum IgE. We conclude that some apparent allergic reactions occurring with CDDP may have a non-allergic etiology, and treatment may be successfully continued in selected patients.

Adult↗

[Photosensitivity following enoxacin and xipamide: combined phototoxic and photo-allergic reaction to enoxacin, photo-allergic reaction to xipamide with subsequent transient light reaction].

In a 51-year-old female patient, we observed a combined phototoxic and photoallergic reaction to Enoxacin, a photoallergic reaction to Xipamide, as well as increased sensitivity to light after withdrawal of the drugs. This unusual diagnosis was based on the clinical picture, graded radiation with UV-A and UV-B, the irradiated intradermal assay, and histological findings. To the best of our knowledge, this is the first report on a photoallergic reaction to Xipamide associated with a combined phototoxic and photoallergic reaction to Enoxacin.

Biopsy↗

Allergic reactions to Erwinia asparaginase in children with acute lymphoblastic leukemia who had previous allergic reactions to Escherichia coli asparaginase.

BACKGROUND: Escherichia coli asparaginase is an active antileukemia agent in the treatment of childhood acute lymphoblastic leukemia. Allergic reactions occurred in 31 of 125 patients (24.8%) treated with weekly high-dose (25,000 IU/m2) intramuscular E. coli asparaginase and necessitated discontinuation of the drug. METHODS: The authors evaluated the toxic effects of Erwinia asparaginase in the 31 children who had allergic reactions to the E. coli preparation. RESULTS: Subsequent allergic reactions to Erwinia asparaginase occurred in 7 of the 31 children (22.6%). In contrast to previous reports with intravenous administration, most allergic reactions to both asparaginase preparations were characterized by mild urticaria that responded to use of diphenhydramine; none of the reactions was life-threatening. CONCLUSIONS: In summary, the authors found Erwinia asparaginase to be an acceptable substitute for E. coli asparaginase for most children who had allergic reactions. Through the use of both E. coli and Erwinia asparaginase, 94% of children could receive their intended asparaginase.

Adolescent↗

Fetal distress during a maternal systemic allergic reaction.

Systemic allergic reactions to food ingestion rarely result in life-threatening situations. When these reactions occur during pregnancy, however, the accompanying physiologic changes may result in fetal distress. A case of repetitive late decelerations in the fetal heart rate during a maternal allergic reaction is presented. Prompt and aggressive medical management brought about total resolution of maternal and fetal compromise.

Adult↗

Recombinant Mycobacterium bovis BCG producing IL-18 reduces IL-5 production and bronchoalveolar eosinophilia induced by an allergic reaction.

BACKGROUND: Allergic reactions occur through the exacerbated induction of a Th2 cell type expression profile and can be prevented by agents favoring a Th1 profile. Bacillus Calmette-Guérin (BCG) is able to induce high IFN-gamma levels and has been shown to decrease experimentally induced allergy. The induction of IFN-gamma is mediated by interleukin (IL)-12 known to be secreted upon mycobacterial infections and can be enhanced by IL-18 acting in synergy with IL-12. OBJECTIVE: We evaluated the ability of a recombinant BCG strain producing IL-18 (rBCG) to modify the Th2 type responses in a murine model of ovalbumin (OVA)-dependent allergic reaction. METHODS: Mice were injected intraperitoneally or intranasally with OVA at days 0 and 15 and exposed to an OVA aerosol challenge at days 29, 30, 31 and 34. At days 0 and 15, two additional groups of mice received OVA together with 5 x 10(6) colony forming units of either rBCG or nonrecombinant BCG. RESULTS: A time-course analysis of OVA-specific immunoglobulin (Ig)E, IgG1 and IgG2a levels indicated no significant difference between the three groups of mice. However, following in vitro stimulation with OVA, lymph node cells from rBCG-treated mice produced less IL-5 and more IFN-gamma than those of mice injected with nonrecombinant BCG. In addition, 48 h after the last OVA challenge, a strong reduction of bronchoalveolar eosinophilia was found in the rBCG-injected mice compared to the nontreated or nonrecombinant BCG-treated groups. CONCLUSION: These results indicate that the production of IL-18 by rBCG may enhance the immunomodulatory properties of BCG that suppress pulmonary Th2 responses and, in particular, decrease airway eosinophilia.

Animals↗

Mechanisms of acute allergic reactions.

Acute allergic reactions range from mild conditions of local tissue swelling and pruritus to severe multisystem syndromes including asthma, urticaria and/or angioedema, gastrointestinal distress, and vascular collapse. Such reactions share a common pathophysiology characterized by vasodilation and postcapillary permeability, resulting in increased extravasation of fluid within minutes after exposure to an eliciting substance. Smooth muscle contraction of the respiratory or gastrointestinal tracts may also be involved. Most of these changes can be explained by the release of chemical mediators from circulating basophilic leukocytes and tissue mast cells. Human basophils and mast cells can be activated to release chemical mediators by several known pathways: crosslinking by allergens of specific immunoglobulin E antibodies attached to basophils and mast cells; anaphylatoxin formation following immune complex activation of the classical complement pathway; anaphylatoxin formed from direct activation of the alternative complement pathway by negatively charged surfaces; non-complement-, non-antibody-mediated direct histamine release; and idiosyncratic mechanisms involving physical exercise, psychological stress, or aspirin intolerance. Any or all of these mechanisms could be operative in patients experiencing acute allergic reactions at the commencement of hemodialysis.

Anaphylaxis↗

Allergic reactions to drugs.

Allergic reactions can result from virtually any drug. In the pharmacopeia the possibility of an allergic reaction to a drug must be considered in any instance when a patient reports an adverse effect to a drug. Although most allergic reactions to drugs are mild, they may be severe and at times fatal. Thus, it is imperative that every physician understand the spectra of drug allergy, the methods for diagnosing, and the means of treating allergic reactions to drugs. This review places drug allergies within the context of the over-all spectra of adverse reaction to drugs, defines the spectra of allergic reactions in terms of the organ systems involved and the severity of the reactions, suggests mechanisms for diagnosing drug allergy by historical evaluation, and where possible, by skin testing procedures and provocative dose challenges, and provides a variety of methods for reintroduction of drugs to which patients have been demonstrated to be allergic. The most important aspect of allergic reactions to drugs, however, is the understanding on the part of the physician that any drug has the potential for causing an allergic reaction and that extreme vigilance in terms of the diagnosis and treatment of these reactions is necessary.

Desensitization, Immunologic↗

IgE reactivity to vaccine components in dogs that developed immediate-type allergic reactions after vaccination.

Allergic reactions after vaccination are considered as an important practical problem in dogs; however, their immunological mechanism has not been well understood. The present study was designed to investigate the relationship between IgE reactivity to the vaccines and immediate-type allergic reactions after vaccination in dogs. Sera from 10 dogs that developed immediate-type allergic reactions such as circulatory collapse, cyanosis, dyspnea, facial edema, and vomiting within 1h after vaccination with non-rabies monovalent or combined vaccines and sera from 50 dogs that did not develop allergic reactions after vaccination were collected. Serum IgE reactivity to the injected vaccines was measured by fluorometric ELISA using a mouse monoclonal anti-dog IgE antibody. Then, IgE reactivity to fetal calf serum (FCS) and stabilizer proteins (gelatin, casein, and peptone) included in the vaccines was measured in sera that had high levels of IgE to the vaccines. Levels of serum specific IgE to the vaccines in dogs with immediate-type allergic reactions (59-4173 fluorescence units [FU], mean +/- S.D.: 992.5 +/- 1181.9 FU) were significantly higher than those in control dogs (38-192 FU, 92.4 +/- 43.3 FU) (P < 0.001). Of the eight dogs that developed immediate-type allergic reactions and had high levels of serum specific IgE to the vaccines, seven had specific IgE directed to FCS. The IgE reactivity to the vaccines in sera from these dogs was almost completely inhibited by FCS. The other one dog had serum IgE directed to gelatin and casein included in the vaccine as stabilizers. The results obtained in this study suggest that immediate-type allergic reactions after vaccination in dogs were induced by type I hypersensitivity mediated by IgE directed to vaccine components. In addition, FCS, gelatin, and casein included in vaccines could be the causative allergens that induced immediate-type allergic reactions after vaccination in dogs.

Animals↗

Induction of allergic reactions in guinea pigs with purified house dust mite allergens.

To establish a guinea pig model for house dust mite allergy with purified mite allergens, we studied the immune response to two major mite allergens, native Der f 1 (nDer f 1) and recombinant Der f 2 (rDer f 2) and crude mite extract in Hartley guinea pigs. Animals were immunized with either mite extract, nDer f 1 or rDer f 2, four times at 2- to 3-week intervals. Then the guinea pigs were examined as to the status of sensitization to the sensitizing antigen. Intradermal injection of mite antigens to mite extract-, nDer f 1-, and rDer f 2-sensitized animals induced both immediate and late-phase cutaneous reactions. Allergic airway disease was also provoked by the intranasal instillation of rDer f 2 or mite extract. Anti-nDer f 1 and -rDer f 2 IgE as well as anti-mite extract IgE were produced in the sensitized guinea pigs and IgE titer for three mite antigens were comparable. We concluded that immunization of Hartley guinea pigs with nDer f 1 and rDer f 2 achieved sensitization to mite allergens, which was comparable to that obtained by the immunization with mite extract. A mite-allergic model suitable for immunological and pharmacological studies was established from rDer f 2-sensitized guinea pigs.

Allergens↗

[Immune response and pathophysiology of the allergic reaction].

The allergic immune response is characterized by a number of cellular and molecular interactions. Allergens are taken up through the respiratory or digestion tract or the skin by dendritic cells, B cells or macrophages. After phagocytoses and processing, fragments of allergens are presented to the allergen-specific T cells. By this process, allergen-reactive T cells are induced, which are predominantly of the Th2 type and which secrete the cytokines IL-4, IL-5 and IL-10. In contrast, during a normal immune response to bacterial or viral allergens, T cells of the Th1 type are induced, which produce IFN gamma and IL-2 but not Th2 cytokines. A direct contact of Th2 cells with B cells results in activation of B cells. The Th2 cytokine IL-4 instructs B cells to switch from IgM to IgE antibody production. IgE antibodies play a central role in the induction of allergic diseases. IgE antibodies are taken up by basophils and mast cells by virtue of high-affinity receptors for IgE on these cells. Allergen confrontation leads to the activation of such IgE-sensitized cells, which results in the release of various mediators such as histamine, leukotrienes and prostaglandins; together, they induce the clinical manifestations of allergic reactions. Recent findings have shown that mast cells (and basophils) from atopic tissue are able to produce cytokines such as IL-4 and can thereby induce IgE antibody production. IL-5 generated by allergen-reactive Th2 cells attracts and activates eosinophils, which are responsible for tissue destruction in allergic asthma.(ABSTRACT TRUNCATED AT 250 WORDS)

Allergens↗