These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology (AAAAI); the American College of Allergy, Asthma & Immunology (ACAAI); and the Joint Council of Allergy, Asthma and Immunology. The AAAAI and the ACAAI have jointly accepted responsibility for establishing "Stinging insect hypersensitivity: a practice parameter update II." Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or the ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology. This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. These parameters are not designed for use by pharmaceutical companies in drug promotion. The Joint Task Force understands that the cost of diagnostic tests and therapeutic agents is an important concern that may appropriately influence the work-up and treatment chosen for a given patient. The Joint Task Force recognizes that the emphasis of our primary recommendations regarding a medication may vary, for example, depending on third party payer issues and product patent expiration dates. However, since a given test or agent's cost is so widely variable, and there is a paucity of pharmacoeconomic data, the Joint Task Force generally does not consider cost when formulating Practice Parameter recommendations. In extraordinary circumstances, when the cost benefit of an intervention is prohibitive as supported by pharmacoeconomic data, commentary may be provided.

In the late 1960s, IgE was isolated and characterized and found to have "reaginic" activity. The term reagin was used to identify the immunologic mediator of immediate hypersensitivity reactions. Reaginic antibodies were detected by the Prausnitz-Küstner (PK) reaction. This test was performed by passively sensitizing the skin of a nonallergic recipient with an intradermal injection of serum of an allergic person and challenging the test site 24 to 48 hours later with an injection of an allergen extract. An immediate wheal and flare reaction indicated a positive test. Before IgE was identified, IgA was thought to be the carrier of reaginic activity.The experiments described in this abstract were done after ragweed-specific IgE had been identified. The purpose was to determine whether reaginic antibodies reacting with other allergens were also IgE. The results indicated that a wide variety of allergic models—pollen, dust, food, insects, and drugs—were also mediated by allergen-specific IgE.Over the past 40 years, very refined techniques have evolved for detection and quantitation of allergen-specific IgE. It is the well documented mediator of immediate hypersensitivity reactions. Immune modifiers (omalizumab) have been developed and can decrease serum levels of allergen-specific IgE, providing clinical benefit.In retrospect, the data described in the abstract 40 years ago were the forerunners of the now well-recognized clinical significance of allergen-specific IgE. In the late 1960s, IgE was isolated and characterized and found to have "reaginic" activity. The term reagin was used to identify the immunologic mediator of immediate hypersensitivity reactions. Reaginic antibodies were detected by the Prausnitz-Küstner (PK) reaction. This test was performed by passively sensitizing the skin of a nonallergic recipient with an intradermal injection of serum of an allergic person and challenging the test site 24 to 48 hours later with an injection of an allergen extract. An immediate wheal and flare reaction indicated a positive test. Before IgE was identified, IgA was thought to be the carrier of reaginic activity. The experiments described in this abstract were done after ragweed-specific IgE had been identified. The purpose was to determine whether reaginic antibodies reacting with other allergens were also IgE. The results indicated that a wide variety of allergic models—pollen, dust, food, insects, and drugs—were also mediated by allergen-specific IgE. Over the past 40 years, very refined techniques have evolved for detection and quantitation of allergen-specific IgE. It is the well documented mediator of immediate hypersensitivity reactions. Immune modifiers (omalizumab) have been developed and can decrease serum levels of allergen-specific IgE, providing clinical benefit. In retrospect, the data described in the abstract 40 years ago were the forerunners of the now well-recognized clinical significance of allergen-specific IgE.

Allergic reactions to insulin are no longer a problem since replacement of animal-derived (bovine, porcine) insulins by human insulin. The relationship between the clinical reactions and the immunologic responses described in this abstract has significant current application to successful drug "desensitization" recommended for treatment of people who have prior suspected IgE-mediated allergic drug reactions.The reported patient initially had an allergic reaction to bovine insulin, mediated by IgE antibodies. Subsequently, she developed insulin resistance, which is mediated by high titers of insulin-specific IgG and necessitating extremely large doses of insulin for diabetic control. At that time, the allergic symptoms disappeared despite persistence of insulin-specific IgE. These observations suggest that the insulin-specific IgG also acted as a protective or blocking antibody, preventing the insulin-IgE antibody reaction and resulting allergic manifestations. This IgG antibody function is at least one suggested mechanism responsible for subsequent drug tolerance when people who have had prior suspected IgE-mediated allergic reactions are treated with a desensitization regime. In addition, there are similar corollaries, perhaps not as definitive, to successful venom immunotherapy and immunotherapy for inhalant allergens.Another relevant finding in this case is the difference in the persistence of IgE and IgG antibodies in the absence of drug exposure. Re-exposure to very small amounts of insulin on 2 occasions, about 8 months after daily insulin therapy was stopped, resulted in allergic reactions. At that time, insulin-specific IgE was still present (1 reaction was due to an insulin skin test—not in abstract). Insulin-specific IgG was present in very low titer about 8 months previously. These observations support the current recommendations that people who have had allergic drug reactions will need repeat desensitization each time the drug is prescribed.Also of interest was the detection of low titers of transient insulin-specific IgA and IgM. The significance of these antibodies is unknown, although there are similar findings in people with other allergies, such as ragweed pollen.This case study is an important contribution to defining the clinical approach and understanding the immunopathogenesis for successful drug tolerance for treatment of people with prior allergic reactions. Allergic reactions to insulin are no longer a problem since replacement of animal-derived (bovine, porcine) insulins by human insulin. The relationship between the clinical reactions and the immunologic responses described in this abstract has significant current application to successful drug "desensitization" recommended for treatment of people who have prior suspected IgE-mediated allergic drug reactions. The reported patient initially had an allergic reaction to bovine insulin, mediated by IgE antibodies. Subsequently, she developed insulin resistance, which is mediated by high titers of insulin-specific IgG and necessitating extremely large doses of insulin for diabetic control. At that time, the allergic symptoms disappeared despite persistence of insulin-specific IgE. These observations suggest that the insulin-specific IgG also acted as a protective or blocking antibody, preventing the insulin-IgE antibody reaction and resulting allergic manifestations. This IgG antibody function is at least one suggested mechanism responsible for subsequent drug tolerance when people who have had prior suspected IgE-mediated allergic reactions are treated with a desensitization regime. In addition, there are similar corollaries, perhaps not as definitive, to successful venom immunotherapy and immunotherapy for inhalant allergens. Another relevant finding in this case is the difference in the persistence of IgE and IgG antibodies in the absence of drug exposure. Re-exposure to very small amounts of insulin on 2 occasions, about 8 months after daily insulin therapy was stopped, resulted in allergic reactions. At that time, insulin-specific IgE was still present (1 reaction was due to an insulin skin test—not in abstract). Insulin-specific IgG was present in very low titer about 8 months previously. These observations support the current recommendations that people who have had allergic drug reactions will need repeat desensitization each time the drug is prescribed. Also of interest was the detection of low titers of transient insulin-specific IgA and IgM. The significance of these antibodies is unknown, although there are similar findings in people with other allergies, such as ragweed pollen. This case study is an important contribution to defining the clinical approach and understanding the immunopathogenesis for successful drug tolerance for treatment of people with prior allergic reactions.

The American Academy of Allergy, Asthma and Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) have jointly accepted responsibility for establishing the ‘‘Stinging insect hypersensitivity: A Practice Parameter Update.’’ Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or the ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology.

Allergic reactions to insect stings are a common and often serious medical problem. Estimates of the incidence in the general population of anaphylaxis caused by insect stings over a specified period range from 0.3 to 3 percent13. Some episodes are fatal4. People at risk for anaphylaxis often make substantial changes in their lifestyles and are fearful of subsequent exposure to insects.Over the past 15 years, our understanding of the natural history of allergy to insect stings has grown, purified venoms have become available, and methods of measuring serum venom-specific IgE and IgG have been developed for . . .

Good medical practice is based on the integration of in vivo and in vitro laboratory findings with a carefully performed history and physical examination.However, in some patients, diagnosis of allergic disease and recommendations for allergy injection treatment have been made by laboratories remote from the patient examination.This report describes a comparison of such approaches with usual medical practice in the same patients, as evaluated by highly respected observers.

and the con stant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions.This is particularly important when the recommended agent is a new and/or infrequently employed drug.

Intradermal skin tests with varying concentrations of honeybee, yellow jacket, white-faced hornet, yellow hornet, and Polistes venoms were done on 85 patients with histories of insectsting anaphylaxis and on 56 insect-nonallergic subjects. Positive skin tests (wheal ⩾ 5 to 10 mm and flare ⩾ 11 to 20 mm) were present in 67 insect-allergic patients at venom concentrations ranging from 0.001 μg/ml to 0.1 μg/ml. Seven additional allergic patients had positive skin tests with the 1.0 μg/ml venom concentration. Twenty-six nonallergic subjects had positive skin tests at the venom concentration of 1.0 μg/ml, and two patients had positive skin tests at the lower venom concentrations (0.001 to 0.1 μg/ml). These results confirm venom skin tests as a highly sensitive method of detecting venom-specific IgE in the evaluation of patients with stinging-insect hypersensitivity. Since a large percentage of insect-nonallergic subjects reacted to the 1.0 μg/ml concentration, clinical judgment and further in vitro testing should be considered in the evaluation of patients who react only at this venom concentration.

This case report demonstrates the lack of correlation between clinical sensitivity to insect venoms and immunologic reactivity as indicated by the presence of venom-specific IgE. A 20-yr-old venom collector was monitored over a 3-yr period with measurements of venom-specific IgE (skin test and RAST) and venom-specific IgG. In the first year of venom collection, multiple stings were tolerated with no reaction. In the second season, she had an anaphylactic reaction after a yellow jacket sting. Subsequently, there was a rising titer of serum yellow jacket and bee venom-specific IgE and positive skin-test reactions. In the third season, yellow jacket, hornet, and bee venom skin tests remained positive and serum IgE antibody titers remained elevated. Stings from all three insects were tolerated with no reaction. Throughout the 3-yr course, serum venom-specific IgG remained low and unchanged. The factors other than IgE-modulating clinical anaphylaxis, perhaps responsible for this clinical and immunologic dichotomy, are unknown. These observations add a further complication to the choice of patients for venom immunotherapy.