Stinging insect hypersensitivity: a practice parameter update 2011

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.     

Stinging and biting insect allergy: an Australian experience.

BACKGROUND: Stings and bites from various insects are responsible for many anaphylactic events. OBJECTIVE: To document the clinical features of specific forms of anaphylaxis and investigate clinical concerns regarding stinging and biting insect allergy. METHODS: All patients presenting for evaluation of adverse reactions to insect stings or bites between December 1980 and December 1997 had the clinical details of their reactions recorded and their reactions classified. RESULTS: The spectrum of clinical symptoms and signs is similar to that seen in anaphylaxis from other sources; stings on the head or neck are not more likely to cause life-threatening reactions than stings elsewhere on the body; a lesser reaction will not necessarily lead to a more serious reaction from a future sting; asthmatic patients do appear to have an increased risk of asthma as a feature of their anaphylactic response; anaphylaxis is usually confined to a particular insect species for the individual patient; patients who have had multiple stings at one time may have experienced true anaphylaxis and not a "toxic" response; and patients who have had anaphylaxis from other sources are at no greater risk than that of the general population of reacting similarly to insect stings or bites. CONCLUSIONS: Anaphylactic events from insect stings show the same clinical features as those from other sources. Systemic reactions seem confined to a specific insect species. Patients who experience RXN3 reactions from multiple stings at one time should undergo specific venom testing, because many have experienced true anaphylaxis and not a toxic response. Future consideration should be given to the role of beta-adrenergic antagonists and ACE inhibitors in patients with systemic reactions.     

Stinging insect allergy: sensitization to vespids in Madrid and surroundings

The study comprised 28 patients from the centre of Spain (Madrid and surroundings) who had suffered systemic reactions when stung by vespids. Specific IgE antibodies to Vespula spp. and Polistes spp. venoms were measured by RAST. All patients had positive RAST to Vespula venom and half of them also had positive RAST to Polistes venom. A patient can be sensitive to both venoms due to either a clinical sensitization to both venoms, or common antigenic determinants. To differentiate these states we used a RAST inhibition assay. We could inhibit Polistes RAST with either Polistes or Vespula venom to a similar degree. Inhibition of Vespula RAST was possible with Vespula venom, but only to a limited degree with Polistes venom. Direct RAST and RAST inhibition studies indicate that in our geographic region sensitization to Vespula venom is more common than to Polistes venom and Polistes might have cross-reactivity in our patients.     

Stinging insect allergy: Natural history and modification with venom immunotherapy

The natural history of stinging insect allergy and its modification by venom immunotherapy was investigated by follow-up observations of patients with histories of venom anaphylaxis and detectable venom-specific IgE. The patients were divided into three categories: (1) receiving venom immunotherapy, (2) declined venom immunotherapy, and (3) terminated venom immunotherapy. One hundred twenty-seven patients were evaluated after 6 mo to 9 yr of venom immunotherapy. Most received top venom doses of 50 μg of yellow jacket and/or honeybee venoms every 4 wk. There were 87 restings in 48 patients resulting in two systemic reactions, only one of which could be considered a treatment failure (1%). Fifty-six patients never received venom immunotherapy. In this group there were 40 restings in 28 patients with 14 systemic reactions (35%). In 88 patients who stopped venom immunotherapy, 61 restings in 41 patients led to 11 systemic reactions (17%). Patients with cardiovascular/or respiratory symptoms with initial sting anaphylaxis were at risk for subsequent reactions. With one exception, patients with hives and edema only as the initial reaction either had a similar or no reaction when they were restung. These results confirm the efficacy of venom immunotherapy but also suggest that there are factors other than the presence of venom-specific IgE modulating the occurrence of clinical anaphylaxis.     

Stinging insect allergy: Detection and clinical significance of venom IgE antibodies

Venom-specific IgE antibodies in 109 sera from patients who had had immediate systemic allergic reactions following insect stings were measured by the radioallergosorbent (RAST) procedure. The majority of sera contained IgE antibodies to either bee, yellow jacket, or hornet venoms. Some sera had positive RAST reactions with 2 or 3 venoms, but others contained single venom-specific IgE antibodies. Of 24 patients who had large local reactions, the sera of 12 contained venom IgE antibodies. The RAST procedure provides an accurate means of documenting IgE-mediated allergic sensitivity to stinging insects.     

A controlled trial of immunotherapy in insect hypersensitivity.

Insect hypersensitivity is currently treated by immunization using whole-body extracts. We compared this regimen with immunotherapy using insect venoms or placebo in groups of 20 patients matched for history and sensitivity, as judged by venom skin test, histamine release and IgE antibody to venom. After six to 10 weeks of immunization, systemic reactions to stings occurred in seven of 12, seven of 11, and one of 18 patients treated with placebo, whole-body extract, and venom, respectively. Placebo and whole-body extract gave similar results and were significantly less effective than venom immunotherapy (P less than 0.01). The 14 patients with failure of treatment with whole-body extract and placebo were subsequently provided with venom immunotherapy; one reacted to a subsequent sting. We conclude that venom immunotherapy is clinically superior to therapy on whole-body extract or placebo.     

Beta-lactams and Beta-lactamase-inhibitors in current- or potential-clinical practice: A comprehensive update

The use of successive generations of β-lactams has selected successive generations of β-lactamases including CTX-M ESBLs, AmpC β-lactamases, and KPC carbapenamases in Enterobacteriaceae. Moreover, this cephalosporin resistance, along with rising resistance to fluoroquinolones, is now driving the use of carbapenems and unfortunately the carbapenem resistance has emerged markedly, especially in Acinetobacter spp. due to OXA- and metallo-carbapenemases. The industry responded to the challenge of rising resistance and recently developed some novel β-lactams such as ceftobiprole, ceftaroline etc. and many β-lactam compounds, including β-lactamase-inhibitors, such as BMS-247243, S-3578, RWJ-54428, CS-023, SMP-601, NXL 104, BAL 30376, LK 157, and so on are under trials. This review provides the comprehensive accounts of the developments in penicillins, cephalosporins, carbapenems, and β-lactamase-inhibitors, and the insight about medicinal chemistry, mechanism(s) of action and resistance, potential strategies to overcome resistance due to β-lactamases, and also the recent advancements in the development of newer β-lactam compounds; some of which are still under trials and yet to be classified. This review will fill the gap since previously published reviews and will serve as a comprehensive update on the current topic.