An evaluation of the sensitivity of subjects with peanut allergy to very low doses of peanut protein: A randomized, double-blind, placebo-controlled food challenge study (original) (raw)
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Peanut allergy: An increasingly common life-threatening disorder
Journal of the American Academy of Dermatology, 2012
Allergic reactions to peanuts in children have become a significant medical and legal concern worldwide, with a rising incidence of this potentially fatal condition. Peanut allergy represents an immunoglobulin E (IgE)emediated hypersensitivity reaction to peanut proteins and is responsible for the majority of cases of food-induced anaphylaxis. Even trace quantities of peanut in a sensitized individual can be fatal, with rapid onset of symptoms often including the cutaneous findings of urticaria, angioedema, or a diffuse nonspecific dermatitis. Peanut allergy is usually a lifelong condition, since only about 20% of affected individuals outgrow it. Some schools ban peanut butter and jelly sandwiches, once a common dietary option, as fear of medical and legal consequences is escalating. Children with peanut allergy and their families should be knowledgeable about management strategies, including carrying and properly administering self-injectable epinephrine. New immunotherapeutic options are being investigated and appear promising.
Current Controversies and Future Prospects for Peanut Allergy Prevention, Diagnosis and Therapies
Journal of Asthma and Allergy
Peanut allergy has increased substantially in the past few decades, both in developed and developing countries. Peanut allergy has become a major public health concern, affecting up to 1 in 50 children, with repercussions for school and airline policies. Recent research findings have shown that, contrary to the long-standing teaching of "delayed" introduction of allergens, early introduction of peanut protein is of benefit as an allergy prevention strategy, especially in high-risk cases. Ideal dose, frequency and duration of "proactive" peanut therapy for maximum protection remain to be determined in order for it to become acceptable and practical on a large scale. Logistics around widespread screening of high-risk patients remain complex. The correct diagnosis of peanut allergy is crucial and diagnostic tests have been fine-tuned in the past 2 decades in order to help differentiate true allergy from false-positive sensitization through cross-reactivity. Component-resolved diagnostics have become routinely available, and the use of basophil activation tests has increased, although standardization and availability remain issues. Future tests, including epitope testing and histamine-release assays, promise to be even more specific in ruling out false positives and reducing the need for incremental food challenges. Stringent peanut avoidance and prompt treatment of reactions remain the cornerstone of treatment. The concept of exposing the allergic body to small amounts of peanut protein in a cautious, orderly, escalating fashion in the form of desensitization has been widely applied in the past 10-15 years, mainly in the research domain, but of late spilling over into everyday practice. However, desensitization does not equate to a cure, and has significant safety concerns and practical ramifications; probably requiring lifelong-controlled peanut ingestion for ongoing protection. Further strategies to enhance the safety and efficacy of immunotherapy are under exploration, many with a non-specific immune-modifying effect. Despite recent advances in peanut allergy, we still need to go back to basics with accurate diagnosis, nutritional counselling, well-organized allergy action plans and accessible emergency kits.
Rising prevalence of allergy to peanut in children: Data from 2 sequential cohorts
Journal of Allergy and Clinical Immunology, 2002
Background: Allergy to peanut is common. However, it is not known whether the prevalence of sensitization and clinical allergy to peanut is increasing. Objective: We sought to determine any change in the prevalence of peanut sensitization and reactivity in early childhood in 2 sequential cohorts in the same geographic area 6 years apart. Methods: Of 2878 children born between September 1, 1994, and August 31, 1996, living on the Isle of Wight, 1273 completed questionnaires, and 1246 had skin prick tests at the age of 3 to 4 years. Those with positive skin prick test responses to peanut were subjected to oral peanut challenges, unless there was a history of immediate systemic reaction. These data were compared with information on sensitization and clinical allergy to peanut available from a previous cohort born in 1989 in the same geographic area. Results: There was a 2-fold increase in reported peanut allergy (0.5% [6/1218] to 1.0% [13/1273]), but the difference was nonsignificant (P = .2). Peanut sensitization increased 3-fold, with 41 (3.3%) of 1246 children sensitized in 1994 to 1996 compared with 11 (1.1%) of 981 sensitized 6 years ago (P = .001). Of 41 sensitized children in the current study, 10 reported a convincing clinical reaction to peanut, and 8 had positive oral challenge results, giving an overall estimate of peanut allergy of 1.5% (18/1246). Conclusions: Sensitization to peanut had increased between 1989 and 1994 to 1996. There was a strong but statistically nonsignificant trend for increase in reported peanut allergy. (J Allergy Clin Immunol 2002;110:784-9.)
Acta Clinica Belgica, 2016
Peanut allergy shows distinct clinical patterns that can be predicted by component resolved diagnosis. However data about peanut sensitization profiles in populations with a broad agestratification are scarce. Methods Sera of 89 peanut allergic patients (age 1-70 years), 21 infants (< 1y) with atopic dermatitis (AD) sensitized to peanut, 24 age matched peanut tolerant individuals with positive sIgE to peanut and 15 healthy individuals were tested for sIgE reactivity to rAra h 1, rAra h 2, rAra h 3, rAra h 8, rAra h 9 and rBet v 1 (FEIA ImmunoCAP, Thermo Fisher Scientific). Results In infants with AD, Ara h 1, Ara h 2 and Ara h 3 enabled to explain 14/21 (67%) of peanut sensitizations. No sensitization to Ara h 8 or Bet v 1 was observed. Patients with generalized reactions were more frequently sensitized to Ara h 1, Ara h 2 and Ara h 3 compared to patients with an oral allergy syndrome (OAS) and peanut tolerant patients. Sensitization to Ara h 8 was significantly more observed in patients with an OAS. Ara h 2 showed to be the best marker to distinguish patients with generalized reactions from patients with an OAS and/or peanut sensitized patients but tolerating the legume. Conclusion Faber et al., 4 Sensitization to Ara h 1, Ara h 2 and Ara h 3 can have early onset and is predominantly associated with a more severe outcome. Ara h 2 is the best marker of a generalized peanut allergy.