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The current management of a primary IgE-mediated peanut allergy consists of the two basic pillars “exposure prophylaxis” with avoidance of the allergen and “emergency therapy” with short-term treatment of an acute allergic reaction after accidental ingestion. Accidental reactions are common despite attempted avoidance. The severity of an allergic or even anaphylactic reaction after accidental ingestion is difficult to assess prior to reaction. In addition, reaction thresholds may vary depending on the accompanying augmentation factor. Therefore, every peanut allergic patient should receive individual dietary counseling as well as instructions for the use of the emergency kit and a structured patient education program (anaphylaxis group training), if necessary. For the first time, since fall 2021 a causal treatment option with a drug for oral immunotherapy will now be available for 4‑ to 17-year-old peanut-allergic children and adolescents. The oral immunotherapy with peanut protein as defatted powder of Arachis hypogaea L., semen (peanuts) leads to desensitization with a good efficacy record and an acceptable safety profile. Other treatment options with different therapeutic approaches are also under development and will probably expand the range for treatment in the coming years.
Genetic factors and mechanisms underlying food allergy are largely unknown. Due to heterogeneity of symptoms a reliable diagnosis is often difficult to make. Here, we report a genome-wide association study on food allergy diagnosed by oral food challenge in 497 cases and 2387 controls. We identify five loci at genome-wide significance, the clade B serpin (SERPINB) gene cluster at 18q21.3, the cytokine gene cluster at 5q31.1, the filaggrin gene, the C11orf30/LRRC32 locus, and the human leukocyte antigen (HLA) region. Stratifying the results for the causative food demonstrates that association of the HLA locus is peanut allergy-specific whereas the other four loci increase the risk for any food allergy. Variants in the SERPINB gene cluster are associated with SERPINB10 expression in leukocytes. Moreover, SERPINB genes are highly expressed in the esophagus. All identified loci are involved in immunological regulation or epithelial barrier function, emphasizing the role of both mechanisms in food allergy.