Marie-Thérèse Guinnepain

Exercise-Induced Anaphylaxis: Useful Screening of Food Sensitization

BACKGROUND AND OBJECTIVES Exercise-induced anaphylaxis is a well-defined entity as described by Sheffer and Austen. Exercise-induced anaphylaxis can be associated with ingestion of a specific food. We report our experience with a series of cases of exercise-induced anaphylaxis in which anaphylaxis was considered to be associated with food allergy. METHODS We observed 19 patients in whom severe systemic signs of anaphylaxis occurred during or immediately after exercise, while the severity of reactions excluded challenge testing. The causal relationship with various foods was systematically investigated in all cases, even in the absence of any history of allergy. RESULTS Sensitization to wheat flour was demonstrated in 12 patients, to peanut in seven, and to tree nuts in six cases with skin tests and/or RAST. Sensitivity to various other foods was found less often. Further, avoidance of specific foods according to results of skin tests and RAST was systematically observed during the five hours prior to exercise and no symptom occurred, suggesting a role of specific food intake in the pathogenesis of exercise-induced anaphylaxis. With such elimination diets, most of these young patients were able to engage in regular vigorous exercises (more than twice a week in some cases) without any clinical manifestation with a median followup of 2 years. In two patients, however, recurrence of exercise-induced anaphylaxis was subsequently explained by concomitant ingestion of other foods such as rice and peanut. Additional avoidance of these foods before exercise was then effective in 14 cases (median follow up: 2 years). CONCLUSIONS Investigations to detect food sensitization, in particular to wheat, peanut and/or tree nuts, and specific avoidance of these foods five hours before exercise appear essential in cases of exercise-induced anaphylaxis.

Human Basophils Express the Glycosylphosphatidylinositol-Anchored Low-Affinity IgG Receptor FcγRIIIB (CD16B)

Basophils express not only high-affinity IgE receptors, but also low-affinity IgG receptors. Which, among these receptors, are expressed by human basophils is poorly known. Low-affinity IgG receptors comprise CD32 (FcγRIIA, FcγRIIB, and FcγRIIC) and CD16 (FcγRIIIA and FcγRIIIB). FcγRIIA, FcγRIIC, and FcγRIIIA are activating receptors, FcγRIIB are inhibitory receptors, FcγRIIIB are GPI-anchored receptors whose function is poorly understood. Basophils were reported to express FcγRII, but not FcγRIII. We aimed at further identifying basophil IgG receptors. Basophils from normal donors and from patients suffering from an allergic skin disease (atopic dermatitis), allergic respiratory diseases (allergic rhinitis and asthma), or a nonallergic skin disease (chronic urticaria) were examined. We found that normal basophils contain FcγRIII transcripts and express FcγRIIIB, but not FcγRIIIA, which were detected on 24–81% basophils from normal donors and on 12–100% basophils from patients. Noticeably, the proportion of FcγRIIIB+ basophils was significantly lower in atopic dermatitis patients than in other subjects. This decreased FcγRIII expression was not correlated with an activated phenotype of basophils in atopic dermatitis patients, although FcγRIIIB expression was down-regulated upon basophil activation by anti-IgE. Our results challenge the two dogmas 1) that basophils do not express FcγRIII and 2) that FcγRIIIB is exclusively expressed by neutrophils. They suggest that a proportion of basophils may be lost during enrichment procedures in which FcγRIII+ cells are discarded by negative sorting using anti-CD16 Abs. They unravel an unexpected complexity of IgG receptors susceptible to modulate basophil activation. They identify a novel systemic alteration in atopic dermatitis.

Angioedema associated with C1 inhibitor deficiency.

ConclusionAngioedema associated with C1 INH deficiency requires diagnosis as soon as the first symptoms of the disease are manifest, and laboratory measurement of complement component levels at the least suspicion, in order to institute preventive and curative treatments. However, different clinical, laboratory, and genetic forms of this disease account for the diversity in the indications for treatment.