Journal of Investigational Allergology and Clinical Immunology最新文献

Background and objectives: Background: Many fish-allergic patients only react to certain fish species and may tolerate others, mostly because of IgE-mediated recognition of specific epitopes on the major allergen parvalbumin. However, the considerable number of fish species consumed makes it challenging to identify which species are allergenic and which are tolerated by individual patients. Objective: In order to improve the diagnosis of fish allergy, we investigated IgE-mediated reactivity to parvalbumins from 12 freshwater fish species that are largely underrepresented in diagnostic tests.

Methods: Parvalbumins were purified from 12 freshwater fish species belonging to 8 families, and their isoform composition was analyzed using mass spectrometry. IgE specific for each parvalbumin was quantified in serum samples from 66 fish-allergic individuals, and basophil activation tests were performed for 5 patients. Crosswise inhibition assays were carried out for all parvalbumins for 7 patients to investigate cross-reactivity between the parvalbumins from the different species.

Results: IgE binding and cross-linking potency of the parvalbumins differed, with the strongest reactivities observed for 4 parvalbumins from the salmonid family (results positive for 89%-95% of patients) and the weakest for parvalbumins from Wels catfish, European eel, and tench (results negative for ≥50% of patients). Ninety percent of the patients with negative results for Wels catfish parvalbumin also had negative results for additional parvalbumins from multiple species. Inhibition assays revealed variable recognition of epitopes by several patients, with the primary sensitizers most frequently being parvalbumins from salmonids and percids.

Conclusions: Including freshwater salmonids in the diagnostic work-up for fish allergy may help to identify most fish-allergic patients. IgE to Wels catfish could help distinguish between polysensitized and oligosensitized patients.

The terms refractory anaphylaxis and near-fatal anaphylaxis have gained prominence in the last 5-10 years. Refractory anaphylaxis has a clinical justification in that patients often do not respond to successive doses of adrenaline. Near-fatal anaphylaxis facilitates the study of fatal anaphylaxis, which is 10 times less frequent. In terms of epidemiology, refractory anaphylaxis and near-fatal anaphylaxis overlap, since refractory anaphylaxis can prove fatal, and the more severe the anaphylaxis (including cardiorespiratory arrest), the greater the need for adrenaline and fluid infusion. However, no specific pathogenesis or treatment has been described for either condition. Consequently, these are not distinct clinical entities, but different manifestations of severity. The risk factors for both types of anaphylaxis are the same as those described for severe anaphylaxis, namely, patient age, cardiac and respiratory comorbidities, and the (controversial) role of ß-blockers and angiotensin-converting enzyme inhibitors. If volume expansion and adrenaline infusion prove ineffective, treatment is based on intubation, ventilation, intravenous vasopressors, and glucagon. Patients should be transferred to the intensive care unit. This review provides a panoramic epidemiologic vision of both manifestations of severe anaphylaxis. We conclude that they share many risk factors and often occur together in severe anaphylaxis. Therefore, each should be considered a manifestation of severe anaphylaxis.