D1.399 - Selective IgE Mediated Anaphylaxis to Gadobutrol and type I Kounis with tolerance to Gadoxetate Disodium

Background

Immediate hypersensitivity reactions to gadolinium based contrast agents (GBCAs) are rare, and their immunopathogenesis remains incompletely understood. While many reactions are attributed to non specific mast cell activation, increasing evidence supports IgE mediated mechanisms in selected patients. Cross reactivity patterns among structurally distinct GBCAs macrocyclic versus linear, ionic versus non ionic are insufficiently defined. Structural determinants potentially influencing hapten formation and antigenicity remain speculative. Coronary involvement during GBCA induced anaphylaxis is exceptionally reported.

Methods

We report a severe immediate reaction following intravenous administration of gadobutrol, a non ionic macrocyclic GBCA, acute and baseline serum tryptase were measured, alternative etiologies, including thromboembolism, infection, and structural cardiac disease, were excluded. Six weeks later allergological evaluation included skin prick tests (SPT) and intradermal tests (IDT) with gadobutrol, gadoterate meglumine (macrocyclic ionic), and gadoxetate disodium (linear ionic), carried out using a 1:10 dilution. Monitored intravenous drug provocation test (DPT) with gadoxetate disodium was performed.

Results

A 60 year old male without prior drug allergy developed generalized erythema, hypotensive syncope, hypoxemia, and cardiovascular collapse 15 minutes after gadobutrol exposure, requiring intensive care management including epinephrine.Acute tryptase reached 46.7 µg/L versus a baseline of 7.25 µg/L, transient troponin elevation occurred without ischemic ECG changes, consistent with type I Kounis syndrome secondary to anaphylaxis. SPT were negative for all tested agents. IDT was strongly positive to gadobutrol (20×16 mm) and negative to both gadoterate meglumine and gadoxetate disodium. Controlled DPT with gadoxetate disodium (5 mL) was fully tolerated.

Conclusion

This case provides compelling evidence of selective IgE mediated sensitization to gadobutrol with objective mast cell activation and secondary coronary involvement. The absence of cross reactivity and tolerance to gadoxetate disodium may be explained by structural differences affecting haptenization capacity and epitope presentation, particularly the non ionic macrocyclic configuration and side chain composition of gadobutrol. These findings support systematic allergological assessment and suggest that structural heterogeneity among GBCAs may have clinically relevant immunological implications.