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PubMed · 13679969

[Anaphylaxis].

C Rubio·E Lasa·E Arroabarren·S Garrido·B E García·A I Tabar
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Abstract

Anaphylaxis is a potentially mortal, underdiagnosed clinical picture. The most frequent triggering agents are drugs and foodstuffs. The first therapeutic option, adrenaline, although clearly indicated, is not carried out with the desired frequency due basically to the high number of cases of anaphylaxis that are not diagnosed as such. In patients with a first episode of anaphylaxis, posterior aetiological diagnosis is crucial to avoid the appearance of new episodes. The only case of anaphylaxis in which immunotherapy with the allergen must be evaluated, is that in which the causal agent is the poison of hymenopters.

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C Rubio, E Lasa, E Arroabarren, S Garrido, B E García, A I Tabar. 2003. [Anaphylaxis].. https://pubmed.ncbi.nlm.nih.gov/13679969/

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Anaphylaxis↗
PubMed2003

Anaphylactic shock caused by immunoglobulin E sensitization after retreatment with the chimeric anti-interleukin-2 receptor monoclonal antibody basiliximab.

BACKGROUND: Repeated administration of chimeric or humanized monoclonal antibodies is generally well tolerated. Anti-idiotypic sensitization is rare and is considered to be of no clinical significance. We observed a child who experienced anaphylactic shock when he received a second course of basiliximab at the time of his second renal transplantation. We therefore searched for the presence of anti-basiliximab immunoglobulin (Ig) E in this patient. METHODS: Serum levels of anti-basiliximab IgE, assay of the anti-murine reactivity of circulating anti-basiliximab IgE, and assays for serum anti-mouse antibodies and global anti-basiliximab anti-idiotypic antibodies were carried out by enzyme-linked immunosorbent assay. Anti-basiliximab IgE antibodies on circulating basophils were evaluated by the ability of the patient's blood to produce leukotrienes in vitro after exposure to basiliximab. RESULTS: Sequential assays of serum samples by enzyme-linked immunosorbent assay indicated that anti-basiliximab IgE antibodies appeared after the second basiliximab course. There was no IgE reactivity toward a control murine IgG2a monoclonal antibody (mAb), indicating that the IgE response was directed exclusively against basiliximab idiotypes. There was no IgE reactivity against the humanized anti-interleukin-2 receptor mAb daclizumab, which was derived from a distinct parental murine mAb. Patient basophils harvested months after the anaphylactic shock produced leukotrienes in vitro on exposure to basiliximab. CONCLUSIONS: Patients exposed to chimeric antibodies may develop an anti-idiotypic IgE response that can trigger anaphylactic shock on further exposure. Specific anti-idiotypic IgE may be bound to basophils even in the absence of circulating IgE.

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