A useful review of AI (aspirin Intolerance) with relevance to asa desensitizatio

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Pathogenesis,diagnosis, and treatment of aspirin intolerance,Jennek et al,Ann

Allergy Asthma immunol,Vo 99,July2007,pgs13-21.

This summary discusses two groups of AI. One hypothesis proposes that AI

results directly from an unspecific,non IgE-dependant degranulation of mast

cells and eosinophils in an pseudoallergic reaction in which symtoms appear

after the first intake of the drug (ASA or another NSAID).These reactions were

associated with increased Cys-LTs and eosinophilic cationic protein( ie

reactions related to COX-1 inhibition ) reflecting activation of eosinophils

and an increase in prostaglandin D2 which mirrors mast cell activation.Studies

showing increased histamine and trytase levels after taking asa in AI

individuals without detection of asa specific IgE supports the pseudoallergic

theory as a cause for AI in most cases.Desensitization for these individuals

would seem a safer procedure.

However in another group of AI individuals exposure to an NSAID can result in

anaphylaxis(IgE mediated reaction).Anaphylactoid reactions with acute urticaria

and angioedema or even anaphylactic shock. Repeated exposure(desensitization) to

an NSAID leads to saturation of anti-NSAID IgE antibody binding sites on mast

cells and basophils.Desenitization in this group of AI individuals only under

medical supervision where equipped to handle anaphylaxis.Cross reactivity is not

as generallized as in the first group( ie antibody specfic)

Correct me if I am wrong but the urticaria can exist in both groups.Also it

would make sense that these two groups might overlap to some extent.An

interesting discussion would involve when an individual with AI develops the IgE

specific reactions because this must be mostly where the desensitization risks

lie. Wayne