ASPIRIN IDIOSYNCRASY IN SYSTEMIC MAST-CELL DISEASE - A NEW LOOK AT MEDIATOR RELEASE DURING ASPIRIN DESENSITIZATION

Objective: To report the clinical responses and mediator-release profi les of an aspirin-sensitive man with systemic mast cell disease during aspirin desensitization. Material and Methods: We quantified the rele ase of six mediators during aspirin desensitization. Results: Although aspirin was administered cautiously with an initial dose of 20 mg, su ccessful aspirin desensitization necessitated complete monitoring and resuscitation capabilities of a medical intensive-care unit for 4.5 da ys because of frequent, severe anaphylactoid responses. To our knowled ge, this is the first report of a pronounced increase in plasma levels of the vasodilator peptide calcitonin gene-related peptide during epi sodes of aspirin-induced hypotension, Increases in plasma levels of ca lcitonin and serum levels of tryptase paralleled those of calcitonin g ene-related peptide, but plasma levels of calcitonin remained increase d for up to 18 hours, Urinary excretion of histamine and 1-methyl-4-im idazoleacetic acid also showed precipitous, although delayed, increase s. Excretion of the prostaglandin D-2 metabolite 11 beta-prostaglandin F-2 alpha a followed a bimodal pattern during aspirin desensitization ; after severe hypotensive responses, the maximal value was more than 490,000 pg/mL, but the level decreased to less than 100 pg/mL after th erapeutic serum levels of salicylate were attained, Conclusion: These data suggest that the hypotensive responses to aspirin in some patient s with systemic mast cell disease may result from the combined effects of several mediators.