Aspirin idiosyncrasy in systemic mast cell disease: a new look at mediator release during aspirin desensitization.

Abstract:

OBJECTIVE:To report the clinical responses and mediator-release profiles of an aspirin-sensitive man with systemic mast cell disease during aspirin desensitization. MATERIAL AND METHODS:We quantified the release of six mediators during aspirin desensitization. RESULTS:Although aspirin was administered cautiously with an initial dose of 20 mg, successful aspirin desensitization necessitated complete monitoring and resuscitation capabilities of a medical intensive-care unit for 4.5 days because of frequent, severe anaphylactoid responses. To our knowledge, this is the first report of a pronounced increase in plasma levels of the vasodilator peptide calcitonin gene-related peptide during episodes of aspirin-induced hypotension. Increases in plasma levels of calcitonin and serum levels of tryptase paralleled those of calcitonin gene-related peptide, but plasma levels of calcitonin remained increased for up to 18 hours. Urinary excretion of histamine and 1-methyl-4-imidazoleacetic acid also showed precipitous, although delayed, increases. Excretion of the prostaglandin D2 metabolite 11 beta-prostaglandin F2 alpha 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 therapeutic serum levels of salicylate were attained. CONCLUSION:These data suggest that the hypotensive responses to aspirin in some patients with systemic mast cell disease may result from the combined effects of several mediators.

journal_name

Mayo Clin Proc

journal_title

Mayo Clinic proceedings

authors

Butterfield JH,Kao PC,Klee GC,Yocum MW

doi

10.4065/70.5.481

subject

Has Abstract

pub_date

1995-05-01 00:00:00

pages

481-7

issue

5

eissn

0025-6196

issn

1942-5546

pii

S0025-6196(11)63888-3

journal_volume

70

pub_type

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