title: Autoreactivity is highly prevalent in patients with multiple intolerances to NSAIDs.
abstract: BACKGROUND
  A subset of drug-allergic patients show a marked propensity to react against several, chemically unrelated nonsteroidal anti-inflammatory drugs (NSAIDs). The pathogenesis of such multiple drug reactions is unclear. Approximately 30% of patients with chronic idiopathic urticaria, a condition frequently characterized by autoreactivity on autologous serum skin test (ASST), experience flares of hives after taking chemically unrelated NSAIDs.
  
  
  OBJECTIVE
  To detect whether a clinically unapparent autoreactivity may represent the nonspecific mechanism facilitating drug-induced histamine release in patients with a history of urticaria/angioedema induced by several, chemically unrelated NSAIDs.
  
  
  METHODS
  Thirty-six adults with a history of acute NSAID-induced urticaria (22 with multiple NSAID sensitivity [MNS]; 14 with single NSAID sensitivity [SNS]; and 20 atopic controls without a history of drug allergy) underwent ASST. Sera from 14 MNS and 4 SNS subjects (all ASST-positive) underwent histamine release assay with basophils from normal donors. Sera from five MNS patients were tested on autologous basophils as well.
  
  
  RESULTS
  Twenty of 22 (91%) MNS subjects versus 5 of 14 (36%) SNS subjects were positive on ASST (P < 0.01). No atopic control was ASST-positive. Sera from 4 of 14 (29%) MNS patients versus 0/4 SNS subjects (P = NS) induced significant histamine release from basophils of normal donors. The use of autologous basophils did not significantly change these results.
  
  
  CONCLUSIONS
  Most patients with multiple NSAID intolerance and approximately one-third of those with single NSAID hypersensitivity are characterized by the presence of circulating histamine-releasing factors. Their nature is still unclear, but the fact that only a minority of sera from ASST+ subjects were able to induce histamine release from normal basophils in vitro suggests that these factors might not differ from those involved in most patients with chronic urticaria. These factors might play a relevant pathogenic role in NSAID-induced urticaria reactions.
authors.affiliation: Allergy Unit, Ospedale Caduti Bollatesi, Bollate, MI, Italy. r.asero@libero.it
authors.forename: Riccardo
authors.initials: R
authors.lastname: Asero
authors.forename: Alberto
authors.initials: A
authors.lastname: Tedeschi
authors.forename: Maurizio
authors.initials: M
authors.lastname: Lorini
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000276:immunology; D001491:Basophils / Q000276:immunology; D004342:Drug Hypersensitivity / Q000097:blood / Q000276:immunology*; D005260:Female; D006636:Histamine Release; D006801:Humans; D008297:Male; D008875:Middle Aged; D012882:Skin Tests; D014581:Urticaria / Q000139:chemically induced / Q000276:immunology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal