Drug allergy: an updated practice parameter

Information sourced from AHRQ:

Drug allergy: an updated practice parameter

Joint Task Force on Practice Parameters, American Academy of Allergy, Asthma and Immunology, American College of Allergy, Asthma and Immunology, Joint Council of Allergy, Asthma and Immunology. Drug allergy: an updated practice parameter. Ann Allergy Asthma Immunol 2010 Oct;105(4):259-273.e78.

[Free full-text Ann Allergy Asthma Immunol article PDF | PubMed ® abstract | National Guideline Clearinghouse version]

[EXCERPTS]

Major Recommendations

Aspirin and NSAIDs

  • One type of adverse reaction to aspirin/NSAIDs is AERD, a clinical entity characterized by aspirin- and NSAID-induced respiratory reactions in patients with underlying asthma and/or rhinitis or sinusitis. (B)
  • The mechanism of AERD appears to be related to aberrant arachidonic acid metabolism. (B)
  • Controlled oral provocation with aspirin is considered to be the most conclusive way to confirm the diagnosis of AERD. (B)
  • Aspirin and NSAIDs that inhibit cyclooxygenase-1 (COX-1) cross-react and cause respiratory reactions in AERD, whereas selective COX-2 inhibitors almost never cause reactions in patients with AERD and can typically be taken safely. (B)
  • Aspirin desensitization followed by daily aspirin therapy to perpetuate the aspirin tolerant state in patients with AERD is indicated in patients with AERD if aspirin or NSAIDs are therapeutically necessary for treatment of some other condition, such as cardiac or rheumatologic diseases. (D)
  • Aspirin desensitization followed by daily aspirin has been associated with improved outcomes in patients with AERD who are poorly controlled with medical and/or surgical management. (D)
  • A second reaction type to aspirin and NSAIDs is exacerbation of urticaria and angioedema in approximately 20% to 40% of patients with underlying chronic idiopathic urticaria. (C) Drugs that inhibit COX-1 cross-react to cause this reaction, whereas selective COX-2 inhibitors typically are better tolerated by these patients. (C)
  • A third reaction type to aspirin and NSAIDs is suggestive of an IgE-mediated mechanism and manifests as urticaria or angioedema or anaphylaxis, and it occurs in patients with no underlying respiratory or cutaneous disease. (C) These reactions appear to be drug specific, and there is no cross-reactivity with other NSAIDs. (D)
  • A fourth reaction type to aspirin and NSAIDs is urticaria or angioedema caused by all drugs that inhibit COX-1, and it occurs in patients without a prior history of chronic urticaria. (C)
  • Rarely, patients exhibit combined (“blended”) respiratory and cutaneous reaction to aspirin or NSAIDs and hence cannot be classified into 1 of the 4 reaction types described above. (C)

Management and Prevention of Drug Allergic Reactions

Pharmacologic induction of drug tolerance to aspirin (e.g., aspirin desensitization) is primarily intended for patients with aspirin-exacerbated respiratory disease (AERD), and unlike other types of desensitization, its purpose is to cautiously induce (rather than prevent) a reaction, after which patients become tolerant of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). (B)

The adverse reaction is predictable (e.g., toxicity, side effect, drug interaction) or due to idiosyncrasy, intolerance, or pseudoallergic effects of the drug.

Aspirin-induced tinnitus at therapeutic or subtherapeutic doses is an example of drug intolerance.

[Definitions Levels of Evidence available online]

[Link to free full-text guideline: Ann Allergy Asthma Immunol article PDF | NGC version online]

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