|
NSAID or nonsteroidal anti-inflammatory drug hypersensitivity reactions encompasses a broad range of allergic or allergic-like symptoms that occur within minutes to hours after ingesting aspirin or other NSAID nonsteroidal anti-inflammatory drugs. Hypersensitivity drug reactions differ from drug toxicity reactions in that drug toxicity reactions result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual (see nonsteroidal anti-inflammatory drugs section on adverse reactions for NSAID-induced toxic reactions); hypersensitivity reactions are idiosyncratic reactions to a drug.〔Allergy Asthma Immunol Res. 2015 Jul;7(4):312-20. doi: 10.4168/aair.2015.7.4.312〕 The broad range of hypersensitivity syndromes evoked by NSAID has recently been classified by the European Academy of Allergy and Clinical Immunology Task Force on NSAIDs Hypersensitivity.〔Allergy. 2013 Oct;68(10):1219-32. doi: 10.1111/all.12260〕 The classification organizes the hypersensitivity reactions to NSAIDs into the following five categories: * 1) NSAIDs-exacerbated respiratory disease (NERD) is an acute (immediate to several hours) exacerbation of bronchoconstriction and other symptoms of asthma (see aspirin-induced asthma) in individuals with a history of asthma and/or nasal congestion, rhinorrhea or other symptoms of rhinitis and sinusitis in individuals with a history of rhinosinusitis after ingestion of various NSAIDs, particularly those that act by inhibiting the COX-1 enzyme. NERD does not appear to be due to a true allergic reaction to NSAIDs but rather at least in part to the more direct effects of these drugs to promote the production and/or release of certain mediators of allergy. That is, inhibition of cellular COX activity deprives tissues of its anti-inflammatory product(s), particularly prostaglandin E2 while concurrently shuttling its substrate, arachidonic acid, into other metabolizing enzymes, particularly 5-lipoxygenase (ALOX5) to overproduce pro-inflammatory leukotriene and 5-Hydroxyicosatetraenoic acid metabolites and 15-lipoxygenase (ALOX15) to overproduce pro-inflammatory 15-Hydroxyicosatetraenoic acid metabolites, including eoxins; the condition is also is associated with a reduction in the anti-inflammatory metabolite, lipoxin A4, and increases in certain pro-allergic chemokines such as eotaxin-2 and CCL7.〔Prostaglandins Other Lipid Mediat. 2009 Sep;89(3-4):120-5. doi: 10.1016/j.prostaglandins.2008.12.003.〕〔Respir Med. 2010 Oct;104(10):1404-9. doi: 10.1016/j.rmed.2010.04.017〕〔Allergy. 2011 Jul;66(7):818-29. doi: 10.1111/j.1398-9995.2011.02557.x.〕〔J Allergy Clin Immunol Pract. 2014 Nov-Dec;2(6):653-7. doi: 10.1016/j.jaip.2014.09.009〕〔Curr Opin Allergy Clin Immunol. 2014 Feb;14(1):1-6. doi: 10.1097/ACI.0000000000000021〕 * 2) NSAIDs-exacerbated cutaneous disease (NECD) is an acute exacerbation of wheals and/or angioedema in individuals with a history of chronic urticaria. NECD also appears due to the non-allergic action of NSAIDs in inhibiting the production of COX anti-inflammatory metabolites while promoting the production 5-lipoxygenase and 15-lipoxygenase pro-inflammatory metabolites and the overproduction of certain pro-allergic chemokines}, e.g. eotaxin-1, eotaxin-2, RANTES, and interleukin-5.〔Immunol Allergy Clin North Am. 2013 May;33(2):163-76. doi: 10.1016/j.iac.2012.11.002〕〔Curr Allergy Asthma Rep. 2015 Mar;15(3):508. doi: 10.1007/s11882-014-0508-7〕 * 3) NSAIDs-induced urticarial disease (NEUD) is the acute development of wheals and/or angioedema in individuals with no history of chronic NSAIDs-induced urticaria or related diseases. The mechanism behind NEUD is unknown but may be due to the non-allergic action of NSAIDs in promoting the production and/or release of allergy mediators.〔Allergy. 2011 Jul;66(7):818-29. doi: 10.1111/j.1398-9995.2011.02557.x〕 * 4) Single NSAID-induced urticarial/angioedema or anaphylaxis (SNIUAA) is the acute development of urticarial, angioedema, or anaphylaxis in response to a single type of NSAID and/or a single group of NSAIDs with a similar structure but not to other structurally unrelated NSAIDs in individuals with no history of underlying relevant chronic diseases. SNIUAA is due to a true IgE-mediated allergy reaction.〔J Allergy Clin Immunol 2003;111:882–888.〕〔Allergy. 2013 Oct;68(10):1219-32. doi: 10.1111/all.12260〕 * 5 Single NSAID-induced delayed reactions (SNIDR) are a set of delayed onset (usually more than 24 hour) reactions to NSAIDs. SNIDR are most commonly skin reactions that may be relatively mild moderately severe such as maculopapular rash, fixed drug eruptions, photosensitivity reactions, delayed urticaria, and contact dermatitis or extremely severe such as the DRESS syndrome, acute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis (also termed Lyell's syndrome). SNIDR result from the drug-specific stimulation of CD4+ T lymphocytes and CD8+ Cytotoxic T cells to elicit a delayed type hypersensitivity reaction.〔Curr Opin Allergy Clin Immunol 2009;9:305–310.〕〔Allergy. 2013 Oct;68(10):1219-32. doi: 10.1111/all.12260〕 ==References== 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「NSAID hypersensitivity reactions」の詳細全文を読む スポンサード リンク
|