DOI QR코드

DOI QR Code

What we know about nonsteroidal anti-inflammatory drug hypersensitivity

  • Pham, Duy Le (Department of Allergy and Clinical Immunology, Ajou University School of Medicine) ;
  • Kim, Ji-Hye (Department of Allergy and Clinical Immunology, Ajou University School of Medicine) ;
  • Trinh, Tu Hoang Kim (Department of Allergy and Clinical Immunology, Ajou University School of Medicine) ;
  • Park, Hae-Sim (Department of Allergy and Clinical Immunology, Ajou University School of Medicine)
  • Received : 2016.02.14
  • Accepted : 2016.03.05
  • Published : 2016.05.01

Abstract

Nonsteroidal anti-inf lammatory drugs (NSAIDs) are widely prescribed for the treatment of inflammatory diseases, but their use is frequently related to hypersensitivity reactions. This review outlines our current knowledge of NSAID hypersensitivity (NHS) with regard to its pathogenic, molecular, and genetic mechanisms, as well as diagnosis and treatment. The presentation of NHS varies from a local (skin and/or airways) reaction to systemic reactions, including anaphylaxis. At the molecular level, NHS reactions can be classified as cross-reactive (mediated by cyclooxygenase inhibition) or selective (specific activation of immunoglobulin E antibodies or T cells). Genetic polymorphisms and epigenetic factors have been shown to be closely associated with NHS, and may be useful as predictive markers. To diagnose NHS, inhalation or oral challenge tests are applied, with the exclusion of any cross-reactive NSAIDs. For patients diagnosed with NHS, absolute avoidance of NSAIDs/aspirin is essential, and pharmacological treatment, including biologics, is often used to control their respiratory and cutaneous symptoms. Finally, desensitization is recommended only for selected patients with NHS. However, further research is required to develop new diagnostic methods and more effective treatments against NHS.

Keywords

Acknowledgement

Supported by : Ministry of Health and Welfare

References

  1. Conaghan PG. A turbulent decade for NSAIDs: update on current concepts of classification, epidemiology, comparative efficacy, and toxicity. Rheumatol Int 2012;32:1491-1502. https://doi.org/10.1007/s00296-011-2263-6
  2. Kowalski ML, Makowska JS. Seven steps to the diagnosis of NSAIDs hypersensitivity: how to apply a new classification in real practice? Allergy Asthma Immunol Res 2015;7:312-320. https://doi.org/10.4168/aair.2015.7.4.312
  3. Kasper L, Sladek K, Duplaga M, et al. Prevalence of asthma with aspirin hypersensitivity in the adult population of Poland. Allergy 2003;58:1064-1066. https://doi.org/10.1034/j.1398-9995.2003.00267.x
  4. Erbagci Z. Multiple NSAID intolerance in chronic idiopathic urticaria is correlated with delayed, pronounced and prolonged autoreactivity. J Dermatol 2004;31:376-382. https://doi.org/10.1111/j.1346-8138.2004.tb00688.x
  5. Ye YM, Kim MK, Kang HR, et al. Predictors of the severity and serious outcomes of anaphylaxis in Korean adults: a multicenter retrospective case study. Allergy Asthma Immunol Res 2015;7:22-29. https://doi.org/10.4168/aair.2015.7.1.22
  6. Demoly P, Adkinson NF, Brockow K, et al. International Consensus on drug allergy. Allergy 2014;69:420-437. https://doi.org/10.1111/all.12350
  7. Kowalski ML, Makowska JS, Blanca M, et al. Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs). Classification, diagnosis and management: review of the EAACI/ENDA(#) and GA2LEN/HANNA*. Allergy 2011;66:818-829. https://doi.org/10.1111/j.1398-9995.2011.02557.x
  8. Gomez F, Perkins JR, Garcia-Martin E, Canto G, Cornejo-Garcia JA. Genetic basis of hypersensitivity reactions to nonsteroidal anti-inflammatory drugs. Curr Opin Allergy Clin Immunol 2015;15:285-293. https://doi.org/10.1097/ACI.0000000000000178
  9. Dona I, Blanca-Lopez N, Cornejo-Garcia JA, et al. Characteristics of subjects experiencing hypersensitivity to non-steroidal anti-inflammatory drugs: patterns of response. Clin Exp Allergy 2011;41:86-95. https://doi.org/10.1111/j.1365-2222.2010.03651.x
  10. Kowal-Bielecka O, Kowal K, Distler O, Gay S. Mechanisms of disease: leukotrienes and lipoxins in scleroderma lung disease. Insights and potential therapeutic implications. Nat Clin Pract Rheumatol 2007;3:43-51. https://doi.org/10.1038/ncprheum0375
  11. Hofmeier KS. Hypersensitivity reactions to modern antiplatelet and anticoagulant drugs. Allergo J Int 2015;24:58-66.
  12. Blanca-Lopez N, Cornejo-Garcia JA, Plaza-Seron MC, et al. Hypersensitivity to nonsteroidal anti-inflammatory drugs in children and adolescents: cross-intolerance reactions. J Investig Allergol Clin Immunol 2015;25:259-269.
  13. Stone SF, Phillips EJ, Wiese MD, Heddle RJ, Brown SG. Immediate-type hypersensitivity drug reactions. Br J Clin Pharmacol 2014;78:1-13. https://doi.org/10.1111/bcp.12297
  14. Cho YS, Moon HB. The role of oxidative stress in the pathogenesis of asthma. Allergy Asthma Immunol Res 2010;2:183-187. https://doi.org/10.4168/aair.2010.2.3.183
  15. Palikhe S, Palikhe NS, Kim SH, Yoo HS, Shin YS, Park HS. Elevated platelet activation in patients with chronic urticaria: a comparison between aspirin-intolerant and aspirin-tolerant groups. Ann Allergy Asthma Immunol 2014;113:276-281. https://doi.org/10.1016/j.anai.2014.06.011
  16. Matsuo H, Yokooji T, Morita H, et al. Aspirin augments IgE-mediated histamine release from human peripheral basophils via Syk kinase activation. Allergol Int 2013;62:503-511. https://doi.org/10.2332/allergolint.13-OA-0536
  17. Kacprzak D, Pawliczak R. Does aspirin-induced oxidative stress cause asthma exacerbation? Arch Med Sci 2015;11:494-504.
  18. Bruno A, Tacconelli S, Patrignani P. Variability in the response to non-steroidal anti-inflammatory drugs: mechanisms and perspectives. Basic Clin Pharmacol Toxicol 2014;114:56-63. https://doi.org/10.1111/bcpt.12117
  19. Reiss AB, Edelman SD. Recent insights into the role of prostanoids in atherosclerotic vascular disease. Curr Vasc Pharmacol 2006;4:395-408. https://doi.org/10.2174/157016106778521652
  20. Hedi H, Norbert G. 5-Lipoxygenase pathway, dendritic cells, and adaptive immunity. J Biomed Biotechnol 2004;2004:99-105. https://doi.org/10.1155/S1110724304310041
  21. Meade EA, Smith WL, DeWitt DL. Differential inhibition of prostaglandin endoperoxide synthase (cyclooxygenase) isozymes by aspirin and other non-steroidal anti-inflammatory drugs. J Biol Chem 1993;268:6610-6614.
  22. Vane JR. The mode of action of aspirin and similar compounds. J Allergy Clin Immunol 1976;58:691-712. https://doi.org/10.1016/0091-6749(76)90181-0
  23. Kupczyk M, Antczak A, Kuprys-Lipinska I, Kuna P. Lipoxin A4 generation is decreased in aspirin-sensitive patients in lysine-aspirin nasal challenge in vivo model. Allergy 2009;64:1746-1752. https://doi.org/10.1111/j.1398-9995.2009.02047.x
  24. Kowalski ML, Asero R, Bavbek S, et al. Classification and practical approach to the diagnosis and management of hypersensitivity to nonsteroidal anti-inflammatory drugs. Allergy 2013;68:1219-1232. https://doi.org/10.1111/all.12260
  25. Sastre B, del Pozo V. Role of PGE2 in asthma and nonasthmatic eosinophilic bronchitis. Mediators Inflamm 2012;2012:645383.
  26. Ricciotti E, FitzGerald GA. Prostaglandins and inflammation. Arterioscler Thromb Vasc Biol 2011;31:986-1000. https://doi.org/10.1161/ATVBAHA.110.207449
  27. Beller TC, Maekawa A, Friend DS, Austen KF, Kanaoka Y. Targeted gene disruption reveals the role of the cysteinyl leukotriene 2 receptor in increased vascular permeability and in bleomycin-induced pulmonary fibrosis in mice. J Biol Chem 2004;279:46129-46134. https://doi.org/10.1074/jbc.M407057200
  28. Paruchuri S, Tashimo H, Feng C, et al. Leukotriene E4-induced pulmonary inflammation is mediated by the P2Y12 receptor. J Exp Med 2009;206:2543-2555. https://doi.org/10.1084/jem.20091240
  29. Gauvreau GM, Parameswaran KN, Watson RM, O'Byrne PM. Inhaled leukotriene E(4), but not leukotriene D(4), increased airway inflammatory cells in subjects with atopic asthma. Am J Respir Crit Care Med 2001;164(8 Pt 1):1495-1500. https://doi.org/10.1164/ajrccm.164.8.2102033
  30. Cummings HE, Liu T, Feng C, et al. Cutting edge: leukotriene C4 activates mouse platelets in plasma exclusively through the type 2 cysteinyl leukotriene receptor. J Immunol 2013;191:5807-5810. https://doi.org/10.4049/jimmunol.1302187
  31. Sanak M, Levy BD, Clish CB, et al. Aspirin-tolerant asthmatics generate more lipoxins than aspirin-intolerant asthmatics. Eur Respir J 2000;16:44-49. https://doi.org/10.1034/j.1399-3003.2000.16a08.x
  32. Fierro IM, Colgan SP, Bernasconi G, et al. Lipoxin A4 and aspirin-triggered 15-epi-lipoxin A4 inhibit human neutrophil migration: comparisons between synthetic 15 epimers in chemotaxis and transmigration with microvessel endothelial cells and epithelial cells. J Immunol 2003;170:2688-2694. https://doi.org/10.4049/jimmunol.170.5.2688
  33. Bonnans C, Levy BD. Lipid mediators as agonists for the resolution of acute lung inflammation and injury. Am J Respir Cell Mol Biol 2007;36:201-205. https://doi.org/10.1165/rcmb.2006-0269TR
  34. Hsieh CW, Lee JW, Liao EC, Tsai JJ. A disease marker for aspirin-induced chronic urticaria. Int J Mol Sci 2014;15:12591-12603. https://doi.org/10.3390/ijms150712591
  35. Blanca M, Perez E, Garcia JJ, et al. Angioedema and IgE antibodies to aspirin: a case report. Ann Allergy 1989;62:295-298.
  36. Bolze S, Bromet N, Gay-Feutry C, Massiere F, Boulieu R, Hulot T. Development of an in vitro screening model for the biosynthesis of acyl glucuronide metabolites and the assessment of their reactivity toward human serum albumin. Drug Metab Dispos 2002;30:404-413. https://doi.org/10.1124/dmd.30.4.404
  37. Berkes EA. Anaphylactic and anaphylactoid reactions to aspirin and other NSAIDs. Clin Rev Allergy Immunol 2003;24:137-148. https://doi.org/10.1385/CRIAI:24:2:137
  38. Altrichter S, Peter HJ, Pisarevskaja D, Metz M, Martus P, Maurer M. IgE mediated autoallergy against thyroid peroxidase: a novel pathomechanism of chronic spontaneous urticaria? PLoS One 2011;6:e14794. https://doi.org/10.1371/journal.pone.0014794
  39. Shin YS, Suh DH, Yang EM, Ye YM, Park HS. Serum specific IgE to thyroid peroxidase activates basophils in aspirin intolerant urticaria. J Korean Med Sci 2015;30:705-709.
  40. Gibbs BF, Rathling A, Zillikens D, Huber M, Haas H. Initial Fc epsilon RI-mediated signal strength plays a key role in regulating basophil signaling and deactivation. J Allergy Clin Immunol 2006;118:1060-1067. https://doi.org/10.1016/j.jaci.2006.07.022
  41. Wojnar RJ, Hearn T, Starkweather S. Augmentation of allergic histamine release from human leukocytes by nonsteroidal anti-inflammatory-analgesic agents. J Allergy Clin Immunol 1980;66:37-45. https://doi.org/10.1016/0091-6749(80)90136-0
  42. Hyman MH. Delayed drug hypersensitivity reactions. Ann Intern Med 2004;140:W35. https://doi.org/10.7326/0003-4819-140-9-200405040-00028-w1
  43. Gallo PM, Gallucci S. The dendritic cell response to classic, emerging, and homeostatic danger signals. Implications for autoimmunity. Front Immunol 2013;4:138.
  44. Antczak A, Montuschi P, Kharitonov S, Gorski P, Barnes PJ. Increased exhaled cysteinyl-leukotrienes and 8-isoprostane in aspirin-induced asthma. Am J Respir Crit Care Med 2002;166:301-306. https://doi.org/10.1164/rccm.2101021
  45. Dworski R, Murray JJ, Roberts LJ 2nd, et al. Allergen-induced synthesis of F(2)-isoprostanes in atopic asthmatics. Evidence for oxidant stress. Am J Respir Crit Care Med 1999;160:1947-1951. https://doi.org/10.1164/ajrccm.160.6.9903064
  46. Idzko M, Pitchford S, Page C. Role of platelets in allergic airway inflammation. J Allergy Clin Immunol 2015;135:1416-1423. https://doi.org/10.1016/j.jaci.2015.04.028
  47. Chandrashekar L, Rajappa M, Sundar I, et al. Platelet activation in chronic urticaria and its correlation with disease severity. Platelets 2014;25:162-165. https://doi.org/10.3109/09537104.2013.786822
  48. Szczeklik A, Nizankowska E, Duplaga M. Natural history of aspirin-induced asthma. AIANE Investigators. European Network on Aspirin-Induced Asthma. Eur Respir J 2000;16:432-436. https://doi.org/10.1034/j.1399-3003.2000.016003432.x
  49. Losol P, Yoo HS, Park HS. Molecular genetic mechanisms of chronic urticaria. Allergy Asthma Immunol Res 2014;6:13-21. https://doi.org/10.4168/aair.2014.6.1.13
  50. Sanak M, Pierzchalska M, Bazan-Socha S, Szczeklik A. Enhanced expression of the leukotriene C(4) synthase due to overactive transcription of an allelic variant associated with aspirin-intolerant asthma. Am J Respir Cell Mol Biol 2000;23:290-296. https://doi.org/10.1165/ajrcmb.23.3.4051
  51. Mastalerz L, Setkowicz M, Sanak M, Rybarczyk H, Szczeklik A. Familial aggregation of aspirin-induced urticaria and leukotriene C synthase allelic variant. Br J Dermatol 2006;154:256-260. https://doi.org/10.1111/j.1365-2133.2005.06851.x
  52. Van Sambeek R, Stevenson DD, Baldasaro M, et al. 5' Flanking region polymorphism of the gene encoding leukotriene C4 synthase does not correlate with the aspirin-intolerant asthma phenotype in the United States. J Allergy Clin Immunol 2000;106(1 Pt 1):72-76. https://doi.org/10.1067/mai.2000.107603
  53. Choi JH, Park HS, Oh HB, et al. Leukotriene-related gene polymorphisms in ASA-intolerant asthma: an association with a haplotype of 5-lipoxygenase. Hum Genet 2004;114:337-344. https://doi.org/10.1007/s00439-004-1082-1
  54. Kawagishi Y, Mita H, Taniguchi M, et al. Leukotriene C4 synthase promoter polymorphism in Japanese patients with aspirin-induced asthma. J Allergy Clin Immunol 2002;109:936-942. https://doi.org/10.1067/mai.2002.124466
  55. Kim SH, Oh JM, Kim YS, et al. Cysteinyl leukotriene receptor 1 promoter polymorphism is associated with aspirin-intolerant asthma in males. Clin Exp Allergy 2006;36:433-439. https://doi.org/10.1111/j.1365-2222.2006.02457.x
  56. Kim SH, Ye YM, Hur GY, et al. CysLTR1 promoter polymorphism and requirement for leukotriene receptor antagonist in aspirin-intolerant asthma patients. Pharmacogenomics 2007;8:1143-1150. https://doi.org/10.2217/14622416.8.9.1143
  57. Park JS, Chang HS, Park CS, et al. Association analysis of cysteinyl-leukotriene receptor 2 (CYSLTR2) polymorphisms with aspirin intolerance in asthmatics. Pharmacogenet Genomics 2005;15:483-492. https://doi.org/10.1097/01.fpc.0000166456.84905.a0
  58. Sousa AR, Parikh A, Scadding G, Corrigan CJ, Lee TH. Leukotriene-receptor expression on nasal mucosal inflammatory cells in aspirin-sensitive rhinosinusitis. N Engl J Med 2002;347:1493-1499. https://doi.org/10.1056/NEJMoa013508
  59. Adamusiak AM, Stasikowska-Kanicka O, Lewandowska-Polak A, et al. Expression of arachidonate metabolism enzymes and receptors in nasal polyps of aspirin-hypersensitive asthmatics. Int Arch Allergy Immunol 2012;157:354-362. https://doi.org/10.1159/000329744
  60. Szczeklik W, Sanak M, Szczeklik A. Functional effects and gender association of COX-2 gene polymorphism G-765C in bronchial asthma. J Allergy Clin Immunol 2004;114:248-253. https://doi.org/10.1016/j.jaci.2004.05.030
  61. Kim SH, Choi JH, Holloway JW, et al. Leukotriene-related gene polymorphisms in patients with aspirin-intolerant urticaria and aspirin-intolerant asthma: differing contributions of ALOX5 polymorphism in Korean population. J Korean Med Sci 2005;20:926-931. https://doi.org/10.3346/jkms.2005.20.6.926
  62. Cornejo-Garcia JA, Jagemann LR, Blanca-Lopez N, et al. Genetic variants of the arachidonic acid pathway in non-steroidal anti-inflammatory drug-induced acute urticaria. Clin Exp Allergy 2012;42:1772-1781. https://doi.org/10.1111/j.1365-2222.2012.04078.x
  63. Lee HY, Kim SH, Ye YM, Choi GS, Park HS. Lack of association of ALOX12 and ALOX15 polymorphisms with aspirin-exacerbated respiratory disease in Korean patients. Ann Allergy Asthma Immunol 2009;103:84-86. https://doi.org/10.1016/S1081-1206(10)60152-4
  64. Palikhe NS, Kim SH, Lee HY, Kim JH, Ye YM, Park HS. Association of thromboxane A2 receptor (TBXA2R) gene polymorphism in patients with aspirin-intolerant acute urticaria. Clin Exp Allergy 2011;41:179-185. https://doi.org/10.1111/j.1365-2222.2010.03642.x
  65. Kim SH, Kim YK, Park HW, et al. Association between polymorphisms in prostanoid receptor genes and aspirin-intolerant asthma. Pharmacogenet Genomics 2007;17:295-304. https://doi.org/10.1097/01.fpc.0000239977.61841.fe
  66. Kim SH, Choi JH, Park HS, et al. Association of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma. Clin Exp Allergy 2005;35:585-590. https://doi.org/10.1111/j.1365-2222.2005.02220.x
  67. Oh SH, Kim YH, Park SM, et al. Association analysis of thromboxane A synthase 1 gene polymorphisms with aspirin intolerance in asthmatic patients. Pharmacogenomics 2011;12:351-363. https://doi.org/10.2217/pgs.10.181
  68. Vidal C, Porras-Hurtado L, Cruz R, et al. Association of thromboxane A1 synthase (TBXAS1) gene polymorphism with acute urticaria induced by nonsteroidal anti-inflammatory drugs. J Allergy Clin Immunol 2013;132:989-991. https://doi.org/10.1016/j.jaci.2013.04.045
  69. Palikhe NS, Sin HJ, Kim SH, et al. Genetic variability of prostaglandin E2 receptor subtype EP4 gene in aspirin-intolerant chronic urticaria. J Hum Genet 2012;57:494-499. https://doi.org/10.1038/jhg.2012.55
  70. Park BL, Park SM, Park JS, et al. Association of PTGER gene family polymorphisms with aspirin intolerant asthma in Korean asthmatics. BMB Rep 2010;43:445-449. https://doi.org/10.5483/BMBRep.2010.43.6.445
  71. Kawakami T, Kashiwakura J, Kawakami Y. Histamine-releasing factor and immunoglobulins in asthma and allergy. Allergy Asthma Immunol Res 2014;6:6-12. https://doi.org/10.4168/aair.2014.6.1.6
  72. Palikhe NS, Kim SH, Cho BY, Ye YM, Hur GY, Park HS. Association of three sets of high-affinity IgE receptor (FcepsilonR1) polymorphisms with aspirin-intolerant asthma. Respir Med 2008;102:1132-1139. https://doi.org/10.1016/j.rmed.2008.03.017
  73. Bae JS, Kim SH, Ye YM, et al. Significant association of FcepsilonRIalpha promoter polymorphisms with aspirin-intolerant chronic urticaria. J Allergy Clin Immunol 2007;119:449-456. https://doi.org/10.1016/j.jaci.2006.10.006
  74. Yamauchi K, Sekizawa K, Suzuki H, et al. Structure and function of human histamine N-methyltransferase: critical enzyme in histamine metabolism in airway. Am J Physiol 1994;267(3 Pt 1):L342-L349.
  75. Kim SH, Kang YM, Kim SH, et al. Histamine N-methyltransferase 939A>G polymorphism affects mRNA stability in patients with acetylsalicylic acid-intolerant chronic urticaria. Allergy 2009;64:213-221. https://doi.org/10.1111/j.1398-9995.2008.01795.x
  76. Pope SM, Brandt EB, Mishra A, et al. IL-13 induces eosinophil recruitment into the lung by an IL-5- and eotaxin-dependent mechanism. J Allergy Clin Immunol 2001;108:594-601. https://doi.org/10.1067/mai.2001.118600
  77. McLeod JJ, Baker B, Ryan JJ. Mast cell production and response to IL-4 and IL-13. Cytokine 2015;75:57-61. https://doi.org/10.1016/j.cyto.2015.05.019
  78. Kim BS, Park SM, Uhm TG, et al. Effect of single nucleotide polymorphisms within the interleukin-4 promoter on aspirin intolerance in asthmatics and interleukin-4 promoter activity. Pharmacogenet Genomics 2010;20:748-758.
  79. Palikhe NS, Kim SH, Choi GS, Ye YM, Park HS. No evidence of association between interleukin-13 gene polymorphism in aspirin intolerant chronic urticaria. Allergy Asthma Immunol Res 2009;1:36-40. https://doi.org/10.4168/aair.2009.1.1.36
  80. Palikhe NS, Kim SH, Cho BY, et al. IL-13 gene polymorphisms are associated with rhinosinusitis and eosinophilic inflammation in aspirin intolerant asthma. Allergy Asthma Immunol Res 2010;2:134-140. https://doi.org/10.4168/aair.2010.2.2.134
  81. Kohyama K, Abe S, Kodaira K, et al. IL-13 and IL-17A gene polymorphisms in Japanese patients with aspirin-exacerbated respiratory disease. Ann Allergy Asthma Immunol 2011;107:510-516. https://doi.org/10.1016/j.anai.2011.09.003
  82. Choi JH, Kim MA, Park HS. An update on the pathogenesis of the upper airways in aspirin-exacerbated respiratory disease. Curr Opin Allergy Clin Immunol 2014;14:1-6. https://doi.org/10.1097/ACI.0000000000000021
  83. Losol P, Kim SH, Shin YS, Ye YM, Park HS. A genetic effect of IL-5 receptor ${\alpha}$ polymorphism in patients with aspirin-exacerbated respiratory disease. Exp Mol Med 2013;45:e14. https://doi.org/10.1038/emm.2013.24
  84. Choi JH, Kim SH, Cho BY, et al. Association of TNF-alpha promoter polymorphisms with aspirin-induced urticaria. J Clin Pharm Ther 2009;34:231-238. https://doi.org/10.1111/j.1365-2710.2008.00979.x
  85. Szabo K, Kiricsi A, Revesz M, et al. The -308 G>A SNP of TNFA is a factor predisposing to chronic rhinosinusitis associated with nasal polyposis in aspirin-sensitive Hungarian individuals: conclusions of a genetic study with multiple stratifications. Int Immunol 2013;25:383-388. https://doi.org/10.1093/intimm/dxs162
  86. Kim SH, Son JK, Yang EM, Kim JE, Park HS. A functional promoter polymorphism of the human IL18 gene is associated with aspirin-induced urticaria. Br J Dermatol 2011;165:976-984. https://doi.org/10.1111/j.1365-2133.2011.10467.x
  87. Palikhe NS, Kim SH, Jin HJ, Nam YH, Park HS. Association of interleukin 10 promoter polymorphism at -819 T>C with aspirin-induced urticaria in a Korean population. Ann Allergy Asthma Immunol 2011;107:544-546. https://doi.org/10.1016/j.anai.2011.08.014
  88. Park JS, Park BL, Kim MO, et al. Association of single nucleotide polymorphisms on Interleukin 17 receptor A (IL17RA) gene with aspirin hypersensitivity in asthmatics. Hum Immunol 2013;74:598-606. https://doi.org/10.1016/j.humimm.2012.11.002
  89. Bronietzki AW, Schuster M, Schmitz I. Autophagy in T-cell development, activation and differentiation. Immunol Cell Biol 2015;93:25-34. https://doi.org/10.1038/icb.2014.81
  90. Dekker JW, Nizankowska E, Schmitz-Schumann M, et al. Aspirin-induced asthma and HLA-DRB1 and HLA-DPB1 genotypes. Clin Exp Allergy 1997;27:574-577. https://doi.org/10.1111/j.1365-2222.1997.tb00747.x
  91. Choi JH, Lee KW, Oh HB, et al. HLA association in aspirin-intolerant asthma: DPB1*0301 as a strong marker in a Korean population. J Allergy Clin Immunol 2004;113:562-564. https://doi.org/10.1016/j.jaci.2003.12.012
  92. Kim SH, Ye YM, Lee SK, et al. Association of TNF-alpha genetic polymorphism with HLA DPB1*0301. Clin Exp Allergy 2006;36:1247-1253. https://doi.org/10.1111/j.1365-2222.2006.02567.x
  93. Lympany PA, Welsh KI, Christie PE, Schmitz-Schumann M, Kemeny DM, Lee TH. An analysis with sequence-specific oligonucleotide probes of the association between aspirin-induced asthma and antigens of the HLA system. J Allergy Clin Immunol 1993;92(1 Pt 1):114-123. https://doi.org/10.1016/0091-6749(93)90045-H
  94. Shin SW, Park BL, Chang H, et al. Exonic variants associated with development of aspirin exacerbated respiratory diseases. PLoS One 2014;9:e111887. https://doi.org/10.1371/journal.pone.0111887
  95. Esmaeilzadeh H, Nabavi M, Amirzargar AA, et al. HLADRB and HLA-DQ genetic variability in patients with aspirin-exacerbated respiratory disease. Am J Rhinol Allergy 2015;29:e63-e69.
  96. Kim SH, Choi JH, Lee KW, et al. The human leucocyte antigen-DRB1*1302-DQB1*0609-DPB1*0201 haplotype may be a strong genetic marker for aspirin-induced urticaria. Clin Exp Allergy 2005;35:339-344. https://doi.org/10.1111/j.1365-2222.2004.02197.x
  97. Pacor ML, Di Lorenzo G, Mansueto P, et al. Relationship between human leucocyte antigen class I and class II and chronic idiopathic urticarial associated with aspirin and/or NSAIDs hypersensitivity. Mediators Inflamm 2006;2006:62489.
  98. Park TJ, Kim JH, Pasaje CF, et al. Polymorphisms of ATF6B are potentially associated with fev1 decline by aspirin provocation in asthmatics. Allergy Asthma Immunol Res 2014;6:142-148. https://doi.org/10.4168/aair.2014.6.2.142
  99. Kohyama K, Abe S, Kodaira K, et al. Polymorphisms of the CYP2C19 gene in Japanese patients with aspirin-exacerbated respiratory disease. J Allergy Clin Immunol 2011;128:1117-1120. https://doi.org/10.1016/j.jaci.2011.07.013
  100. Kim SH, Choi H, Yoon MG, Ye YM, Park HS. Dipeptidyl-peptidase 10 as a genetic biomarker for the aspirin-exacerbated respiratory disease phenotype. Ann Allergy Asthma Immunol 2015;114:208-213. https://doi.org/10.1016/j.anai.2014.12.003
  101. Losol P, Palikhe NS, Lee JW, et al. Association of P2RY12 polymorphisms with eosinophil and platelet activation in patients with aspirin-exacerbated respiratory disease. Ann Allergy Asthma Immunol 2015;114:423-424. https://doi.org/10.1016/j.anai.2015.02.009
  102. Cheong HS, Park SM, Kim MO, et al. Genome-wide methylation profile of nasal polyps: relation to aspirin hypersensitivity in asthmatics. Allergy 2011;66:637-644. https://doi.org/10.1111/j.1398-9995.2010.02514.x
  103. Choi JH, Kim JH, Park HS. Upper airways in aspirin-exacerbated respiratory disease. Curr Opin Allergy Clin Immunol 2015;15:21-26. https://doi.org/10.1097/ACI.0000000000000122
  104. Samter M, Beers RF Jr. Concerning the nature of intolerance to aspirin. J Allergy 1967;40:281-293. https://doi.org/10.1016/0021-8707(67)90076-7
  105. Graefe H, Roebke C, Schafer D, Meyer JE. Aspirin sensitivity and chronic rhinosinusitis with polyps: a fatal combination. J Allergy (Cairo) 2012;2012:817910.
  106. Lee RU, Stevenson DD. Aspirin-exacerbated respiratory disease: evaluation and management. Allergy Asthma Immunol Res 2011;3:3-10. https://doi.org/10.4168/aair.2011.3.1.3
  107. Jenkins C, Costello J, Hodge L. Systematic review of prevalence of aspirin induced asthma and its implications for clinical practice. BMJ 2004;328:434. https://doi.org/10.1136/bmj.328.7437.434
  108. Baenkler HW. Salicylate intolerance: pathophysiology, clinical spectrum, diagnosis and treatment. Dtsch Arztebl Int 2008;105:137-142.
  109. Asero R, Bavbek S, Blanca M, et al. Clinical management of patients with a history of urticaria/angioedema induced by multiple NSAIDs: an expert panel review. Int Arch Allergy Immunol 2013;160:126-133. https://doi.org/10.1159/000342424
  110. Parejo PA, Garcia-Agundez JA, Cornejo-Garcia JA, et al. Association study of functional polymorphisms in genes involved in histamine homeostasis and multiple NSAID: triggered urticaria and/or angioedema and anaphylaxis in patients without pre-existing chronic urticaria (MNSAID-UA). J Allergy Clin Immunol 2013;131(2 Suppl):AB169.
  111. Johansson SG, Bieber T, Dahl R, et al. Revised nomenclature for allergy for global use: report of the Nomenclature Review Committee of the World Allergy Organization, October 2003. J Allergy Clin Immunol 2004;113:832-836. https://doi.org/10.1016/j.jaci.2003.12.591
  112. Simons FE, Ardusso LR, Bilo MB, et al. 2012 Update: World Allergy Organization Guidelines for the assessment and management of anaphylaxis. Curr Opin Allergy Clin Immunol 2012;12:389-399. https://doi.org/10.1097/ACI.0b013e328355b7e4
  113. Nizankowska-Mogilnicka E, Bochenek G, Mastalerz L, et al. EAACI/GA2LEN guideline: aspirin provocation tests for diagnosis of aspirin hypersensitivity. Allergy 2007;62:1111-1118. https://doi.org/10.1111/j.1398-9995.2007.01409.x
  114. Scherer K, Brockow K, Aberer W, et al. Desensitization in delayed drug hypersensitivity reactions: an EAACI position paper of the Drug Allergy Interest Group. Allergy 2013;68:844-852. https://doi.org/10.1111/all.12161
  115. Mullol J, Picado C. Rhinosinusitis and nasal polyps in aspirin-exacerbated respiratory disease. Immunol Allergy Clin North Am 2013;33:163-176. https://doi.org/10.1016/j.iac.2012.11.002
  116. Pinto JM, Mehta N, DiTineo M, Wang J, Baroody FM, Naclerio RM. A randomized, double-blind, placebo-controlled trial of anti-IgE for chronic rhinosinusitis. Rhinology 2010;48:318-324.
  117. Vennera Mdel C, Picado C, Mullol J, Alobid I, Bernal-Sprekelsen M. Efficacy of omalizumab in the treatment of nasal polyps. Thorax 2011;66:824-825. https://doi.org/10.1136/thx.2010.152835
  118. Mesonjesi E, Ziu EP, Priftanji A, Qama D. Omalizumab for severe allergic asthma: a life changing drug? Clin Transl Allergy 2015;5(Suppl 2):P18.
  119. Brightling CE, Chanez P, Leigh R, et al. Efficacy and safety of tralokinumab in patients with severe uncontrolled asthma: a randomised, double-blind, placebo-controlled, phase 2b trial. Lancet Respir Med 2015;3:692-701. https://doi.org/10.1016/S2213-2600(15)00197-6
  120. Darveaux J, Busse WW. Biologics in asthma: the next step toward personalized treatment. J Allergy Clin Immunol Pract 2015;3:152-160. https://doi.org/10.1016/j.jaip.2014.09.014
  121. Fainardi V, Pisi G, Chetta A. Mepolizumab in the treatment of severe eosinophilic asthma. Immunotherapy 2016;8:27-34. https://doi.org/10.2217/imt.15.102
  122. Riechelmann H; Europaischen Akademie fur Allergie und Klinische Immunologie (EAACI) und der European Rhinologic Society (ERS). Chronic rhinosinusitis: EPOS 2012 part I. Laryngorhinootologie 2013;92:193-201. https://doi.org/10.1055/s-0033-1333704
  123. Cernadas JR, Brockow K, Romano A, et al. General considerations on rapid desensitization for drug hypersensitivity: a consensus statement. Allergy 2010;65:1357-1366. https://doi.org/10.1111/j.1398-9995.2010.02441.x
  124. White AA, Stevenson DD. Aspirin-exacerbated respiratory disease: update on pathogenesis and desensitization. Semin Respir Crit Care Med 2012;33:588-594. https://doi.org/10.1055/s-0032-1325618
  125. Oh MS, Seong GM, Lee HS, Lim GC, Lee J. Two cases of aspirin sensitive, intractable chronic urticaria successfully controlled by aspirin desensitization. Korean J Asthma Allergy Clin Immunol 2012;32:51-55.

Cited by

  1. KAAACI Standardization Committee Report on the procedures and applications of the diagnostic tests for drug allergy vol.5, pp.5, 2017, https://doi.org/10.4168/aard.2017.5.5.239
  2. Nonsteroidal anti-inflammatory drug hypersensitivity in the Asia-Pacific vol.8, pp.4, 2016, https://doi.org/10.5415/apallergy.2018.8.e38
  3. An update on the management of aspirin-exacerbated respiratory disease vol.12, pp.2, 2016, https://doi.org/10.1080/17476348.2018.1417843
  4. Probable cutaneous adverse drug reaction to piroxicam in a cat vol.4, pp.2, 2018, https://doi.org/10.1177/2055116918786598
  5. Increased Basal Blood Histamine Levels in Patients with Self-Reported Hypersensitivity to Non-Steroidal Anti-Inflammatory Drugs vol.181, pp.1, 2016, https://doi.org/10.1159/000503968
  6. Drug hypersensitivity reactions in Asia: regional issues and challenges vol.10, pp.None, 2016, https://doi.org/10.5415/apallergy.2020.10.e8
  7. Descriptive Analysis of Cross-Reactive Anaphylaxis as a Different Clinical Subtype of Nonsteroidal Anti-Inflammatory Drug (NSAID) Hypersensitivity vol.182, pp.2, 2021, https://doi.org/10.1159/000510335