View source for Atopy

{{Short description|Predisposition towards allergy}}
{{About|the disease|the philosophical use|Atopy (philosophy)}}
{{Infobox medical condition (new)
| name            = Atopy
| synonyms        = Atopic syndrome
| image           = Eczema-arms.jpg
| caption         = [[Eczema]]—a typical atopic manifestation
| pronounce       = {{IPAc-en|ˈ|æ|t|ə|p|iː}}<ref>[http://www.merriam-webster.com/dictionary/atopy Merriam-Webster Dictionary: Atopy]</ref>
| field           = [[Dermatology]], [[immunology]]
| symptoms        =
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| risks           =
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'''Atopy''' is the tendency to produce an exaggerated [[immunoglobulin E]] (IgE) [[immune response]] to otherwise harmless substances in the environment.<ref name=Ralston2018/> [[Allergic disease]]s are clinical manifestations of such inappropriate, '''atopic''' responses.<ref name=Ralston2018>{{Cite book|last=Ralston, Stuart H., Herausgeber. Penman, Ian D., Herausgeber. Strachan, Mark W. J., Herausgeber. Hobson, Richard P., Herausgeber. Britton, Robert, Illustrator. Davidson, Leybourne S. 1894-1981 Begründer des Werks.|title=Davidson's principles and practice of medicine |isbn=978-0-7020-7028-0 |oclc=1040673074 |date=2018-04-23|publisher=Elsevier }}</ref>

Atopy may have a [[heredity|hereditary]] component, although contact with the [[allergen]] or irritant must occur before the [[hypersensitivity]] reaction can develop (characteristically [[Type I hypersensitivity|after re-exposure]]).<ref name="urlMosby's Medical Dictionary:atopy">{{cite web|url=http://www.elsevier.com/wps/find/bookdescription.cws_home/716563/description#description |title=Mosby's Medical Dictionary:atopy |url-status = dead|archive-url=https://web.archive.org/web/20110710192530/http://www.elsevier.com/wps/find/bookdescription.cws_home/716563/description |archive-date=2011-07-10 }}</ref> Maternal psychological trauma during [[pregnancy]] may also be a strong indicator for development of atopy.<ref name=":0">{{Cite journal|last1=Wright|first1=Rosalind J|last2=Enlow|first2=Michelle Bosquet|date=2008-09-01|title=Maternal stress and perinatal programming in the expression of atopy|journal=Expert Review of Clinical Immunology|volume=4|issue=5|pages=535–538|doi=10.1586/1744666X.4.5.535|issn=1744-666X|pmc=2762209|pmid=19838310}}</ref>

The term ''atopy'' was coined by [[Arthur F. Coca]] and [[Robert Cooke (physician)|Robert Cooke]] in 1923<ref>Coca AF, Cooke RA. (1923) [http://www.jimmunol.org/cgi/content/abstract/8/3/163 On the classification of the phenomenon of hypersensitiveness] J Immunol</ref><ref name="RingPrzybilla2006">{{cite book|author1=Johannes Ring|author2=Bernhard Przybilla|author3=Thomas Ruzicka|title=Handbook of atopic eczema|url=https://books.google.com/books?id=jTktMX60bPwC&pg=PA3|access-date=4 May 2010|year=2006|publisher=Birkhäuser|isbn=978-3-540-23133-2|pages=3–}}</ref> from the [[Ancient Greek|Greek]] ἀτοπία meaning "the state of being out of place", "absurdity".<ref>{{cite web |url=https://www.etymonline.com/word/atopy |title=atopy |author=<!--Not stated--> |date=2019 |website=Online Etymology Dictionary |publisher=Douglas Harper |access-date=26 Sep 2019 }}</ref> Many physicians and scientists use the term ''atopy'' for any reaction mediated by IgE (even those that are appropriate and proportional to the antigen), but many [[Pediatrics|pediatricians]] reserve it to refer only to a genetically mediated predisposition to an excessive IgE reaction.<ref name="PawankarHolgate2009">{{cite book|author1=Ruby Pawankar|author2=Stephen T. Holgate|author3=Lanny J. Rosenwasser|title=Allergy Frontiers: Classification and Pathomechanisms|url=https://books.google.com/books?id=TJj3hqINS8sC&pg=PA33|access-date=4 May 2010|date=7 April 2009|publisher=Springer|isbn=978-4-431-88314-2|pages=33–}}</ref>

==Signs and symptoms==
Atopic sensitization is considered in the case of a person having IgE positivity or a prick test positivity to any common food- or air-borne allergen.<ref>{{Cite journal|last1=Simpson|first1=Angela|last2=Tan|first2=Vincent Y. F.|last3=Winn|first3=John|last4=Svensén|first4=Markus|last5=Bishop|first5=Christopher M.|last6=Heckerman|first6=David E.|last7=Buchan|first7=Iain|last8=Custovic|first8=Adnan|date=June 2010|title=Beyond Atopy|journal=American Journal of Respiratory and Critical Care Medicine|volume=181|issue=11|pages=1200–1206|doi=10.1164/rccm.200907-1101oc|pmid=20167852|issn=1073-449X|url=https://pure.manchester.ac.uk/ws/files/20022234/POST-PEER-REVIEW-NON-PUBLISHERS-DOCUMENT.PDF }}</ref> Atopic conditions are considered: [[atopic dermatitis]], [[allergic rhinitis]] (hay fever), [[allergic asthma]], atopic [[keratoconjunctivitis]]. The likelihood of having asthma, rhinitis and atopic dermatitis together is 10 times higher than could be expected by chance.<ref>{{Cite journal|last1=Sun|first1=Hai-Lun|last2=Yeh|first2=Chih-Jung|last3=Ku|first3=Min-Sho|last4=Lue|first4=Ko-Huang|date=2012-01-01|title=Coexistence of allergic diseases: Patterns and frequencies|journal=Allergy and Asthma Proceedings|volume=33|issue=1|pages=e1-4|doi=10.2500/aap.2012.33.3506|pmid=22370527|issn=1088-5412}}</ref>  Atopy is more common among individuals with a number of different conditions, such as [[eosinophilic esophagitis]] and [[non-celiac gluten sensitivity]].<ref name="MansuetoSeidita2014">{{cite journal|vauthors= Mansueto P, Seidita A, D'Alcamo A, Carroccio A|title= Non-celiac gluten sensitivity: literature review|year= 2014|journal= J Am Coll Nutr|volume= 33|issue= 1|pages=39–54|doi=10.1080/07315724.2014.869996|pmid= 24533607|type=Review|hdl= 10447/90208|s2cid= 22521576|url= https://iris.unipa.it/bitstream/10447/90208/1/Journal%20of%20the%20Americal%20College%20of%20Nutrition%202014%2033%2039-54.pdf|hdl-access= free}}</ref><ref name="GonzalezCerveraArias2017">{{cite journal| vauthors=González-Cervera J, Arias Á, Redondo-González O, Cano-Mollinedo MM, Terreehorst I, Lucendo AJ| title=Association between atopic manifestations and eosinophilic esophagitis: A systematic review and meta-analysis. | journal=Ann Allergy Asthma Immunol | year= 2017 | volume= 118 | issue= 5 | pages= 582–590.e2 | pmid=28366582 | doi=10.1016/j.anai.2017.02.006 | type=Systematic Review and Meta-analysis }}</ref>

Allergic reactions can range from sneezing and rhinorrhoea to anaphylaxis and even death.<ref name="tandfonline.com">{{Cite journal|date=July 2008|title=Davidson's Principles and Practice of Medicine, IE Edition, 20th Ed: Medicine—Clinical Medicine|journal=Journal of Endocrinology, Metabolism and Diabetes of South Africa|language=en|volume=13|issue=2|pages=75|doi=10.1080/22201009.2008.10872174|s2cid=220276722|issn=1608-9677|doi-access=free}}</ref>

==Pathophysiology==
In an allergic reaction, initial exposure to an otherwise harmless exogenous substance (known as an allergen) triggers the production of specific IgE antibodies by activated B cells.<ref name="tandfonline.com"/> These IgE antibodies bind to the surface of mast cells via high-affinity IgE receptors, a step that is not itself associated with a clinical response.<ref name="tandfonline.com"/> However, upon re-exposure, the allergen binds to membrane-bound IgE which activates the mast cells, releasing a variety of mediators.<ref name="tandfonline.com"/> This [[Hypersensitivity|type I hypersensitivity]] reaction is the basis of the symptoms of allergic reactions, which range from sneezing and rhinorrhoea to anaphylaxis.<ref name="tandfonline.com"/> Allergens can be a number of different substances, for example [[pollen]], [[dander]], [[dust mites]], and foods.

==Causes==
Atopic reactions are caused by localized [[hypersensitivity]] reactions to an [[allergen]]. Atopy appears to show a strong [[genetic disorder|hereditary component]]. One study concludes that the risk of developing atopic dermatitis (3%) or atopy in general (7%) "increases by a factor of two with each first-degree family member already suffering from atopy".<ref>
{{cite journal  |first1 = W.|last1=Küster|first2=M.|last2=Petersen|first3=E.|last3=Christophers|first4=M.|last4=Goos|first5=W.|last5=Sterry  | title = A family study of atopic dermatitis  | journal = Archives of Dermatological Research  | volume = 282  | issue =  2 / January, 1990  | pages = 98–102  | date = December 12, 2004  | doi = 10.1007/BF00493466  |pmid=2353830|s2cid=9396200}}</ref> As well, maternal stress and perinatal programming is increasingly understood as a root cause of atopy, finding that "...trauma may be a particularly robust potentiator of the cascade of biological events that increase vulnerability to atopy and may help explain the increased risk found in low-income urban populations."<ref name=":0" />

Environmental factors are also thought to play a role in the development of atopy, and the 'hygiene hypothesis' is one of the models that may explain the steep rise in the incidence of atopic diseases, though this hypothesis is incomplete and in some cases, contradictory to findings.<ref name=":0" /> This hypothesis proposes that excess 'cleanliness' in an infant's or child's environment can lead to a decline in the number of infectious stimuli that are necessary for the proper development of the immune system. The decrease in exposure to infectious stimuli may result in an imbalance between the infectious-response ("protective") elements and the allergic-response ("false alarm") elements within the immune system.<ref>{{cite journal | author = Grammatikos AP | year = 2008 | title = The genetic and environmental basis of atopic diseases | journal = Ann. Med. | volume = 40 | issue = 7| pages = 482–95 | doi = 10.1080/07853890802082096 | pmid = 18608118 | s2cid = 188280 | doi-access = free }}</ref>

Some studies also suggest that the maternal diet during pregnancy may be a causal factor in atopic diseases (including asthma) in offspring, suggesting that consumption of antioxidants, certain lipids, and/or a [[Mediterranean diet]] may help to prevent atopic diseases.

A Swedish research study titled "Atopy In Children Of Families With An Anthroposophic Lifestyle" comparing the rate of bronchial asthma, allergies, dermatitis, and other atopic diseases among [[Waldorf education|Steiner school]] pupils and pupils in public schools originally appeared in the May 1, 1999, edition of the British medical journal The Lancet.  The findings indicated that Steiner school pupils were "at a significantly lower risk of atopy" than children attending public schools.  The researchers investigated a variety of factors in the lives of the Steiner school pupils that might have contributed to this lower rate of atopy, which included breastfeeding, reduced immunization, avoidance of antibiotics and medications that reduce fevers, consumption of bio-dynamic and organic foods, and other physical aspects of the children's lives. <ref>{{cite journal |last1=Alm |first1=Johan S |last2=Swartz |first2=Jackie |last3=Lilja |first3=Gunnar |last4=Scheynius |first4=Annika |last5=Pershagen |first5=Göran |title=Atopy in children of families with an anthroposophic lifestyle |journal=The Lancet |date=May 1999 |volume=353 |issue=9163 |pages=1485–1488 |doi=10.1016/S0140-6736(98)09344-1|pmid=10232315 |s2cid=27540120 |citeseerx=10.1.1.586.4628 }}</ref>

The multicenter PARSIFAL study in 2006, involving 6,630 children age 5 to 13 in 5 European countries, suggested that reduced use of [[antibiotic]]s and [[antipyretic]]s is associated with a reduced risk of allergic disease in children.<ref name="Flöistrup 2006">{{cite journal | url=http://www.louisbolk.nl/downloads/mhuber/0601allergic.pdf | pmid=16387585 | doi=10.1016/j.jaci.2005.09.039 | volume=117 | title=Allergic disease and sensitization in Steiner school children | date=January 2006 | author=Flöistrup H, Swartz J, Bergström A | display-authors=etal | journal=J. Allergy Clin. Immunol. | issue=1 | pages=59–66 | access-date=2007-07-18 | archive-date=2007-09-27 | archive-url=https://web.archive.org/web/20070927025458/http://www.louisbolk.nl/downloads/mhuber/0601allergic.pdf | url-status=dead }}</ref>

===Genetics===
There is a strong genetic predisposition toward atopic allergies, especially on the maternal side. Because of the strong familial evidence, investigators have tried to map susceptibility genes for atopy.<ref>{{cite journal | author = Blumenthal MN | year = 2005 | title = The Role of Genetics in the Development of Asthma and Atopy | journal = Curr Opin Allergy Clin Immunol | volume = 5 | issue = 141–5| pages = 141–5 | doi = 10.1097/01.all.0000162306.12728.c2 | pmid = 15764904 | s2cid = 30698973 }}</ref><ref>{{cite journal |vauthors=Hoffjan S, Nicolae D, Ober C| year = 2003 | title = Association Studies for Asthma and Atopic Diseases: A Comprehensive Review of the Literature | journal = Respir Res | volume = 4 | issue = 14| page = 14748924 | doi = 10.1186/1465-9921-4-14 | pmid = 14748924 | pmc = 314398 | doi-access = free }}</ref> Genes for atopy ([[C11orf30]], [[STAT6]], [[SLC25A46]], [[HLA-DQB1]], IL1RL1/IL18R1, TLR1/TLR6/TLR10, LPP, MYC/PVT1, IL2/ADAD1, HLA-B/MICA)<ref>{{cite journal|last1=Bønnelykke|first1=Klaus|last2=Matheson|first2=Melanie C|last3=Pers|first3=Tune H|last4=Granell|first4=Raquel|last5=Strachan|first5=David P|last6=Alves|first6=Alexessander Couto|last7=Linneberg|first7=Allan|last8=Curtin|first8=John A|last9=Warrington|first9=Nicole M|last10=Standl|first10=Marie|last11=Kerkhof|first11=Marjan|last12=Jonsdottir|first12=Ingileif|last13=Bukvic|first13=Blazenka K|last14=Kaakinen|first14=Marika|last15=Sleimann|first15=Patrick|last16=Thorleifsson|first16=Gudmar|last17=Thorsteinsdottir|first17=Unnur|last18=Schramm|first18=Katharina|last19=Baltic|first19=Svetlana|last20=Kreiner-Møller|first20=Eskil|last21=Simpson|first21=Angela|last22=Pourcain|first22=Beate St|last23=Coin|first23=Lachlan|last24=Hui|first24=Jennie|last25=Walters|first25=Eugene H|last26=Tiesler|first26=Carla M T|last27=Duffy|first27=David L|last28=Jones|first28=Graham|last29=Ring|first29=Susan M|last30=McArdle|first30=Wendy L|last31=Price|first31=Loren|last32=Robertson|first32=Colin F|last33=Pekkanen|first33=Juha|last34=Tang|first34=Clara S|last35=Thiering|first35=Elisabeth|last36=Montgomery|first36=Grant W|last37=Hartikainen|first37=Anna-Liisa|last38=Dharmage|first38=Shyamali C|last39=Husemoen|first39=Lise L|last40=Herder|first40=Christian|last41=Kemp|first41=John P|last42=Elliot|first42=Paul|last43=James|first43=Alan|last44=Waldenberger|first44=Melanie|last45=Abramson|first45=Michael J|last46=Fairfax|first46=Benjamin P|last47=Knight|first47=Julian C|last48=Gupta|first48=Ramneek|last49=Thompson|first49=Philip J|last50=Holt|first50=Patrick|last51=Sly|first51=Peter|last52=Hirschhorn|first52=Joel N|last53=Blekic|first53=Mario|last54=Weidinger|first54=Stephan|last55=Hakonarsson|first55=Hakon|last56=Stefansson|first56=Kari|last57=Heinrich|first57=Joachim|last58=Postma|first58=Dirkje S|last59=Custovic|first59=Adnan|last60=Pennell|first60=Craig E|last61=Jarvelin|first61=Marjo-Riitta|last62=Koppelman|first62=Gerard H|last63=Timpson|first63=Nicholas|last64=Ferreira|first64=Manuel A|last65=Bisgaard|first65=Hans|last66=Henderson|first66=A John|title=Meta-analysis of genome-wide association studies identifies ten loci influencing allergic sensitization|journal=Nature Genetics|date=30 June 2013|volume=45|issue=8|pages=902–906|doi=10.1038/ng.2694|pmid=23817571|pmc=4922420}}</ref> tend to be involved in allergic responses or other components of the immune system. The gene C11orf30 seems to be the most relevant for atopy as it may increase susceptibility to poly-sensitization.<ref>{{cite journal|last1=Amaral|first1=André F. S.|last2=Minelli|first2=Cosetta|last3=Guerra|first3=Stefano|last4=Wjst|first4=Matthias|last5=Probst-Hensch|first5=Nicole|last6=Pin|first6=Isabelle|last7=Svanes|first7=Cecilie|last8=Janson|first8=Christer|last9=Heinrich|first9=Joachim|last10=Jarvis|first10=Deborah L.|title=The locus increases susceptibility to poly-sensitisation|journal=Allergy|date=December 2014|pages=328–333|doi=10.1111/all.12557|volume=70|issue=3|pmid=25546184|hdl=10044/1/21574|s2cid=25960081|url=http://spiral.imperial.ac.uk/bitstream/10044/1/21574/6/Amaral_Allergy_revised_unmarked_forSPIRAL_11-3-2015.pdf|hdl-access=free}}</ref>

===''Staphylococcus aureus''===
Bleach baths provide temporary control of eczema.<ref>{{Cite journal | last1 = Nguyen | first1 = T. | last2 = Zuniga | first2 = R. | title = Skin conditions: New drugs for managing skin disorders | journal = FP Essentials | volume = 407 | pages = 11–16 | year = 2013 | pmid = 23600334}}</ref> [[Ciprofloxacin]] is an allergen that may cause [[contact dermatitis]], symptoms of which are indistinguishable from eczema.<ref>{{Cite journal | last1 = Lee | first1 = S. W. | last2 = Cheong | first2 = S. H. | last3 = Byun | first3 = J. Y. | last4 = Choi | first4 = Y. W. | last5 = Choi | first5 = H. Y. | title = Occupational hand eczema among nursing staffs in Korea: Self-reported hand eczema and contact sensitization of hospital nursing staffs | doi = 10.1111/1346-8138.12036 | journal = The Journal of Dermatology | volume = 40 | issue = 3 | pages = 182–187 | year = 2013 | pmid = 23294332 | s2cid = 33771711 }}</ref> [[Filaggrin]] mutations are associated with atopic eczema and may contribute to the excessive dryness of the skin and the loss of the barrier function of normal skin.<ref>{{cite journal |vauthors=O'Regan GM, Sandilands A, McLean WH, Irvine AD| year = 2008 | title = Filaggrin in Atopic Dermatitis | doi = 10.1016/j.jaci.2008.08.002 | journal = J Allergy Clin Immunol | volume = 122 | issue = 4 | pages = 689–93| pmid = 18774165 }}</ref> It may be possible that the filaggrin mutations and the loss of the normal skin barrier expose crevices that make it possible for ''Staphylococcus aureus'' to colonize the skin.<ref>{{cite journal | author = Breuer K, [[Alexander Kapp (dermatologist and allergist)|Kapp A]], Werfel T | year = 2001 | title = Bacterial Infections and Atopic Dermatitis | journal = Allergy | volume = 56 | issue = 11 | pages = 1034–41| pmid = 11703215 | doi = 10.1034/j.1398-9995.2001.00146.x | s2cid = 28897487 | doi-access = free }}</ref> Atopic eczema is often associated with genetic defects in genes that control allergic responses. Thus, some investigators have proposed that atopic eczema is an allergic response to increased ''Staphylococcus aureus'' colonization of the skin.<ref>{{cite journal |vauthors=Abramson JS, Dahl MV, Walsh G, Blumenthal MN, Douglas SD, Quie PG| year = 1982 | title = Antistaphylococcal IgE in Patients with Atopic Dermatitis | journal = J Am Acad Dermatol | volume = 7 | issue = 1 | pages = 105–110| doi = 10.1016/s0190-9622(82)80017-0 | pmid = 7107990 }}</ref> A hallmark indicator of atopic eczema is a positive [[wheal and flare]] reaction to a skin test of ''S. aureus'' antigens. In addition, several studies have documented that an IgE-mediated response to ''S. aureus'' is present in people with atopic eczema.<ref>{{cite journal |vauthors=Parish WE, Welbourn E, Champion RH| year = 1976 | title = Hypersensitivity to Bacteria in Eczema. Ii. Titre and Immunoglobulin Class of Antibodies to Staphylococci and Micrococci | journal = Br J Dermatol | volume = 95 | issue = 3 | pages = 285–93| doi = 10.1111/j.1365-2133.1976.tb07016.x | pmid = 974019 | s2cid = 5842899 }}</ref><ref>{{cite journal |vauthors=Motala C, Potter PC, Weinberg EG, Malherbe D, Hughes J| year = 1986 | title = Anti-''Staphylococcus aureus''-Specific IgE in Atopic Dermatitis | journal = J Allergy Clin Immunol | volume = 78 | issue = 4 Pt 1 | pages = 583–9| pmid = 3771950 | doi = 10.1016/0091-6749(86)90075-8 }}</ref>

== Changes in prevalence over time ==
In adults, the prevalence of IgE sensitization to allergens from [[house dust mite]] and cat, but not grass, seems to decrease over time as people age.<ref>{{cite journal|last1=Amaral|first1=André F.S.|last2=Newson|first2=Roger B.|last3=Abramson|first3=Michael J.|last4=Antó|first4=Josep M.|last5=Bono|first5=Roberto|last6=Corsico|first6=Angelo G.|last7=de Marco|first7=Roberto|last8=Demoly|first8=Pascal|last9=Forsberg|first9=Bertil|last10=Gislason|first10=Thorarinn|last11=Heinrich|first11=Joachim|last12=Huerta|first12=Ismael|last13=Janson|first13=Christer|last14=Jõgi|first14=Rain|last15=Kim|first15=Jeong-Lim|last16=Maldonado|first16=José|last17=Martinez-Moratalla Rovira|first17=Jesús|last18=Neukirch|first18=Catherine|last19=Nowak|first19=Dennis|last20=Pin|first20=Isabelle|last21=Probst-Hensch|first21=Nicole|last22=Raherison-Semjen|first22=Chantal|last23=Svanes|first23=Cecilie|last24=Urrutia Landa|first24=Isabel|last25=van Ree|first25=Ronald|last26=Versteeg|first26=Serge A.|last27=Weyler|first27=Joost|last28=Zock|first28=Jan-Paul|last29=Burney|first29=Peter G.J.|last30=Jarvis|first30=Deborah L.|title=Changes in IgE sensitization and total IgE levels over 20 years of follow-up|journal=Journal of Allergy and Clinical Immunology|date=November 2015|doi=10.1016/j.jaci.2015.09.037|pmid=26586040|pmc=4889785|volume=137|issue=6|pages=1788–1795.e9}}</ref> However, the biological reasons for these changes are not fully understood.

== Treatments ==
Treatments for atopic disorders depend on the organ(s) involved. They can vary from local treatment options, often topical [[corticosteroid]]s, to systemic treatment options with oral corticosteroids, biological treatments (e.g. [[omalizumab]], [[mepolizumab]]) or [[allergen immunotherapy]].<ref>{{Cite journal|last1=Wollenberg|first1=A.|last2=Barbarot|first2=S.|last3=Bieber|first3=T.|last4=Christen-Zaech|first4=S.|last5=Deleuran|first5=M.|last6=Fink-Wagner|first6=A.|last7=Gieler|first7=U.|last8=Girolomoni|first8=G.|last9=Lau|first9=S.|last10=Muraro|first10=A.|last11=Czarnecka-Operacz|first11=M.|date=May 2018|title=Consensus-based European guidelines for treatment of atopic eczema (atopic dermatitis) in adults and children: part I|journal=Journal of the European Academy of Dermatology and Venereology|language=en|volume=32|issue=5|pages=657–682|doi=10.1111/jdv.14891|pmid=29676534|doi-access=free}}</ref><ref>{{Cite journal|last1=Reddel|first1=Helen K.|last2=Bateman|first2=Eric D.|last3=Becker|first3=Allan|last4=Boulet|first4=Louis-Philippe|last5=Cruz|first5=Alvaro A.|last6=Drazen|first6=Jeffrey M.|last7=Haahtela|first7=Tari|last8=Hurd|first8=Suzanne S.|last9=Inoue|first9=Hiromasa|last10=de Jongste|first10=Johan C.|last11=Lemanske|first11=Robert F.|date=September 2015|title=A summary of the new GINA strategy: a roadmap to asthma control|journal=European Respiratory Journal|language=en|volume=46|issue=3|pages=622–639|doi=10.1183/13993003.00853-2015|issn=0903-1936|pmc=4554554|pmid=26206872}}</ref><ref>{{Cite journal|last1=Klimek|first1=Ludger|last2=Bachert|first2=Claus|last3=Pfaar|first3=Oliver|last4=Becker|first4=Sven|last5=Bieber|first5=Thomas|last6=Brehler|first6=Randolf|last7=Buhl|first7=Roland|last8=Casper|first8=Ingrid|last9=Chaker|first9=Adam|last10=Czech|first10=Wolfgang|last11=Fischer|first11=Jörg|date=2020-02-12|title=Correction to "ARIA guideline 2019: treatment of allergic rhinitis in the German health system"|journal=Allergo Journal International|volume=29|issue=2|pages=63–65|language=en|doi=10.1007/s40629-019-00115-4|s2cid=211089322 |issn=2197-0378|doi-access=}}</ref>

==See also==
*[[Eczema]]
*[[Asthma]] 
*[[Rhinitis]]
*[[Anaphylaxis]]
*[[Allergic march]]

==References==
{{Reflist}}

== External links ==
{{Medical resources
|  DiseasesDB     = 34489
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|  ICD9           = {{ICD9|691.8}}
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|  OMIM           = 147050
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* [https://www.atsdr.cdc.gov/csem/csem.html Case Studies in Environmental Medicine (CSEM): Environmental Triggers of Asthma] – Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services.

{{Hypersensitivity and autoimmune diseases| state=collapsed}}
{{Authority control}}

[[Category:Type I hypersensitivity]]