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| '''For the WikiPatient page for this topic, click [[Allergy (patient information)|here]]'''
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| {{Infobox_Disease |
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| Name = {{PAGENAME}} |
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| Image = |
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| Caption = |
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| DiseasesDB = 33481 |
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| ICD10 = {{ICD10|T|78|4|t|66}} |
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| ICD9 = {{ICD9|995.3}} |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = 000812 |
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| eMedicineSubj = med |
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| eMedicineTopic = 1101 |
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| MeshID = D006967 |
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| {{SI}}
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| {{CMG}}
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| __NOTOC__ | | __NOTOC__ |
| {{Editor Help}}
| | '''For patient information, click [[Allergy (patient information)|here]]''' |
| ==Overview==
| | {{Allergy}} |
| '''Allergy''' is a disorder of the [[immune system]] that is often called [[atopy]]. Allergic reactions occur to environmental substances known as [[allergen]]s; these reactions are [[Acquired disorder|acquired]], predictable and rapid. Strictly, allergy is one of four forms of [[hypersensitivity]] and is called ''type I'' (or ''immediate'') hypersensitivity. It is characterized by excessive activation of certain [[white blood cell]]s called [[mast cell]]s and [[basophil granulocyte|basophils]] by a type of [[antibody]], known as [[IgE]], resulting in an extreme [[Inflammation|inflammatory]] response. Common allergic reactions include [[eczema]], [[urticaria|hives]], [[hay fever]], [[asthma]], [[food allergy|food allergies]], and reactions to the [[venom]] of stinging insects such as wasps and bees.<ref>{{cite journal |author=Kay AB |title=Overview of 'allergy and allergic diseases: with a view to the future' |journal=Br. Med. Bull. |volume=56 |issue=4 |pages=843–64 |year=2000 |pmid=11359624 |doi=}}</ref> | | {{CMG}} {{AE}} {{MMT}} |
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| Mild allergies like [[hay fever]], are highly prevalent in the human [[population]] and cause [[symptom]]s such as [[allergic conjunctivitis]], itchiness and [[rhinorrhea|runny nose]]. Similarly, conditions such as [[asthma]] are common, in which allergy plays a major role. In some people, severe allergies to environmental or dietary allergens, or to [[medication]], occur that may result in life-threatening [[anaphylaxis|anaphylactic reactions]] and potentially death.
| | ==[[Allergy overview|Overview]]== |
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| A variety of tests now exist to diagnose allergic conditions; these include testing the skin for responses to known allergens or analyzing the blood for the presence and levels of allergen-specific IgE. Treatments for allergies include allergen avoidance, use of [[antihistamine]]s, [[steroid]]s or other [[oral]] medications, [[immunotherapy]] to [[Desensitization (medicine)|desensitize]] the response to allergen, and [[targeted therapy]].
| | ==[[Allergy historical perspective|Historical Perspective]]== |
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| ==Classification and history== | | ==[[Allergy classification|Classification]]== |
| The concept "allergy" was originally introduced in 1906 by the Viennese [[pediatrician]] [[Clemens von Pirquet]], after noting that some of his patients were hypersensitive to normally innocuous entities such as dust, [[pollen]], or certain foods.<ref>{{WhoNamedIt|Doctor|2382|Clemens Peter Pirquet von Cesenatico}}</ref> Pirquet called this phenomenon "allergy" from the Greek words ''allos'' meaning "other" and ''ergon'' meaning "work".<ref>{{cite journal|author=Von Pirquet C|year=1906|title=Allergie|journal=Munch Med Wochenschr|volume=53|pages=1457}}</ref> Historically, all forms of hypersensitivity were classified as allergies, and all were thought to be caused by an improper activation of the immune system. Later, it became clear that several different [[disease]] mechanisms were implicated, with the common link to a disordered activation of the immune system. In 1963, a new classification scheme was designed by [[Philip George Houthem Gell|Philip Gell]] and [[Robin Coombs]] that described four types of [[hypersensitivities|hypersensitivity reactions]], known as Type I to Type IV hypersensitivity.<ref name=GellCoombs>{{cite book |author=Gell PGH, Coombs RRA. |title=Clinical Aspects of Immunology |publisher=Blackwell |location=London |year=1963}}</ref> With this new classification, the word "allergy" was restricted to only type I hypersensitivities (also called immediate hypersensitivity), which are characterized as rapidly developing reactions.
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| A major breakthrough in understanding the mechanisms of allergy was the discovery of the antibody class labeled [[immunoglobulin E]] (IgE) - [[Kimishige Ishizaka]] and co-workers were the first to isolate and describe IgE in the 1960s.<ref>{{cite journal |author=Ishizaka K, Ishizaka T, Hornbrook MM |title=Physico-chemical properties of human reaginic antibody. IV. Presence of a unique immunoglobulin as a carrier of reaginic activity |journal=J. Immunol. |volume=97 |issue=1 |pages=75–85 |year=1966 |pmid=4162440 |doi=}}</ref>
| | ==[[Allergy pathophysiology|Pathophysiology]]== |
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| ==Signs and symptoms== | | ==[[Allergy causes|Causes]]== |
| {| class = "prettytable" style = "width:50%; float:right; font-size:90%; margin-left:15px"
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| |+Common symptoms of allergy
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| ! Affected organ || Symptom
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| |[[Nose]]|| swelling of the nasal [[mucous membrane|mucosa]] (allergic rhinitis)
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| |[[Paranasal sinus|Sinuses]]||allergic [[sinusitis]]
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| | [[Eye]]s|| redness and [[itch]]ing of the [[conjunctiva]] (allergic conjunctivitis)
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| |[[Airway]]s|| Sneezing, coughing, [[bronchoconstriction]], [[wheeze|wheezing]] and [[dyspnea]], sometimes outright attacks of [[asthma]], in severe cases the airway constricts due to swelling known as [[angioedema]]
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| |[[Ear]]s|| feeling of fullness, possibly pain, and impaired hearing due to the lack of [[eustachian tube]] drainage.
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| |[[Skin]]|| [[rash]]es, such as [[eczema]] and [[urticaria|hives (urticaria)]]
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| |[[Gastrointestinal tract]]|| [[abdominal pain]], [[bloating]], [[vomiting]], [[Diarrhea]]
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| |}
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| Many allergens are [[wiktionary:airborne|airborne]] particles, such as dust or pollen. In these cases, symptoms arise in areas in contact with air, such as eyes, nose and lungs. For instance, allergic rhinitis, also known as hay fever, causes irritation of the nose, sneezing, and itching and redness of the eyes.<ref>{{cite book |author=Bope, Edward T.; Rakel, Robert E. |title=Conn's Current Therapy 2005 |publisher=W.B. Saunders Company |location=Philadelphia, PA |year= |pages=880 |isbn=0721 6386 43 |oclc= |doi=}}</ref> Inhaled allergens can also lead to asthmatic symptoms, caused by narrowing of the airways ([[bronchoconstriction]]) and increased production of [[mucus]] in the [[lung]]s, shortness of breath ([[dyspnea]]), coughing and wheezing.<ref name=holgate98>
| | ==[[Allergy differential diagnosis|Differentiating Allergy from other Diseases]]== |
| {{cite journal |author=Holgate ST |title=Asthma and allergy--disorders of civilization? |journal=QJM |volume=91 |issue=3 |pages=171–84 |year=1998 |pmid=9604069 |doi=}}</ref>
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| Aside from these ambient allergens, allergic reactions can result from foods, insect stings, and reactions to [[medication]]s like [[aspirin]], and [[antibiotic]]s such as [[penicillin]]. Symptoms of food allergy include abdominal pain, bloating, vomiting, diarrhoea, itchy skin, and swelling of the skin during hives or [[angiooedema]]. Food allergies rarely cause [[respiratory tract|respiratory]] (asthmatic) reactions, or [[rhinitis]].<ref name=rusznak98>{{cite journal |author=Rusznak C, Davies RJ |title=ABC of allergies. Diagnosing allergy |journal=BMJ |volume=316 |issue=7132 |pages=686–9 |year=1998 |pmid=9522798 |doi=}}</ref> Insect stings, antibiotics and certain medicines produce a systemic allergic response that is also called [[anaphylaxis]]; multiple systems can be affected including the [[digestive system]], the [[respiratory system]], and the [[circulatory system]].<ref>{{cite journal |author=Golden DB |title=Insect sting anaphylaxis |journal=Immunol Allergy Clin North Am |volume=27 |issue=2 |pages=261–72, vii |year=2007 |pmid=17493502 |doi=10.1016/j.iac.2007.03.008}}</ref><ref>{{cite journal |author=Schafer JA, Mateo N, Parlier GL, Rotschafer JC |title=Penicillin allergy skin testing: what do we do now? |journal=Pharmacotherapy |volume=27 |issue=4 |pages=542–5 |year=2007 |pmid=17381381 |doi=10.1592/phco.27.4.542}}</ref><ref name=tang03>{{cite journal |author=Tang AW |title=A practical guide to anaphylaxis |journal=Am Fam Physician |volume=68 |issue=7 |pages=1325–32 |year=2003 |pmid=14567487 |doi=}}</ref> Depending of the rate of severity, it can cause [[cutaneous]] reactions, bronchoconstriction, [[edema]], [[hypotension]], [[coma]] and even [[death]]. This type of reaction can be triggered suddenly or the onset can be delayed. The severity of this type of allergic response often requires injections of [[epinephrine]], sometimes through a device known as the [[Epi-Pen]] auto-injector. The nature of [[anaphylaxis]] is such that the reaction can seemingly be subsiding, but may recur throughout a prolonged period of time. <ref name=tang03/>
| | ==[[Allergy epidemiology and demographics|Epidemiology and Demographics]]== |
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| Substances that come into contact with the skin, such as latex are also common causes of allergic reactions, known as [[contact dermatitis]] or eczema.<ref>{{cite journal |author=Brehler R, Kütting B |title=Natural rubber latex allergy: a problem of interdisciplinary concern in medicine |journal=Arch. Intern. Med. |volume=161 |issue=8 |pages=1057–64 |year=2001 |pmid=11322839 |doi=}}</ref> Skin allergies frequently cause rashes, or swelling and inflammation within the skin, in what is known as a "[[wheal]] and flare" reaction characteristic of hives and angioedema.<ref>{{cite journal |author=Muller BA |title=Urticaria and angioedema: a practical approach |journal=Am Fam Physician |volume=69 |issue=5 |pages=1123–8 |year=2004 |pmid=15023012 |doi=}}</ref>
| | ==[[Allergy risk factors|Risk Factors]]== |
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| ==Cause== | | ==[[Allergy screening|Screening]]== |
| Risk factors for allergy can be placed in two general categories, namely [[Host (biology)|host]] and environmental factors. Host factors include [[heredity]], [[gender|sex]], [[Race (classification of human beings)|race]] and age, with heredity being by far the most important. There are recent increases in the incidence of allergic disorders, however, that cannot be explained by genetic factors alone. The four main candidate environmental factors are alterations in exposure to [[infectious disease]]s during early childhood, environmental pollution, allergen levels, and [[Diet (nutrition)|dietary]] changes.<ref name=Janeway>{{cite book | last = Janeway | first = Charles | authorlink = Charles Janeway | coauthors = Paul Travers, Mark Walport, and Mark Shlomchik | title = Immunobiology; Fifth Edition | publisher = Garland Science | date= 2001 | location = New York and London| pages = e-book | url = http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=imm.TOC&depth=10| doi = | id = ISBN 0-8153-4101-6}}.</ref>
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| ===Genetic basis=== | | ==[[Allergy natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| Allergic diseases are strongly familial: [[Identical_twins#Identical_twins|identical twins]] are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in [[twin#Fraternal_twins|non-identical twins]].<ref>{{cite journal |author=Galli SJ |title=Allergy |journal=Curr. Biol. |volume=10 |issue=3 |pages=R93–5 |year=2000 |pmid=10679332 |doi=}}</ref> Allergic parents are more likely to have allergic children,<ref name=DeSwert>{{cite journal |author=De Swert LF |title=Risk factors for allergy |journal=Eur. J. Pediatr. |volume=158 |issue=2 |pages=89–94 |year=1999 |pmid=10048601 |doi=}}</ref> and their allergies are likely to be stronger than those from non-allergic parents. However some allergies are not consistent along [[Genealogy|genealogies]]; parents who are allergic to peanuts, may have children who are allergic to ragweed, or siblings that are allergic to different things. It seems that the likelihood of developing allergies is [[Heredity|inherited]] and due to some irregularity in the way the immune system works, but the specific allergen, which causes the development of an allergy, is not.<ref name=DeSwert/>
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| The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk.<ref name=Croner>{{cite journal |author=Croner S |title=Prediction and detection of allergy development: influence of genetic and environmental factors |journal=J. Pediatr. |volume=121 |issue=5 Pt 2 |pages=S58–63 |year=1992 |pmid=1447635 |doi=}}</ref> Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years.<ref name=Croner/> The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.<ref>Jarvis D, Burney P (1997) Epidemiology of atopy and atopic disease In: Kay AB (ed) Allergy and allergic diseases, vol 2. Blackwell Science London, pp 1208–1224</ref> Overall, boys have a higher risk of developing allergy than girls,<ref name=DeSwert/> although for some diseases, namely asthma in young adults, females are more likely to be affected.<ref>{{cite journal |author=Anderson HR, Pottier AC, Strachan DP |title=Asthma from birth to age 23: incidence and relation to prior and concurrent atopic disease |journal=Thorax |volume=47 |issue=7 |pages=537–42 |year=1992 |pmid=1412098 |doi=}}</ref> Sex differences tend to decrease in adulthood.<ref name=DeSwert/> Ethnicity may play a role in some allergies, however racial factors have been difficult to separate from environmental influences and changes due to migration.<ref name=DeSwert/> Interestingly, with regards to asthma, it has been suggested that different [[Locus (genetics)|genetic loci]] are responsible for asthma in people of Caucasian, Hispanic, Asian, and African origins.<ref>{{cite journal |author=Barnes KC, Grant AV, Hansel NN, Gao P, Dunston GM |title=African Americans with asthma: genetic insights |url= http://pats.atsjournals.org/cgi/content/full/4/1/58 |journal=Proc Am Thorac Soc |volume=4 |issue=1 |pages=58–68 |year=2007 |pmid=17202293 |doi=10.1513/pats.200607-146JG}}</ref>
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| ===Environmental factors===
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| International differences have been associated with the number of individuals within a population that suffer from allergy. Allergic diseases are more common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations, although these differences are becoming less defined.<ref name = cooper04>{{cite journal |author=Cooper PJ |title=Intestinal worms and human allergy |journal=Parasite Immunol. |volume=26 |issue=11-12 |pages=455–67 |year=2004 |pmid=15771681 |doi=10.1111/j.0141-9838.2004.00728.x}}</ref>
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| Exposure to allergens, especially in early life, is an important [[Risk factor|risk factor]] for allergy. Alterations in exposure to [[microorganism]]s is the most plausible explanation, at present, for the increase in [[Atopy|atopic allergy]].<ref name= Janeway/> Since children that live in large families or overcrowded households, or attend day care, have a reduced incidence of allergic disease, a relationship has been proposed between exposures to [[bacteria]] and [[virus]]es during childhood, and protection against the development of allergy, which has been called – the "[[hygiene hypothesis]]".<ref name = cooper04/> Exposure to [[endotoxin]] and other components of bacteria may reduce atopic diseases.<ref name="pmid12063508">{{cite journal |author=von Mutius E |title=Environmental factors influencing the development and progression of pediatric asthma |journal=J. Allergy Clin. Immunol. |volume=109 |issue=6 Suppl |pages=S525–32 |year=2002 |pmid=12063508 |doi=}}</ref> Endotoxin exposure reduces release of inflammatory [[cytokine]]s such as [[tumor necrosis factor alpha|TNF-α]], [[interferon-gamma|IFNγ]], [[interleukin-10]], and [[interleukin-12]] from white blood cells ([[leukocytes]]) that circulate in the [[blood]].<ref name="pmid12239255">{{cite journal |author=Braun-Fahrländer C, Riedler J, Herz U, ''et al'' |title=Environmental exposure to endotoxin and its relation to asthma in school-age children |journal=N. Engl. J. Med. |volume=347 |issue=12 |pages=869–77 |year=2002 |pmid=12239255 |doi=10.1056/NEJMoa020057}}</ref> Certain microbe-sensing [[protein]]s, known as [[Toll-like receptor]]s, found on the surface of cells in the body are also thought to be involved in these processes.<ref>{{cite journal |author=Garn H, Renz H |title=Epidemiological and immunological evidence for the hygiene hypothesis |journal=Immunobiology |volume=212 |issue=6 |pages=441–52 |year=2007 |pmid=17544829 |doi=10.1016/j.imbio.2007.03.006}}</ref>
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| Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine [[chlorination]] and purification of drinking water supplies.<ref>{{cite journal |author=Macpherson CN, Gottstein B, Geerts S |title=Parasitic food-borne and water-borne zoonoses |journal=Rev. - Off. Int. Epizoot. |volume=19 |issue=1 |pages=240–58 |year=2000 |pmid=11189719 |doi=}}</ref> Recent research has shown that some common [[parasite]]s, such as [[Intestinal parasite|intestinal worm]]s (e.g. [[hookworm]]s), secrete chemicals into the gut wall (and hence the bloodstream) that [[immunosuppressant|suppress]] the immune system and prevent the body from attacking the parasite.<ref>{{cite journal |author=Carvalho EM, Bastos LS, Araújo MI |title=Worms and allergy |journal=Parasite Immunol. |volume=28 |issue=10 |pages=525–34 |year=2006 |pmid=16965288 |doi=10.1111/j.1365-3024.2006.00894.x}}</ref> This gives rise to a new slant on the hygiene hypothesis theory — that co-evolution of man and parasites has led to an immune system that only functions correctly in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive.<ref>{{cite journal |author=Yazdanbakhsh M, Kremsner PG, van Ree R |title=Allergy, parasites, and the hygiene hypothesis |journal=Science |volume=296 |issue=5567 |pages=490–4 |year=2002 |pmid=11964470 |doi=10.1126/science.296.5567.490}}</ref> In particular, research suggests that allergies may coincide with the delayed establishment of [[gut flora]] in [[infant]]s.<ref name="pmid17382394">{{cite journal |author=Emanuelsson C, Spangfort MD |title=Allergens as eukaryotic proteins lacking bacterial homologues |journal=Mol. Immunol. |volume=44 |issue=12 |pages=3256–60 |year=2007 |pmid=17382394 |doi=10.1016/j.molimm.2007.01.019}}</ref> However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms.<ref name = cooper04/> Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies.<ref name = falcone05>{{cite journal |author=Falcone FH, Pritchard DI |title=Parasite role reversal: worms on trial |journal=Trends Parasitol. |volume=21 |issue=4 |pages=157–60 |year=2005 |pmid=15780835 |doi=10.1016/j.pt.2005.02.002}}</ref> It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected [[symbiosis]] is at work.<ref name = falcone05/>
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| For more information on this topic, see [[Helminthic therapy]].
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| ==Pathophysiology==
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| The [[pathophysiology]] of allergic responses can be divided into two phases. The first is an [[Acute (medical)|acute response]] that occurs immediately after exposure to an allergen. This phase can either subside or progress into a "late phase reaction" which can substantially prolong the symptoms of a response, and result in tissue damage.
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| ===Acute response===
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| [[Image:Allergy degranulation processes 01.svg|thumb|Degranulation process in allergy.'''1''' - antigen; '''2''' - IgE antibody; '''3''' - FcεRI receptor; '''4''' - preformed mediators (histamine, proteases, chemokines, heparine); '''5''' - [[granules]]; '''6''' - [[mast cell]]; '''7''' - newly formed mediators (prostaglandins, leukotrienes, thromboxanes, PAF)]]
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| In the early stages of allergy, a type I hypersensitivity reaction against an allergen, encountered for the first time, causes a response in a type of immune cell called a [[T helper cell|T<sub>H</sub>2 lymphocyte]], which belongs to a subset of [[T cell]]s that produce a [[cytokine]] called [[interleukin-4]] (IL-4). These T<sub>H</sub>2 cells interact with other [[lymphocytes]] called [[B cell]]s, whose role is production of antibodies. Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of [[Fc receptor]] called [[FcεRI]]) on the surface of other kinds of immune cells called [[mast cell]]s and [[basophil]]s, which are both involved in the acute inflammatory response. The IgE-coated cells, at this stage are sensitized to the allergen.<ref name=Janeway/>
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| If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule, and activates the sensitized cell. Activated mast cells and basophils undergo a process called [[degranulation]], during which they release [[histamine]] and other inflammatory chemical mediators ([[cytokine]]s, [[interleukin]]s, [[leukotriene]]s, and [[prostaglandin]]s) from their [[granule]]s into the surrounding tissue causing several systemic effects, such as [[vasodilation]], [[mucous]] secretion, [[nerve]] stimulation and [[smooth muscle]] contraction. This results in [[rhinorrhea]], itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system and eczema is localized to the [[dermis]].<ref name=Janeway/>
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| ===Late-phase response===
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| After the chemical mediators of the acute response subside, late phase responses can often occur. This is due to the migration of other [[leukocyte]]s such as [[neutrophil]]s, [[lymphocyte]]s, [[eosinophil]]s and [[macrophage]]s to the initial site. The reaction is usually seen 2-24 hours after the original reaction.<ref>{{cite journal |author=Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ |title=Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses |journal=Curr. Opin. Immunol. |volume=18 |issue=6 |pages=751–60 |year=2006 |pmid=17011762 |doi=10.1016/j.coi.2006.09.011}}</ref> Cytokines from mast cells may also play a role in the persistence of long-term effects. Late phase responses seen in [[asthma]] are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils, and are still dependent on activity of T<sub>H</sub>2 cells.<ref>{{cite journal |author=Holt PG, Sly PD |title=Th2 cytokines in the asthma late-phase response |journal=Lancet |volume=370 |issue=9596 |pages=1396–8 |year=2007 |pmid=17950849 |doi=10.1016/S0140-6736(07)61587-6}}</ref>
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| ==Diagnosis== | | ==Diagnosis== |
| [[Image:Allergy testing machine.jpg|right|thumb|An allergy testing machine being operated in the diagnostic immunology lab at Lackland Air Force Base]] | | [[Allergy diagnostic study of choice|Diagnostic study of choice]] | [[Allergy history and symptoms|History and Symptoms]] | [[Allergy physical examination|Physical Examination]] | [[Allergy laboratory findings|Laboratory Findings]] | [[Allergy electrocardiogram|Electrocardiogram]] | [[Allergy x ray|X-Ray Findings]] | [[Allergy echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Allergy CT scan|CT-Scan Findings]] | [[Allergy MRI|MRI Findings]] | [[Allergy other imaging findings|Other Imaging Findings]] | [[Allergy other diagnostic studies|Other Diagnostic Studies]] |
| Before a diagnosis of allergic disease can be confirmed, the other possible causes of the presenting symptoms should be carefully considered.<ref>Emedicine|Allergic and Environmental Asthma -
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| Includes discussion of differentials</ref> [[Vasomotor rhinitis]], for example, is one of many [[Illness|maladies]] that shares symptoms with allergic rhinitis, underscoring the need for professional differential diagnosis.<ref name="pmid16190503">{{cite journal |author=Wheeler PW, Wheeler SF |title=Vasomotor rhinitis |journal=American family physician |volume=72 |issue=6 |pages=1057–62 |year=2005 |pmid=16190503 |doi= |url=http://www.aafp.org/afp/20050915/1057.html}}</ref> Once a diagnosis of asthma, rhinitis, anaphylaxis, or other allergic disease has been made, there are several methods for discovering the causative agent of that allergy.
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| ===Skin testing===
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| [[Image:Allergy skin testing.JPG|thumb|right|Skin Testing]]For assessing the presence of allergen-specific IgE antibodies, allergy skin testing is preferred over blood allergy tests because it is more sensitive and specific, simpler to use, and less expensive.<ref name="pmid7630219">{{cite journal |author=Ten RM, Klein JS, Frigas E |title=Allergy skin testing |journal=Mayo Clin. Proc. |volume=70 |issue=8 |pages=783–4 |year=1995 |pmid=7630219 |doi= |url=http://www.mayoclinicproceedings.com/inside.asp?AID=3978&UID=}}</ref> [[Skin allergy testing|Skin testing]] is also known as "puncture testing" and "prick testing" due to the series of tiny puncture or pricks made into the patient's skin. Small amounts of suspected allergens and/or their extracts (pollen, grass, mite proteins, peanut extract, etc.) are introduced to sites on the skin marked with pen or dye (the ink/dye should be carefully selected, lest it cause an allergic response itself). A small plastic or metal device is used to puncture or prick the skin. Sometimes, the allergens are injected "intradermally" into the patient's skin, with a needle and syringe. Common areas for testing include the inside forearm and the back. If the patient is allergic to the substance, then a visible inflammatory reaction will usually occur within 30 minutes. This response will range from slight reddening of the skin to a full-blown [[hive]] (called "wheal and flare") in more sensitive patients. Interpretation of the results of the skin prick test is normally done by allergists on a scale of severity, with +/- meaning borderline reactivity, and 4+ being a large reaction. Increasingly, allergists are measuring and recording the diameter of the wheal and flare reaction. Interpretation by well-trained allergists is often guided by relevant literature.<ref name="pmid16164451">{{cite journal |author=Verstege A, Mehl A, Rolinck-Werninghaus C, ''et al'' |title=The predictive value of the skin prick test weal size for the outcome of oral food challenges |journal=Clin. Exp. Allergy |volume=35 |issue=9 |pages=1220–6 |year=2005 |pmid=16164451 |doi=10.1111/j.1365-2222.2005.2324.x}}</ref> Some patients may believe they have determined their own allergic sensitivity from observation, but a skin test has been shown to be much better than patient observation to detect allergy.<ref name="pmid11101180">{{cite journal |author=Li JT, Andrist D, Bamlet WR, Wolter TD |title=Accuracy of patient prediction of allergy skin test results |journal=Ann. Allergy Asthma Immunol. |volume=85 |issue=5 |pages=382–4 |year=2000 |pmid=11101180 |doi=}}</ref> | |
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| If a serious life threatening anaphylactic reaction has brought a patient in for evaluation, some allergists will prefer an initial blood test prior to performing the skin prick test. Skin tests may not be an option if the patient has widespread skin disease or has not avoided [[antihistamines]] for several days.
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| ===Blood testing===
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| Various blood allergy testing methods are also available for detecting allergy to specific substances. This kind of testing measures a "total IgE level" - an estimate of IgE contained within the patient's [[blood plasma|serum]]. This can be determined through the use of radiometric and [[colorimetry|colormetric]] [[immunoassay]]s. Radiometric assays include the [[radioallergosorbent test]] (RAST) test method, which uses IgE-binding (anti-IgE) antibodies labeled with [[radioactive isotope]]s for quantifying the levels of IgE antibody in the blood.<ref name="pmid7630219"/> Other newer methods use colorimetric or fluorometric technology in the place of radioactive isotopes. Some "screening" test methods are intended to provide qualitative test results, giving a "yes" or "no" answer in patients with suspected allergic sensitization. One such method has a sensitivity of about 70.8% and a positive predictive value of 72.6% according to a large study.<ref name="pmid16047713">{{cite journal |author=Vidal C, Gude F, Boquete O, ''et al'' |title=Evaluation of the phadiatop test in the diagnosis of allergic sensitization in a general adult population |journal=Journal of investigational allergology & clinical immunology |volume=15 |issue=2 |pages=124–30 |year=2005 |pmid=16047713 |doi=}}</ref>
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| A low total IgE level is not adequate to rule out sensitization to commonly inhaled allergens.<ref name="pmid12911420">{{cite journal |author=Kerkhof M, Dubois AE, Postma DS, Schouten JP, de Monchy JG |title=Role and interpretation of total serum IgE measurements in the diagnosis of allergic airway disease in adults |journal=Allergy |volume=58 |issue=9 |pages=905–11 |year=2003 |pmid=12911420 |doi=10.1034/j.1398-9995.2003.00230.x}}</ref> [[statistics|Statistical methods]], such as [[ROC curve]]s, predictive value calculations, and likelihood ratios have been used to examine the relationship of various testing methods to each other. These methods have shown that patients with a high total IgE have a high probability of allergic sensitization, but further investigation with specific allergy tests for a carefully chosen allergens is often warranted.
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| ==Treatment== | | ==Treatment== |
| There have been enormous improvements in the medical treatments used to treat allergic conditions. With respect to anaphylaxis and hypersensitivity reactions to foods, drugs, and insects and in allergic skin diseases, advances have included the identification of food proteins to which IgE binding is associated with severe reactions and development of low-allergen foods, improvements in skin prick test predictions; evaluation of the [[atopy]] patch test; in wasp sting outcomes predictions and a rapidly disintegrating epinephrine tablet, and anti-IL-5 for eosinophilic diseases.<ref>{{cite journal |author=Sicherer SH, Leung DY |title=Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects |journal=J. Allergy Clin. Immunol. |volume=119 |issue=6 |pages=1462-9 |year=2007 |pmid=17412401 |doi=10.1016/j.jaci.2007.02.013}}</ref>
| | [[Allergy medical therapy|Medical Therapy]] | [[Allergy interventions|Interventions]] | [[Allergy surgery|Surgery]] | [[Allergy primary prevention|Primary Prevention]] | [[Allergy secondary prevention|Secondary Prevention]] | [[Allergy cost-effectiveness of therapy| Cost-Effectiveness of Therapy]] | [[Allergy future or investigational therapies|Future or Investigational Therapies]] |
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| Traditionally treatment and management of allergies involved simply avoiding the allergen in question or otherwise reducing exposure. For instance, people with cat allergies were encouraged to avoid them. While avoidance may help to reduce symptoms and avoid life-threatening anaphylaxis, it is difficult to achieve for those with pollen or similar air-borne allergies. Strict avoidance still has a role in management though, and is often used in managing food allergies.
| | ==Case Studies== |
| | [[Allergy case study one|Case #1]] |
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| ===Pharmacotherapy=== | | ==Related Chapters== |
| Several [[antagonism|antagonistic]] drugs are used to block the action of allergic mediators, or to prevent activation of cells and degranulation processes. These include [[antihistamine]]s, [[cortisone]], [[dexamethasone]], [[hydrocortisone]], [[epinephrine]] (adrenaline), [[theophylline]] and [[cromolyn sodium]]. Anti-[[leukotriene]]s, such as [[Montelukast]] (Singulair) or [[Zafirlukast]] (Accolate), are FDA approved for treatment of allergic diseases. Anti-[[cholinergic]]s, [[decongestant]]s, mast cell stabilizers, and other compounds thought to impair eosinophil [[chemotaxis]], are also commonly used. These drugs help to alleviate the symptoms of allergy, and are imperative in the recovery of acute anaphylaxis, but play little role in chronic treatment of allergic disorders.
| | * [[Allergic inflammation|Allergic Inflammation]] |
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| ===Immunotherapy===
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| Desensitization or [[hyposensitization]] is a treatment in which the patient is gradually [[vaccination|vaccinated]] with progressively larger doses of the allergen in question. This can either reduce the severity or eliminate hypersensitivity altogether. It relies on the progressive skewing of [[IgG]] antibody production, to block excessive IgE production seen in atopys. In a sense, the person builds up immunity to increasing amounts of the allergen in question. Studies have demonstrated the long-term efficacy and the preventive effect of immunotherapy in reducing the development of new allergy.<ref name="pmid10963288">{{cite journal |author=Ross RN, Nelson HS, Finegold I |title=Effectiveness of specific immunotherapy in the treatment of allergic rhinitis: an analysis of randomized, prospective, single- or double-blind, placebo-controlled studies |journal=Clinical therapeutics |volume=22 |issue=3 |pages=342–50 |year=2000 |pmid=10963288 |doi=10.1016/S0149-2918(00)80038-7}}</ref> Meta-analyses have also confirmed efficacy of the treatment in allergic rhinitis in children and in asthma. A review by the Mayo Clinic in Rochester confirmed the safety and efficacy of allergen immunotherapy for allergic rhinitis and conjunctivitis, allergic forms of asthma, and stinging insect based on numerous well-designed scientific studies.<ref name="pmid17803880">{{cite journal |author=Rank MA, Li JT |title=Allergen immunotherapy |journal=Mayo Clin. Proc. |volume=82 |issue=9 |pages=1119–23 |year=2007 |month= Sep |pmid=17803880 |doi=}}</ref> Additionally, national and international guidelines confirm the clinical efficacy of injection immunotherapy in rhinitis and asthma, as well as the safety, provided that recommendations are followed.<ref name="pmid17418661">{{cite journal |author=Passalacqua G, Durham SR |title=Allergic rhinitis and its impact on asthma update: allergen immunotherapy |journal=J. Allergy Clin. Immunol. |volume=119 |issue=4 |pages=881–91 |year=2007 |pmid=17418661 |doi=10.1016/j.jaci.2007.01.045}}</ref>
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| A second form of immunotherapy involves the intravenous injection of [[monoclonal antibody|monoclonal]] anti-IgE antibodies. These bind to free and B-cell associated IgE; signalling their destruction. They do not bind to IgE already bound to the Fc receptor on [[basophil]]s and mast cells, as this would stimulate the allergic inflammatory response. The first agent of this class is [[Omalizumab]]. While this form of immunotherapy is very effective in treating several types of atopy, it should ''not'' be used in treating the majority of people with food allergies.
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| A third type, [[Sublingual immunotherapy]], is an orally-administered therapy which takes advantage of [[immune tolerance|oral immune tolerance]] to non-pathogenic antigens such as foods and resident bacteria. This therapy currently accounts for 40 percent of allergy treatment in Europe. In the United States, sublingual immunotherapy is gaining support among traditional allergists and is endorsed by doctors who treat allergy.
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| ===Unproven or ineffective treatments===
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| An experimental treatment, [[enzyme potentiated desensitization]] (EPD), has been tried for decades but is not generally accepted as effective.<ref name="pmid15042943">{{cite journal |author=Terr AI |title=Unproven and controversial forms of immunotherapy |journal=Clinical allergy and immunology |volume=18 |issue= |pages=703–10 |year=2004 |pmid=15042943 |doi=}}</ref> EPD uses dilutions of allergen and an enzyme, [[beta-glucuronidase]], to which T-regulatory lymphocytes are supposed to respond by favouring desensitization, or down-regulation, rather than sensitization. EPD has also been tried for the treatment of [[autoimmune diseases]] but again is not [[FDA]] approved or of proven effectiveness.<ref name="pmid15042943" />
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| In [[alternative medicine]], a number of allergy treatments are described by its practitioners, particularly [[naturopathic]], [[herbal medicine]], [[homeopathy]], [[traditional Chinese medicine]] and [[kinesiology]]. Systematic literature searches conducted by the Mayo Clinic through 2006, involving hundreds of articles studying multiple conditions, including asthma and upper respiratory tract infection showed no effectiveness of any alternative treatments, and no difference compared with placebo. The authors concluded that, based on rigorous clinical trials of all types of homeopathy for childhood and adolescence ailments, there is no convincing evidence that supports the use of alternative treatments.<ref name="pmid17285788">{{cite journal |author=Altunç U, Pittler MH, Ernst E |title=Homeopathy for childhood and adolescence ailments: systematic review of randomized clinical trials |journal=Mayo Clin. Proc. |volume=82 |issue=1 |pages=69–75 |year=2007 |pmid=17285788 |doi=}}</ref>
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| ==Epidemiology==
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| Many diseases related to inflammation such as [[type 1 diabetes]], [[rheumatoid arthritis]] and allergic diseases—hay fever and asthma—have increased in the Western world over the past 2-3 decades.<ref name=Platts>{{cite journal |author=Platts-Mills TA, Erwin E, Heymann P, Woodfolk J |title=Is the hygiene hypothesis still a viable explanation for the increased prevalence of asthma? |journal=Allergy |volume=60 Suppl 79 |issue= |pages=25–31 |year=2005 |pmid=15842230 |doi=10.1111/j.1398-9995.2005.00854.x}}</ref> Rapid increases in allergic asthma and other atopic disorders in industrialized nations probably began in the 1960s and 1970s, with further increases occurring during the 1980s and 1990s,<ref name= Bloomfield/> although some suggest that a steady rise in sensitization has been occurring since the 1920s.<ref>{{cite journal |author=Isolauri E, Huurre A, Salminen S, Impivaara O |title=The allergy epidemic extends beyond the past few decades |journal=Clin. Exp. Allergy |volume=34 |issue=7 |pages=1007–10 |year=2004 |pmid=15248842 |doi=10.1111/j.1365-2222.2004.01999.x}}</ref> The incidence of atopy in developing countries has generally remained much lower.<ref name= Bloomfield/>
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| {| class = "prettytable" style = "width:70%; float:center; font-size:90%; margin-left:15px"
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| |+ Allergic conditions: Statistics and Epidemiology
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| ! Allergy type || United States || United Kingdom<ref>{{cite web |url= http://www.publications.parliament.uk/pa/ld200607/ldselect/ldsctech/166/16607.htm|title= Chapter 4: The Extent and Burden of Allergy in the United Kingdom |date= 24 July 2007|accessdate=2007-12-03 |format= |work=House of Lords - Science and Technology - Sixth Report}}</ref>
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| | Allergic rhinitis ||35.9 million<ref>{{cite web |url=http://www.aaaai.org/patients/gallery/rhinitissinusitis.asp?item=1a |title=AAAAI - rhinitis, sinusitis, hay fever, stuffy nose, watery eyes, sinus infection |accessdate=2007-12-03 |format= |work=}}</ref> (about 11% of the population<ref>Based on an estimated population of 303 million in 2007 [http://www.census.gov/population/www/popclockus.html U.S. POPClock]. U.S. Census Bureau.</ref>)||3.3 million (about 5.5% of the population<ref>Based on an estimated population of 60.6 million [http://www.statistics.gov.uk/cci/nugget.asp?id=6 UK population grows to 60.6 million]</ref>) | |
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| | Asthma ||10 million suffer from allergic asthma (about 3% of the population). The prevalence of asthma increased 75% from 1980-1994. Asthma prevalence is 39% higher in African Americans than in whites.<ref>{{cite web |url=http://www.aaaai.org/patients/gallery/prevention.asp?item=1a |title=AAAAI - asthma, allergy, allergies, prevention of allergies and asthma, treatment for allergies and asthma |accessdate=2007-12-03 |format= |work=}}</ref> || 5.7 million (about 9.4%). In six and seven year olds asthma increased from 18.4% to 20.9% over five years, during the same time the rate decreased from 31% to 24.7% in 13 to 14 year olds.
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| | Atopic eczema ||About 9% of the population. Between 1960 and 1990 prevalence has increased from 3% to 10% in children.<ref>{{cite web |url=http://www.aaaai.org/patients/gallery/skinallergies.asp?item=1a |title=AAAAI - skin condition, itchy skin, bumps, red irritated skin, allergic reaction, treating skin condition |accessdate=2007-12-03 |format= |work=}}</ref>|| 5.8 million (about 1% severe).
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| | Anaphylaxis || At least 40 deaths per year due to insect venom. About 400 deaths due to penicillin anaphylaxis. About 220 cases of anaphylaxis and 3 deaths per year are due to latex allergy.<ref name=>{{cite web |url=http://www.aaaai.org/patients/gallery/anaphylaxis.asp?item=1a |title=AAAAI - anaphylaxis, cause of anaphylaxis, prevention, allergist, anaphylaxis statistics |accessdate=2007-12-03 |format= |work=}}</ref> An estimated 150 people die annually from anaphylaxis due to food allergy.<ref name=Food/>|| Between 1999 and 2006, 48 deaths occurred in people ranging from five months to 85 years old.
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| | Insect venom ||Around 15% of adults have mild, localized allergic reactions. Systemic reactions occur in 3% of adults and less than 1% of children. <ref>{{cite web |url=http://www.aaaai.org/patients/gallery/insect.asp?item=1a |title=AAAAI - stinging insect, allergic reaction to bug bite, treatment for insect bite |accessdate=2007-12-03 |format= |work=}}</ref>|| Unknown
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| | Drug allergies || Anaphylactic reactions to penicillin cause 400 deaths. || Unknown
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| | Food allergies ||2-4% of children and 1-2% of adults. Peanut and/or tree nut (e.g. walnut, almond and cashew) allergy affects about three million Americans, or 1.1% of the population.<ref name=Food>{{cite web |url=http://www.aaaai.org/patients/gallery/foodallergy.asp?item=1a |title=AAAAI - food allergy, food reactions, anaphylaxis, food allergy prevention |accessdate=2007-12-03 |format= |work=}}</ref> ||5-7% of infants and 1-2% of adults. A 117.3% increase in peanut allergies was observed from 2001 to 2005, an estimated 25,700 people in England are affected.
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| | Multiple allergies<br/>(Asthma, eczema and allergic rhinitis together) ||{{?}} ||2.3 million (about 3.7%), prevalence has increased by 48.9% between 2001 and 2005.
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| Although genetic factors fundamentally govern susceptibility to atopic disease, increases in atopy have occurred within too short a time frame to be explained by a genetic change in the population, thus pointing to environmental or lifestyle changes.<ref name= Bloomfield>{{cite journal |author=Bloomfield SF, Stanwell-Smith R, Crevel RW, Pickup J |title=Too clean, or not too clean: the hygiene hypothesis and home hygiene |journal=Clin. Exp. Allergy |volume=36 |issue=4 |pages=402–25 |year=2006 |pmid=16630145 |doi=10.1111/j.1365-2222.2006.02463.x}}</ref> Several hypotheses have been identified to explain this increased prevalence; increased exposure to perennial allergens due to housing changes and increasing time spent indoors, and changes in cleanliness or hygiene that have resulted in the decreased activation of a common immune control mechanism, coupled with dietary changes, obesity and decline in physical exercise.<ref name=Platts/> The [[hygiene hypothesis]] maintains<ref>{{cite journal |author=Strachan DP |title=Hay fever, hygiene, and household size |journal=BMJ |volume=299 |issue=6710 |pages=1259–60 |year=1989 |pmid=2513902}} {{PMC|1838109}}</ref> that high living standards and hygienic conditions exposes children to fewer infections. It is thought that reduced bacterial and viral infections early in life direct the maturing immune system away from T<sub>H</sub>1 type responses, leading to unrestrained T<sub>H</sub>2 responses that allow for an increase in allergy.<ref>{{cite journal |author=Yazdanbakhsh M, Kremsner PG, van Ree R |title=Allergy, parasites, and the hygiene hypothesis |journal=Science |volume=296 |issue=5567 |pages=490–4 |year=2002 |pmid=11964470 |doi=10.1126/science.296.5567.490}}</ref><ref name=Renz>{{cite journal |author=Renz H, Blümer N, Virna S, Sel S, Garn H |title=The immunological basis of the hygiene hypothesis |journal=Chem Immunol Allergy |volume=91 |issue= |pages=30–48 |year=2006 |pmid=16354947 |doi=10.1159/000090228}}</ref>
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| Changes in rates and types of infection alone however, have been unable to explain the observed increase in allergic disease, and recent evidence has focused attention on the importance of the gastrointestinal microbial environment. Evidence has shown that exposure to food and [[fecal-oral route|fecal-oral]] pathogens, such as [[hepatitis A]], ''[[Toxoplasma gondii]]'', and ''[[Helicobacter pylori]]'' (which also tend to be more prevalent in developing countries), can reduce the overall risk of atopy by more than 60%,<ref>{{cite journal |author=Matricardi PM, Rosmini F, Riondino S, ''et al'' |title=Exposure to foodborne and orofecal microbes versus airborne viruses in relation to atopy and allergic asthma: epidemiological study | journal=BMJ |volume=320 |issue=7232 |pages=412–7 |year=2000 |pmid=10669445 |doi=}} {{PMC|27285}}</ref> and an increased prevalence of parasitic infections has been associated with a decreased prevalence of asthma.<ref>{{cite journal |author=Masters S, Barrett-Connor E |title=Parasites and asthma--predictive or protective? |journal=Epidemiol Rev |volume=7 |issue= |pages=49–58 |year=1985 |pmid=4054238 |doi=}}</ref> It is speculated that these infections exert their effect by critically altering T<sub>H</sub>1/T<sub>H</sub>2 regulation.<ref name= Sheikh/> Important elements of newer hygiene hypotheses also include exposure to [[endotoxin]]s, exposure to pets and growing up on a farm.<ref name= Sheikh>{{cite journal |author=Sheikh A, Strachan DP |title=The hygiene theory: fact or fiction? |journal=Curr Opin Otolaryngol Head Neck Surg |volume=12 |issue=3 |pages=232–6 |year=2004 |pmid=15167035 |doi=}}</ref>
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| ==Medical specialty==
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| In the [[United States]] physicians who hold certification by the American Board of Allergy and Immunology (ABAI) have successfully completed an accredited educational program and an evaluation process, including a secure, proctored examination to demonstrate the knowledge, skills, and experience to the provision of patient care in allergy and immunology.<ref>{{cite web |url=http://www.abai.org/training.asp |title=ABAI: American Board of Allergy and Immunology |accessdate=2007-08-05 |format= |work=}}</ref> An '''allergist-immunologist''' is a physician specially trained to manage and treat asthma and the other allergic diseases. Becoming an allergist-immunologist requires completion of at least nine years of training. After completing medical school and graduating with a medical degree, a physician will then undergo three years of training in internal medicine (to become an internist) or pediatrics (to become a pediatrician). Once physicians have finished training in one of these specialties, they must pass the exam of either the American Board of Pediatrics (ABP) or the American Board of Internal Medicine (ABIM). Internists or pediatricians who wish to focus on the sub-specialty of allergy-immunology then complete at least an additional two years of study, called a fellowship, in an allergy-immunology training program. Allergist-immunologists who are listed as ABAI-certified have successfully passed the certifying examination of the American Board of Allergy and Immunology (ABAI), following their fellowship.<ref>{{cite web |url=http://www.aaaai.org/media/resources/allergist.asp |title=AAAAI - What is an Allergist? |accessdate=2007-08-05 |format= |work=}}</ref>
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| In the United Kingdom, allergy is a subspecialty of [[general medicine]] or [[pediatrics]]. After obtaining postgraduate exams ([[Membership of the Royal College of Physicians|MRCP]] or MRCPCH respectively) a doctor works as several years as a [[specialist registrar]] before qualifying for the [[General Medical Council]] specialist register. Allergy services may also be delivered by [[immunologist]]s. A 2003 [[Royal College of Physicians]] report presented a case for improvement of what were felt to be inadequate allergy services in the UK.<ref>Royal College of Physicians (2003). ''Allergy: the unmet need''. London, UK: Royal College of Physicians. ISBN 1-86016-183-9. {{PDFlink|[http://www.rcplondon.ac.uk/pubs/contents/81e384d6-0328-4653-9cc2-2aa7baa3c56a.pdf PDF version]|1.03 [[Mebibyte|MiB]]<!-- application/pdf, 1089174 bytes -->}}</ref> In 2006, the House of Lords convened a subcommittee that reported in 2007. It concluded likewise that allergy services were insufficient to deal with what the Lords referred to as an "allergy epidemic" and its social cost; it made several other recommendations.<ref>{{cite book |author=House of Lords - Science and Technology Committee |title=Allergy - HL 166-I, 6th Report of Session 2006-07 - Volume 1: Report |year=2007 |publisher=TSO (The Stationery Office) |location=London, UK |isbn=0104011491|url= http://www.publications.parliament.uk/pa/ld200607/ldselect/ldsctech/166/16602.htm}}</ref>
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| ==See also==
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| * [[Allergic inflammation]]
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| * [[Allergen]] | | * [[Allergen]] |
| * [[Hypersensitivity]] | | * [[Hypersensitivity]] |
| * [[Hypoallergenic]] | | * [[Hypoallergenic]] |
| * [[Multiple chemical sensitivity]] (MCS) | | * [[Multiple chemical sensitivity|Multiple Chemical Sensitivity (MCS)]] |
| * [[Urticaria]] | | * [[Urticaria]] |
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| ==References==
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| {{Reflist|2}}
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| ==External links==
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| * [http://www.acaai.org American College of Allergy, Asthma and Immunology]
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| * [http://www.aaaai.org American Academy of Allergy, Asthma & Immunology]
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| * [http://www.aafa.org Asthma and Allergy Foundation of America] – patient advocacy organization
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| * [http://www.aanma.org Allergy & Asthma Network Mothers of Asthmatics]
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| * [http://www.abai.org American Board of Allergy and Immunology] – ABAI establishes qualifications and examines physicians to become recognized specialists in allergy and immunology in the U.S.
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| * [http://www.alert4allergy.org Alert4allergy.org - Food allergy alert service - free for UK residents]
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| {{Allergic conditions}} | | {{Allergic conditions}} |
| {{Consequences of external causes}} | | {{Consequences of external causes}} |
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