atopy

AtopyClassification and external resources

Eczema-arms.jpg

Eczema—a typical atopic manifestation

OMIM 147050 (http://omim.org/entry/147050)

DiseasesDB 34489(http://www.diseasesdatabase.com/ddb34489.htm)

AtopyFrom Wikipedia, the free encyclopedia

Atopy (pron. {ay-top-pee}); Greek ἀτοπία -placelessness, out of place, special, unusual,extraordinary) or atopic syndrome is a predispositiontoward developing certain allergic hypersensitivity[1]

reactions. Atopy may have a hereditary component,although contact with the allergen must occur before thehypersensitivity reaction can develop.[2]

The term "atopy" was coined by Coca and Cooke in1923.[3][4] Many physicians and scientists use the term"atopy" for any IgE-mediated reaction (even those thatare appropriate and proportional to the antigen), but manypediatricians reserve the word "atopy" for a geneticallymediated predisposition to an excessive IgE reaction.[5]

Contents

1 Signs and symptoms2 Pathophysiology3 Causes

3.1 Genetics3.2 Staphylococcus aureus

4 Treatments5 References6 External links

Signs and symptoms

Atopy (atopic syndrome) is a syndrome characterized by a tendency to be “hyperallergic”. A person withatopy typically presents with one or more of the following: eczema (atopic dermatitis), allergic rhinitis (hayfever), allergic conjunctivitis, or allergic asthma. Patients with atopy also have a tendency to have foodallergies.

Patients with atopy usually develop what is referred to as the “allergic triad” of symptoms, i.e., eczema(atopic dermatitis), hay fever (allergic rhinitis), and allergy-induced asthma (allergic asthma). They also havea tendency to have food allergies, and other symptoms characterized by their hyperallergic state. Forexample, eosinophilic esophagitis is found associated with atopic allergies.

Atopic syndrome can be fatal for those who experience serious allergic reactions, such as anaphylaxis,brought on by reactions to food or environment.

Pathophysiology

Atopy - Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Atopy

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The individual components of atopy are all caused at least in part by allergy (type I hypersensitivityreactions). Therefore, atopic responses appear after the body is exposed to various allergens, for examplepollen, dander, dust mites, certain foods, or chemical/physical irritants.

Although atopy has various definitions, in general, it is defined by the presence of elevated levels of totaland allergen-specific IgE in the serum, leading to positive skin-prick tests to common allergens.

Causes

Atopic reactions are caused by localized hypersensitivity reaction to an allergen. Atopy appears to show astrong hereditary component. One study concludes that the risk of developing atopic dermatitis (3%) oratopy in general (7%) "increases by a factor of two with each first-degree family member already sufferingfrom atopy".[6]

Environmental factors are also thought to play a role in the development of atopy, and the 'hygienehypothesis' is one of the models that may explain the steep rise in the incidence of atopic diseases. Thishypothesis proposes that excess 'cleanliness' in an infant's or child's environment can lead to a decline in thenumber of infectious stimuli that are necessary for the proper development of the immune system. Thedecrease 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.[7]

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 aMediterranean diet may help to prevent atopic diseases.[8]

The multicenter PARSIFAL study in 2006, involving 6630 children age 5 to 13 in 5 European countries,suggested that reduced use of antibiotics and antipyretics is associated with a reduced risk of allergic diseasein children.[9]

Genetics

There is a strong genetic predisposition toward atopic allergies, especially on the maternal side. Because ofthe strong familial evidence, investigators have tried to map susceptibility genes for atopy. These have beenreviewed,.[10][11] Genes for atopy tend to be involved in allergic responses or other components of theimmune system.

Staphylococcus aureus

Bleach baths provide temporary control of eczema.[12] Ciprofloxacin is an allergen that may cause contactdermatitis, symptoms of which are indistinguishable from eczema.[13] Filaggrin mutations are associated withatopic eczema, and may contribute to the excessive dryness of the skin and the loss of the barrier function ofnormal skin.[14] It may be possible that the filaggrin mutations and the loss of the normal skin barrier exposecrevices that make it possible for Staphylococcus aureus to colonize the skin.[15] Atopic eczema is oftenassociated with genetic defects in genes that control allergic responses. Thus, some investigators haveproposed that atopic eczema is an allergic response to increased Staphylococcus aureus colonization of theskin.[16] 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 ispresent in patients with atopic eczema.[17][18]

Treatments


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Corticosteroids: For years, there was no treatment for atopic eczema. Atopy was believed to be allergic inorigin due to the patients’ extremely high serum IgE levels, but standard therapies at the time did not help.Oral prednisone was sometimes prescribed for severe cases. Wet wraps (covering the patients with gauze likea mummy) were sometimes used in hospitals to control itching. However, the discovery of corticosteroids inthe 1950s, and their subsequent incorporation in topical creams and ointments, provided a significantadvancement in the treatment of atopic eczema and other conditions. Thus, the use of topical steroidsavoided many of the undesirable side-effects of systemic administration of corticosteroids. Topical steroidscontrol the itching and the rash that accompany atopic eczema. Side-effects of topical steroid use areplentiful, and the patient is advised to use topical steroids in moderation and only as needed.

Immune modulators: Pimecrolimus and tacrolimus creams and ointments became available in the 1980s,and are sometimes prescribed for atopic eczema. They act by interfering with T cells, but have been linkedto the development of cancer.

Avoiding dry skin: Dry skin is a common feature of patients with atopic eczema (see also eczema forinformation), and can exacerbate atopic eczema.

Avoiding allergens and irritants: See eczema for information.

References

^ "Dorlands Medical Dictionary:atopy"(http://www.mercksource.com/pp/us/cns/cns_hl_dorlands_split.jsp?pg=/ppdocs/us/common/dorlands/dorland/one/000010034.htm).

1.

^ "Mosby's Medical Dictionary:atopy"(http://www.elsevier.com/wps/find/bookdescription.cws_home/716563/description#description).

2.

^ Coca AF, Cooke RA. (1923) On theclassification of the phenomenon ofhypersensitiveness (http://www.jimmunol.org/cgi/content/abstract/8/3/163) J Immunol

3.

^ Johannes Ring; Bernhard Przybilla; ThomasRuzicka (2006). Handbook of atopic eczema(http://books.google.com/?id=jTktMX60bPwC&pg=PA3). Birkhäuser. pp. 3–.ISBN 978-3-540-23133-2. Retrieved 4 May 2010.

4.

^ Ruby Pawankar; Stephen T. Holgate; Lanny J.Rosenwasser (7 April 2009). Allergy Frontiers:Classification and Pathomechanisms(http://books.google.com/?id=TJj3hqINS8sC&pg=PA33). Springer. pp. 33–.ISBN 978-4-431-88314-2. Retrieved 4 May 2010.

5.

^ Küster, W.; W. Küster , M. Petersen, E.Christophers, M. Goos and W. Sterry (December12, 2004). "A family study of atopic dermatitis".Archives of Dermatological Research (SpringerBerlin / Heidelberg) 282 (2 / January, 1990):98–102. doi:10.1007/BF00493466(http://dx.doi.org/10.1007%2FBF00493466).

6.

^ Grammatikos AP. The genetic and environmentalbasis of atopic diseases. Ann Med. 2008;40(7):482-95.PMID 18608118

7.


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^ A Swedish research study titled “Atopy InChildren Of Families With An AnthroposophicLifestyle” comparing the rate of bronchial asthma,allergies, dermatitis, and other atopic diseasesamong Steiner school pupils and pupils in publicschools originally appeared in the May 1, 1999edition of the British medical journal The Lancet.The findings indicated that Steiner school pupilswere “at a significantly lower risk of atopy” thanchildren attending public schools. The researchersinvestigated a variety of factors in the lives of theSteiner school pupils that might have contributed tothis lower rate of atopy, which includedbreastfeeding, lack of immunization, avoidance ofantibiotics and medications that reduce fevers,consumption of bio-dynamic and organic foods,and other physical aspects of the children’s lives.Devereux, Graham; Devereux G and Seaton A(December 2004). "Diet as a risk factor for atopyand asthma". J Allergy Clin Immunol. 115 (6):1109–1117. doi:10.1016/j.jaci.2004.12.1139(http://dx.doi.org/10.1016%2Fj.jaci.2004.12.1139).PMID 15940119 (https://www.ncbi.nlm.nih.gov/pubmed/15940119).

8.

^ Flöistrup, H., Swartz, J., Bergström, A., Alm, J.S., Scheynius, A., et al. (2006). Allergic diseaseand sensitization in Steiner school children. TheJournal of Allergy and Clinical Immunology,117(1), 59-66. PMID 16387585 Reprint copy(http://www.louisbolk.nl/downloads/mhuber/0601allergic.pdf)

9.

^ Blumenthal, MN (2005) The Role of Genetics inthe Development of Asthma and Atopy. Curr OpinAllergy Clin Immunol, 5, 141-5 15764904.

10.

^ Hoffjan, S, D Nicolae, C Ober (2003)Association Studies for Asthma and AtopicDiseases: A Comprehensive Review of theLiterature. Respir Res, 4, 14 14748924.

11.

^ Nguyen, T.; Zuniga, R. (2013). "Skin conditions:New drugs for managing skin disorders". FPessentials 407: 11–16. PMID 23600334(https://www.ncbi.nlm.nih.gov/pubmed/23600334).

12.

^ Lee, S. W.; Cheong, S. H.; Byun, J. Y.; Choi, Y.W.; Choi, H. Y. (2013). "Occupational handeczema among nursing staffs in Korea:Self-reported hand eczema and contactsensitization of hospital nursing staffs". TheJournal of Dermatology 40 (3): 182–187.doi:10.1111/1346-8138.12036 (http://dx.doi.org/10.1111%2F1346-8138.12036). PMID 23294332(https://www.ncbi.nlm.nih.gov/pubmed/23294332).

13.

^ O'Regan, GM, A Sandilands, WH McLean, ADIrvine (2008) Filaggrin in Atopic Dermatitis. JAllergy Clin Immunol, 122, 689-93 18774165.

14.

^ Breuer, K, A Kapp, T Werfel (2001) BacterialInfections and Atopic Dermatitis. Allergy, 56,1034-41 11703215.

15.

^ Abramson, JS, MV Dahl, G Walsh, MNBlumenthal, SD Douglas, PG Quie (1982)Antistaphylococcal IgE in Patients with AtopicDermatitis. J Am Acad Dermatol, 7, 105-1107107990.

16.

^ Parish, WE, E Welbourn, RH Champion (1976)Hypersensitivity to Bacteria in Eczema. Ii. Titreand Immunoglobulin Class of Antibodies toStaphylococci and Micrococci. Br J Dermatol, 95,285-93 974019.

17.

^ Motala, C, PC Potter, EG Weinberg, D Malherbe,J Hughes (1986) Anti-Staphylococcus Aureus-Specific Ige in Atopic Dermatitis. J Allergy ClinImmunol, 78, 583-9 3771950.

18.

External links

Case Studies in Environmental Medicine (CSEM): Environmental Triggers of Asthma(http://www.atsdr.cdc.gov/HEC/CSEM/asthma/) – Agency for Toxic Substances and Disease Registry,U.S. Department of Health and Human Services.


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