Atopy

This article is about the disease. For the philosophical use, see Atopy (philosophy).
Atopy
atopic syndrome

Eczema—a typical popatopic manifestation
Classification and external resources
Pronunciation /ˈætəpiː/[1]
ICD-9-CM 691.8
OMIM 147050
DiseasesDB 34489

Atopy is a predisposition toward developing certain allergic hypersensitivity[2] reactions.

Atopy may have a hereditary component, although contact with the allergen or irritant must occur before the hypersensitivity reaction can develop.[3]

The term atopy was coined by Coca and Cooke in 1923.[4][5] Many physicians and scientists use the term "atopy" for any IgE-mediated reaction (even those that are appropriate and proportional to the antigen), but many pediatricians reserve the word "atopy" for a genetically mediated predisposition to an excessive IgE reaction.[6] The terms if from Greek ἀτοπία meaning "placelessness".

Signs and symptoms

Atopy (atopic syndrome) is a syndrome characterized by a tendency to be “hyperallergic”. A person with atopy typically presents with one or more of the following : eczema (atopic dermatitis), allergic rhinitis (hay fever), or allergic asthma. Some patients with atopy display what is referred to as the “allergic triad” of symptoms, i.e. all three of the aforementioned conditions. Patients with atopy also have a tendency to have food allergies, allergic conjunctivitis, and other symptoms characterized by their hyperallergic state. For example, eosinophilic esophagitis is found to be 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

The individual components of atopy are all caused at least in part by allergy (type I hypersensitivity reactions). Therefore, atopic responses appear after the body is exposed to various allergens, for example pollen, 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 total and 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 a strong 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".[7]

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. 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.[8]

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.[9]

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 disease in children.[10]

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.[11][12] Genes for atopy (C11orf30, STAT6, SLC25A46, HLA-DQB1, IL1RL1/IL18R1, TLR1/TLR6/TLR10, LPP, MYC/PVT1, IL2/ADAD1, HLA-B/MICA)[13] tend to be involved in allergic responses or other components of the immune system. C11orf30 seems to be the most relevant for atopy as it may increase susceptibility to poly-sensitization.[14]

Staphylococcus aureus

Bleach baths provide temporary control of eczema.[15] Ciprofloxacin is an allergen that may cause contact dermatitis, symptoms of which are indistinguishable from eczema.[16] 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.[17] 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.[18] 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.[19] 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 patients with atopic eczema.[20][21]

Changes in prevalence

In adults, the prevalence of IgE sensitization to allergens from house dust mite and cat, but not grass, seem to decrease over time as people age.[22] However, the biological reasons for these changes are not fully understood.

Treatments

Corticosteroids: For years, there was no treatment for atopic eczema. Atopy was believed to be allergic in origin 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) were sometimes used in hospitals to control itching. However, the discovery of corticosteroids in the 1950s, and their subsequent incorporation in topical creams and ointments, provided a significant advancement in the treatment of atopic eczema and other conditions. Thus, the use of topical steroids avoided many of the undesirable side-effects of systemic administration of corticosteroids. Topical steroids control the itching and the rash that accompany atopic eczema. Side-effects of topical steroid use are plentiful, 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 linked to the development of cancer.

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

Avoiding allergens and irritants: See eczema for information.

See also

References

  1. ↑ Merriam-Webster Dictionary: Atopy
  2. ↑ "Dorlands Medical Dictionary:atopy".
  3. ↑ "Mosby's Medical Dictionary:atopy". Archived from the original on 2011-07-10.
  4. ↑ Coca AF, Cooke RA. (1923) On the classification of the phenomenon of hypersensitiveness J Immunol
  5. ↑ Johannes Ring; Bernhard Przybilla; Thomas Ruzicka (2006). Handbook of atopic eczema. Birkhäuser. pp. 3–. ISBN 978-3-540-23133-2. Retrieved 4 May 2010.
  6. ↑ Ruby Pawankar; Stephen T. Holgate; Lanny J. Rosenwasser (7 April 2009). Allergy Frontiers: Classification and Pathomechanisms. Springer. pp. 33–. ISBN 978-4-431-88314-2. Retrieved 4 May 2010.
  7. ↑ Küster, W.; Petersen, M.; Christophers, E.; Goos, M.; Sterry, W. (December 12, 2004). "A family study of atopic dermatitis". Archives of Dermatological Research. Springer Berlin / Heidelberg. 282 (2 / January, 1990): 98–102. doi:10.1007/BF00493466.
  8. ↑ Grammatikos AP. The genetic and environmental basis of atopic diseases. Ann Med. 2008; 40(7):482-95.PMID 18608118
  9. ↑ 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 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, lack of 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. Devereux, Graham; Seaton, A. (December 2004). "Diet as a risk factor for atopy and asthma". J Allergy Clin Immunol. 115 (6): 1109–1117. doi:10.1016/j.jaci.2004.12.1139. PMID 15940119.
  10. ↑ Flöistrup, H., Swartz, J., Bergström, A., Alm, J. S., Scheynius, A., et al. (2006). Allergic disease and sensitization in Steiner school children. The Journal of Allergy and Clinical Immunology, 117(1), 59-66. PMID 16387585 Reprint copy Archived September 27, 2007, at the Wayback Machine.
  11. ↑ Blumenthal, MN (2005) The Role of Genetics in the Development of Asthma and Atopy. Curr Opin Allergy Clin Immunol, 5, 141-5 15764904.
  12. ↑ Hoffjan, S, D Nicolae, C Ober (2003) Association Studies for Asthma and Atopic Diseases: A Comprehensive Review of the Literature. Respir Res, 4, 14 14748924.
  13. ↑ Bønnelykke, Klaus; Matheson, Melanie C; Pers, Tune H; Granell, Raquel; Strachan, David P; Alves, Alexessander Couto; Linneberg, Allan; Curtin, John A; Warrington, Nicole M; Standl, Marie; Kerkhof, Marjan; Jonsdottir, Ingileif; Bukvic, Blazenka K; Kaakinen, Marika; Sleimann, Patrick; Thorleifsson, Gudmar; Thorsteinsdottir, Unnur; Schramm, Katharina; Baltic, Svetlana; Kreiner-Møller, Eskil; Simpson, Angela; Pourcain, Beate St; Coin, Lachlan; Hui, Jennie; Walters, Eugene H; Tiesler, Carla M T; Duffy, David L; Jones, Graham; Ring, Susan M; McArdle, Wendy L; Price, Loren; Robertson, Colin F; Pekkanen, Juha; Tang, Clara S; Thiering, Elisabeth; Montgomery, Grant W; Hartikainen, Anna-Liisa; Dharmage, Shyamali C; Husemoen, Lise L; Herder, Christian; Kemp, John P; Elliot, Paul; James, Alan; Waldenberger, Melanie; Abramson, Michael J; Fairfax, Benjamin P; Knight, Julian C; Gupta, Ramneek; Thompson, Philip J; Holt, Patrick; Sly, Peter; Hirschhorn, Joel N; Blekic, Mario; Weidinger, Stephan; Hakonarsson, Hakon; Stefansson, Kari; Heinrich, Joachim; Postma, Dirkje S; Custovic, Adnan; Pennell, Craig E; Jarvelin, Marjo-Riitta; Koppelman, Gerard H; Timpson, Nicholas; Ferreira, Manuel A; Bisgaard, Hans; Henderson, A John (30 June 2013). "Meta-analysis of genome-wide association studies identifies ten loci influencing allergic sensitization". Nature Genetics. 45 (8): 902–906. doi:10.1038/ng.2694.
  14. ↑ Amaral, André F. S.; Minelli, Cosetta; Guerra, Stefano; Wjst, Matthias; Probst-Hensch, Nicole; Pin, Isabelle; Svanes, Cecilie; Janson, Christer; Heinrich, Joachim; Jarvis, Deborah L. (December 2014). "The locus increases susceptibility to poly-sensitisation". Allergy: n/a–n/a. doi:10.1111/all.12557.
  15. ↑ Nguyen, T.; Zuniga, R. (2013). "Skin conditions: New drugs for managing skin disorders". FP essentials. 407: 11–16. PMID 23600334.
  16. ↑ Lee, S. W.; Cheong, S. H.; Byun, J. Y.; Choi, Y. W.; Choi, H. Y. (2013). "Occupational hand eczema among nursing staffs in Korea: Self-reported hand eczema and contact sensitization of hospital nursing staffs". The Journal of Dermatology. 40 (3): 182–187. doi:10.1111/1346-8138.12036. PMID 23294332.
  17. ↑ O'Regan, GM, A Sandilands, WH McLean, AD Irvine (2008) Filaggrin in Atopic Dermatitis. J Allergy Clin Immunol, 122, 689-93 18774165.
  18. ↑ Breuer, K, A Kapp, T Werfel (2001) Bacterial Infections and Atopic Dermatitis. Allergy, 56, 1034-41 11703215.
  19. ↑ Abramson, JS, MV Dahl, G Walsh, MN Blumenthal, SD Douglas, PG Quie (1982) Antistaphylococcal IgE in Patients with Atopic Dermatitis. J Am Acad Dermatol, 7, 105-110 7107990.
  20. ↑ Parish, WE, E Welbourn, RH Champion (1976) Hypersensitivity to Bacteria in Eczema. Ii. Titre and Immunoglobulin Class of Antibodies to Staphylococci and Micrococci. Br J Dermatol, 95, 285-93 974019.
  21. ↑ Motala, C, PC Potter, EG Weinberg, D Malherbe, J Hughes (1986) Anti-Staphylococcus Aureus-Specific Ige in Atopic Dermatitis. J Allergy Clin Immunol, 78, 583-9 3771950.
  22. ↑ Amaral, André F.S.; Newson, Roger B.; Abramson, Michael J.; Antó, Josep M.; Bono, Roberto; Corsico, Angelo G.; de Marco, Roberto; Demoly, Pascal; Forsberg, Bertil; Gislason, Thorarinn; Heinrich, Joachim; Huerta, Ismael; Janson, Christer; Jõgi, Rain; Kim, Jeong-Lim; Maldonado, José; Martinez-Moratalla Rovira, Jesús; Neukirch, Catherine; Nowak, Dennis; Pin, Isabelle; Probst-Hensch, Nicole; Raherison-Semjen, Chantal; Svanes, Cecilie; Urrutia Landa, Isabel; van Ree, Ronald; Versteeg, Serge A.; Weyler, Joost; Zock, Jan-Paul; Burney, Peter G.J.; Jarvis, Deborah L. (November 2015). "Changes in IgE sensitization and total IgE levels over 20 years of follow-up". Journal of Allergy and Clinical Immunology. doi:10.1016/j.jaci.2015.09.037.

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