Atopy - Wikipedia, the free encyclopedia

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Atopy
From Wikipedia, the free encyclopedia

Atopy (pron. {ay-top-pee}); Greek placelessness, out of place, special, unusual,

extraordinary) or atopic syndrome is a predisposition
toward developing certain allergic hypersensitivity[1]
reactions. Atopy may have a hereditary component,
although contact with the allergen must occur before the
hypersensitivity reaction can develop.[2]
The term "atopy" was coined by Coca and Cooke in
1923.[3][4] 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.[5]

Atopy
Classification and external resources
Eczema-arms.jpg

Eczemaa typical atopic manifestation

OMIM

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

Contents

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

1 Signs and symptoms

2 Pathophysiology
3 Causes
3.1 Genetics
3.2 Staphylococcus aureus
4 Treatments
5 References
6 External links

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), allergic conjunctivitis, or allergic asthma. Patients with atopy also have a tendency to have food
allergies.
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 have
a tendency to have food allergies, and other symptoms characterized by their hyperallergic state. For
example, 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

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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".[6]
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.[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 a
Mediterranean 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 disease
in children.[9]

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. These have been
reviewed,.[10][11] Genes for atopy tend to be involved in allergic responses or other components of the
immune system.

Staphylococcus aureus
Bleach baths provide temporary control of eczema.[12] Ciprofloxacin is an allergen that may cause contact
dermatitis, symptoms of which are indistinguishable from eczema.[13] 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.[14] 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.[15] 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.[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 is
present 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 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 like
a mummy) 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.

References
1. ^ "Dorlands Medical Dictionary:atopy"

6. ^ Kster, W.; W. Kster , M. Petersen, E.

(http://www.mercksource.com/pp/us

Christophers, M. Goos and W. Sterry (December

/cns/cns_hl_dorlands_split.jsp?pg=/ppdocs

12, 2004). "A family study of atopic dermatitis".

/us/common/dorlands/dorland/one/000010034.htm).

Archives of Dermatological Research (Springer

2. ^ "Mosby's Medical Dictionary:atopy"

Berlin / Heidelberg) 282 (2 / January, 1990):

(http://www.elsevier.com/wps/find

98102. doi:10.1007/BF00493466

/bookdescription.cws_home/716563

(http://dx.doi.org/10.1007%2FBF00493466).

/description#description).
3. ^ Coca AF, Cooke RA. (1923) On the
classification of the phenomenon of

7. ^ Grammatikos AP. The genetic and environmental

basis of atopic diseases. Ann Med. 2008;
40(7):482-95.PMID 18608118

hypersensitiveness (http://www.jimmunol.org
/cgi/content/abstract/8/3/163) J Immunol
4. ^ Johannes Ring; Bernhard Przybilla; Thomas
Ruzicka (2006). Handbook of atopic eczema
(http://books.google.com/?id=jTktMX60bPwC&
pg=PA3). Birkhuser. pp. 3.
ISBN 978-3-540-23133-2. Retrieved 4 May 2010.
5. ^ 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.

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8. ^ A Swedish research study titled Atopy In

http://en.wikipedia.org/wiki/Atopy

11. ^ Hoffjan, S, D Nicolae, C Ober (2003)

Children Of Families With An Anthroposophic

Association Studies for Asthma and Atopic

Lifestyle comparing the rate of bronchial asthma,

Diseases: A Comprehensive Review of the

allergies, dermatitis, and other atopic diseases

Literature. Respir Res, 4, 14 14748924.

among Steiner school pupils and pupils in public

12. ^ Nguyen, T.; Zuniga, R. (2013). "Skin conditions:

schools originally appeared in the May 1, 1999

New drugs for managing skin disorders". FP

edition of the British medical journal The Lancet.

essentials 407: 1116. PMID 23600334

The findings indicated that Steiner school pupils

(https://www.ncbi.nlm.nih.gov/pubmed/23600334).

were at a significantly lower risk of atopy than

13. ^ Lee, S. W.; Cheong, S. H.; Byun, J. Y.; Choi, Y.

children attending public schools. The researchers

W.; Choi, H. Y. (2013). "Occupational hand

investigated a variety of factors in the lives of the

eczema among nursing staffs in Korea:

Steiner school pupils that might have contributed to

Self-reported hand eczema and contact

this lower rate of atopy, which included

sensitization of hospital nursing staffs". The

breastfeeding, lack of immunization, avoidance of

Journal of Dermatology 40 (3): 182187.

antibiotics and medications that reduce fevers,

doi:10.1111/1346-8138.12036 (http://dx.doi.org

consumption of bio-dynamic and organic foods,

/10.1111%2F1346-8138.12036). PMID 23294332

and other physical aspects of the childrens lives.

(https://www.ncbi.nlm.nih.gov/pubmed/23294332).

Devereux, Graham; Devereux G and Seaton A

14. ^ O'Regan, GM, A Sandilands, WH McLean, AD

(December 2004). "Diet as a risk factor for atopy

Irvine (2008) Filaggrin in Atopic Dermatitis. J

and asthma". J Allergy Clin Immunol. 115 (6):

Allergy Clin Immunol, 122, 689-93 18774165.

11091117. doi:10.1016/j.jaci.2004.12.1139

15. ^ Breuer, K, A Kapp, T Werfel (2001) Bacterial

(http://dx.doi.org/10.1016%2Fj.jaci.2004.12.1139).

Infections and Atopic Dermatitis. Allergy, 56,

PMID 15940119 (https://www.ncbi.nlm.nih.gov

1034-41 11703215.

/pubmed/15940119).
9. ^ Flistrup, H., Swartz, J., Bergstrm, A., Alm, J.

16. ^ Abramson, JS, MV Dahl, G Walsh, MN

Blumenthal, SD Douglas, PG Quie (1982)

S., Scheynius, A., et al. (2006). Allergic disease

Antistaphylococcal IgE in Patients with Atopic

and sensitization in Steiner school children. The

Dermatitis. J Am Acad Dermatol, 7, 105-110

Journal of Allergy and Clinical Immunology,

7107990.

117(1), 59-66. PMID 16387585 Reprint copy

17. ^ Parish, WE, E Welbourn, RH Champion (1976)

(http://www.louisbolk.nl/downloads/mhuber

Hypersensitivity to Bacteria in Eczema. Ii. Titre

/0601allergic.pdf)

and Immunoglobulin Class of Antibodies to

10. ^ Blumenthal, MN (2005) The Role of Genetics in

the Development of Asthma and Atopy. Curr Opin
Allergy Clin Immunol, 5, 141-5 15764904.

Staphylococci and Micrococci. Br J Dermatol, 95,

285-93 974019.
18. ^ Motala, C, PC Potter, EG Weinberg, D Malherbe,
J Hughes (1986) Anti-Staphylococcus AureusSpecific Ige in Atopic Dermatitis. J Allergy Clin
Immunol, 78, 583-9 3771950.

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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Categories: Type 1 hypersensitivity

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