Atopy

Last updated
Atopy
Other namesAtopic syndrome
Eczema-arms.jpg
Eczema—a typical atopic manifestation
Pronunciation
Specialty Dermatology, immunology

Atopy is the tendency to produce an exaggerated immunoglobulin E (IgE) immune response to otherwise harmless substances in the environment. [2] Allergic diseases are clinical manifestations of such inappropriate, atopic responses. [2]

Contents

Atopy may have a hereditary component, although contact with the allergen or irritant must occur before the hypersensitivity reaction can develop (characteristically after re-exposure). [3] Maternal psychological trauma in utero may also be a strong indicator for development of atopy. [4]

The term atopy was coined by Arthur F. Coca and Robert Cooke in 1923. [5] [6] 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. [7] The term is from Greek ἀτοπία meaning "the state of being out of place", "absurdity". [8]

Signs and symptoms

Atopic sensitization is considered IgE positivity or prick test positivity to any common food- or air-borne allergen. [9] Atopic conditions are considered: atopic dermatitis, allergic rhinitis (hay fever), allergic asthma, atopic keratoconjunctivitis. The likelihood of having asthma, rhinitis and atopic dermatitis together is 10 times higher than could be expected by chance. [10] Atopy is more common among individuals with a number of different conditions, such as eosinophilic esophagitis and non-celiac gluten sensitivity. [11] [12]

Allergic reactions can range from sneezing and rhinorrhoea to anaphylaxis and even death. [13]

Pathophysiology

In an allergic reaction, initial exposure to an otherwise harmless exogenous substance (known as an allergen) triggers the production of specific IgE antibodies by activated B cells. [13] These IgE antibodies bind to the surface of mast cells via high-affinity IgE receptors, a step that is not itself associated with a clinical response. [13] However, upon re-exposure, the allergen binds to membrane-bound IgE which activates the mast cells, releasing a variety of mediators. [13] This type I hypersensitivity reaction is the basis of the symptoms of allergic reactions, which range from sneezing and rhinorrhoea to anaphylaxis. [13] Allergens can be a number of different substances, for example pollen, dander, dust mites, and foods.

Causes

Atopic reactions are caused by localized hypersensitivity reactions to an allergen. Atopy appears to show a strong 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". [14] As well, maternal stress and perinatal programming is increasingly understood as a root cause of atopy, finding that "...trauma may be a particularly robust potentiator of the cascade of biological events that increase vulnerability to atopy and may help explain the increased risk found in low-income urban populations." [4]

Environmental factors are also thought to play a role in the development of atopy, and the 'hygiene hypothesis' is one of the models that may explain the steep rise in the incidence of atopic diseases, though this hypothesis is incomplete and in some cases, contradictory to findings. [4] 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. [15]

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

A Swedish research study titled "Atopy In Children Of Families With An Anthroposophic Lifestyle" comparing the rate of bronchial asthma, allergies, dermatitis, and other atopic diseases among Steiner school pupils and pupils in public schools originally appeared in the May 1, 1999, edition of the British medical journal The Lancet. The findings indicated that Steiner school pupils were "at a significantly lower risk of atopy" than children attending public schools. The researchers investigated a variety of factors in the lives of the Steiner school pupils that might have contributed to this lower rate of atopy, which included breastfeeding, reduced immunization, avoidance of antibiotics and medications that reduce fevers, consumption of bio-dynamic and organic foods, and other physical aspects of the children's lives. [16]

The multicenter PARSIFAL study in 2006, involving 6,630 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. [17]

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. [18] [19] Genes for atopy (C11orf30, STAT6, SLC25A46, HLA-DQB1, IL1RL1/IL18R1, TLR1/TLR6/TLR10, LPP, MYC/PVT1, IL2/ADAD1, HLA-B/MICA) [20] tend to be involved in allergic responses or other components of the immune system. The gene C11orf30 seems to be the most relevant for atopy as it may increase susceptibility to poly-sensitization. [21]

Staphylococcus aureus

Bleach baths provide temporary control of eczema. [22] Ciprofloxacin is an allergen that may cause contact dermatitis, symptoms of which are indistinguishable from eczema. [23] 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. [24] 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. [25] 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. [26] A hallmark indicator of atopic eczema is a positive wheal and flare reaction to a skin test of S. aureus antigens. In addition, several studies have documented that an IgE-mediated response to S. aureus is present in people with atopic eczema. [27] [28]

Changes in prevalence over time

In adults, the prevalence of IgE sensitization to allergens from house dust mite and cat, but not grass, seems to decrease over time as people age. [29] However, the biological reasons for these changes are not fully understood.

Treatments

Treatments for atopic disorders depend on the organ(s) involved. They can vary from local treatment options, often topical corticosteroids, to systemic treatment options with oral corticosteroids, biological treatments (e.g. omalizumab, mepolizumab) or allergen immunotherapy. [30] [31] [32]

See also

Related Research Articles

<span class="mw-page-title-main">Allergy</span> Immune system response to a substance that most people tolerate well

Allergies, also known as allergic diseases, are various conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment. These diseases include hay fever, food allergies, atopic dermatitis, allergic asthma, and anaphylaxis. Symptoms may include red eyes, an itchy rash, sneezing, coughing, a runny nose, shortness of breath, or swelling. Note that food intolerances and food poisoning are separate conditions.

<span class="mw-page-title-main">Dermatitis</span> Inflammation of the skin

Dermatitis is inflammation of the skin, typically characterized by itchiness, redness and a rash. In cases of short duration, there may be small blisters, while in long-term cases the skin may become thickened. The area of skin involved can vary from small to covering the entire body. Dermatitis is often called eczema, and the difference between those terms is not standardized.

An allergen is a type of antigen that produces an abnormally vigorous immune response in which the immune system fights off a perceived threat that would otherwise be harmless to the body. Such reactions are called allergies.

<span class="mw-page-title-main">Hypersensitivity</span> Medical condition

Hypersensitivity is an abnormal physiological condition in which there is an undesirable and adverse immune response to antigen. It is an abnormality in the immune system that causes immune diseases including allergies and autoimmunity. It is caused by many types of particles and substances from the external environment or from within the body that are recognized by the immune cells as antigens. The immune reactions are usually referred to as an over-reaction of the immune system and they are often damaging and uncomfortable.

<span class="mw-page-title-main">Allergic rhinitis</span> Nasal inflammation due to allergens in the air

Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. Signs and symptoms include a runny or stuffy nose, sneezing, red, itchy, and watery eyes, and swelling around the eyes. The fluid from the nose is usually clear. Symptom onset is often within minutes following allergen exposure, and can affect sleep and the ability to work or study. Some people may develop symptoms only during specific times of the year, often as a result of pollen exposure. Many people with allergic rhinitis also have asthma, allergic conjunctivitis, or atopic dermatitis.

<span class="mw-page-title-main">Immunoglobulin E</span> Immunoglobulin E (IgE) Antibody

Immunoglobulin E (IgE) is a type of antibody that has been found only in mammals. IgE is synthesised by plasma cells. Monomers of IgE consist of two heavy chains and two light chains, with the ε chain containing four Ig-like constant domains (Cε1–Cε4). IgE is thought to be an important part of the immune response against infection by certain parasitic worms, including Schistosoma mansoni, Trichinella spiralis, and Fasciola hepatica. IgE is also utilized during immune defense against certain protozoan parasites such as Plasmodium falciparum. IgE may have evolved as a defense to protect against venoms.

<span class="mw-page-title-main">Food allergy</span> Hypersensitivity reaction to a food

A food allergy is an abnormal immune response to food. The symptoms of the allergic reaction may range from mild to severe. They may include itchiness, swelling of the tongue, vomiting, diarrhea, hives, trouble breathing, or low blood pressure. This typically occurs within minutes to several hours of exposure. When the symptoms are severe, it is known as anaphylaxis. A food intolerance and food poisoning are separate conditions, not due to an immune response.

<span class="mw-page-title-main">Type I hypersensitivity</span> Type of allergic reaction

Type I hypersensitivity, in the Gell and Coombs classification of allergic reactions, is an allergic reaction provoked by re-exposure to a specific type of antigen referred to as an allergen. Type I is distinct from type II, type III and type IV hypersensitivities. The relevance of the Gell and Coombs classification of allergic reactions has been questioned in the modern-day understanding of allergy, and it has limited utility in clinical practice.

<span class="mw-page-title-main">Allergic conjunctivitis</span> Medical condition

Allergic conjunctivitis (AC) is inflammation of the conjunctiva due to allergy. Although allergens differ among patients, the most common cause is hay fever. Symptoms consist of redness, edema (swelling) of the conjunctiva, itching, and increased lacrimation. If this is combined with rhinitis, the condition is termed allergic rhinoconjunctivitis (ARC).

<span class="mw-page-title-main">Atopic dermatitis</span> Long-term form of skin inflammation

Atopic dermatitis (AD), also known as atopic eczema, is a long-term type of inflammation of the skin (dermatitis). It results in itchy, red, swollen, and cracked skin. Clear fluid may come from the affected areas, which can thicken over time. AD may also simply be called eczema, a term that generally refers to a larger group of skin conditions.

<span class="mw-page-title-main">Patch test</span> Medical test to determine substances causing allergic reactions

A patch test is a diagnostic method used to determine which specific substances cause allergic inflammation of a patient's skin.

<span class="mw-page-title-main">Milk allergy</span> Type of food allergy caused by milk

Milk allergy is an adverse immune reaction to one or more proteins in cow's milk. Symptoms may take hours to days to manifest, with symptoms including atopic dermatitis, inflammation of the esophagus, enteropathy involving the small intestine and proctocolitis involving the rectum and colon. However, rapid anaphylaxis is possible, a potentially life-threatening condition that requires treatment with epinephrine, among other measures.

<span class="mw-page-title-main">Egg allergy</span> Type of food allergy caused by eggs

Egg allergy is an immune hypersensitivity to proteins found in chicken eggs, and possibly goose, duck, or turkey eggs. Symptoms can be either rapid or gradual in onset. The latter can take hours to days to appear. The former may include anaphylaxis, a potentially life-threatening condition which requires treatment with epinephrine. Other presentations may include atopic dermatitis or inflammation of the esophagus.

<span class="mw-page-title-main">Allergic inflammation</span>

Allergic inflammation is an important pathophysiological feature of several disabilities or medical conditions including allergic asthma, atopic dermatitis, allergic rhinitis and several ocular allergic diseases. Allergic reactions may generally be divided into two components; the early phase reaction, and the late phase reaction. While the contribution to the development of symptoms from each of the phases varies greatly between diseases, both are usually present and provide us a framework for understanding allergic disease.

<span class="mw-page-title-main">Wheat allergy</span> Medical condition

Wheat allergy is an allergy to wheat which typically presents itself as a food allergy, but can also be a contact allergy resulting from occupational exposure. Like all allergies, wheat allergy involves immunoglobulin E and mast cell response. Typically the allergy is limited to the seed storage proteins of wheat. Some reactions are restricted to wheat proteins, while others can react across many varieties of seeds and other plant tissues. Wheat allergy is rare. Prevalence in adults was found to be 0.21% in a 2012 study in Japan.

Oat sensitivity represents a sensitivity to the proteins found in oats, Avena sativa. Sensitivity to oats can manifest as a result of allergy to oat seed storage proteins either inhaled or ingested. A more complex condition affects individuals who have gluten-sensitive enteropathy in which there is an autoimmune response to avenin, the glutinous protein in oats similar to the gluten within wheat. Sensitivity to oat foods can also result from their frequent contamination by wheat, barley, or rye particles.

<span class="mw-page-title-main">Fish allergy</span> Type of food allergy caused by fish

Fish allergy is an immune hypersensitivity to proteins found in fish. Symptoms can be either rapid or gradual in onset. The latter can take hours to days to appear. The former may include anaphylaxis, a potentially life-threatening condition which requires treatment with epinephrine. Other presentations may include atopic dermatitis or inflammation of the esophagus. Fish is one of the eight common food allergens which are responsible for 90% of allergic reactions to foods: cow's milk, eggs, wheat, shellfish, peanuts, tree nuts, fish, and soy beans.

<span class="mw-page-title-main">Dust mite allergy</span> Medical condition

Dust mite allergy, also known as house dust allergy, is a sensitization and allergic reaction to the droppings of house dust mites. The allergy is common and can trigger allergic reactions such as asthma, eczema or itching. The mite's gut contains potent digestive enzymes that persist in their feces and are major inducers of allergic reactions such as wheezing. The mite's exoskeleton can also contribute to allergic reactions. Unlike scabies mites or skin follicle mites, house dust mites do not burrow under the skin and are not parasitic.

<span class="mw-page-title-main">Shellfish allergy</span> Type of food allergy caused by shellfish

Shellfish allergy is among the most common food allergies. "Shellfish" is a colloquial and fisheries term for aquatic invertebrates used as food, including various species of molluscs such as clams, mussels, oysters and scallops, crustaceans such as shrimp, lobsters and crabs, and cephalopods such as squid and octopus. Shellfish allergy is an immune hypersensitivity to proteins found in shellfish. Symptoms can be either rapid or gradual in onset. The latter can take hours to days to appear. The former may include anaphylaxis, a potentially life-threatening condition which requires treatment with epinephrine. Other presentations may include atopic dermatitis or inflammation of the esophagus. Shellfish is one of the eight common food allergens, responsible for 90% of allergic reactions to foods: cow's milk, eggs, wheat, shellfish, peanuts, tree nuts, fish, and soy beans.

<span class="mw-page-title-main">Sesame allergy</span> Food allergy caused by sesame seeds

A food allergy to sesame seeds has prevalence estimates in the range of 0.1–0.2% of the general population, and are higher in the Middle East and other countries where sesame seeds are used in traditional foods. Reporting of sesame seed allergy has increased in the 21st century, either due to a true increase from exposure to more sesame foods or due to an increase in awareness. Increasing sesame allergy rates have induced more countries to regulate food labels to identify sesame ingredients in products and the potential for allergy. In the United States, sesame became the ninth food allergen with mandatory labeling, effective 1 January 2023.

References

  1. ↑ Merriam-Webster Dictionary: Atopy
  2. 1 2 Ralston, Stuart H., Herausgeber. Penman, Ian D., Herausgeber. Strachan, Mark W. J., Herausgeber. Hobson, Richard P., Herausgeber. Britton, Robert, Illustrator. Davidson, Leybourne S. 1894-1981 Begründer des Werks. (2018-04-23). Davidson's principles and practice of medicine. Elsevier. ISBN   978-0-7020-7028-0. OCLC   1040673074.{{cite book}}: CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  3. ↑ "Mosby's Medical Dictionary:atopy". Archived from the original on 2011-07-10.
  4. 1 2 3 Wright, Rosalind J; Enlow, Michelle Bosquet (2008-09-01). "Maternal stress and perinatal programming in the expression of atopy". Expert Review of Clinical Immunology. 4 (5): 535–538. doi:10.1586/1744666X.4.5.535. ISSN   1744-666X. PMC   2762209 . PMID   19838310.
  5. ↑ Coca AF, Cooke RA. (1923) On the classification of the phenomenon of hypersensitiveness J Immunol
  6. ↑ Johannes Ring; Bernhard Przybilla; Thomas Ruzicka (2006). Handbook of atopic eczema. Birkhäuser. pp. 3–. ISBN   978-3-540-23133-2 . Retrieved 4 May 2010.
  7. ↑ 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.
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  21. ↑ 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" (PDF). Allergy. 70 (3): 328–333. doi:10.1111/all.12557. hdl: 10044/1/21574 . PMID   25546184. S2CID   25960081.
  22. ↑ Nguyen, T.; Zuniga, R. (2013). "Skin conditions: New drugs for managing skin disorders". FP Essentials. 407: 11–16. PMID   23600334.
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  24. ↑ O'Regan GM, Sandilands A, McLean WH, Irvine AD (2008). "Filaggrin in Atopic Dermatitis". J Allergy Clin Immunol. 122 (4): 689–93. doi:10.1016/j.jaci.2008.08.002. PMID   18774165.
  25. ↑ Breuer K, Kapp A, Werfel T (2001). "Bacterial Infections and Atopic Dermatitis". Allergy. 56 (11): 1034–41. doi: 10.1034/j.1398-9995.2001.00146.x . PMID   11703215. S2CID   28897487.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ↑ Abramson JS, Dahl MV, Walsh G, Blumenthal MN, Douglas SD, Quie PG (1982). "Antistaphylococcal IgE in Patients with Atopic Dermatitis". J Am Acad Dermatol. 7 (1): 105–110. doi:10.1016/s0190-9622(82)80017-0. PMID   7107990.
  27. ↑ Parish WE, Welbourn E, Champion RH (1976). "Hypersensitivity to Bacteria in Eczema. Ii. Titre and Immunoglobulin Class of Antibodies to Staphylococci and Micrococci". Br J Dermatol. 95 (3): 285–93. doi:10.1111/j.1365-2133.1976.tb07016.x. PMID   974019. S2CID   5842899.
  28. ↑ Motala C, Potter PC, Weinberg EG, Malherbe D, Hughes J (1986). "Anti-Staphylococcus aureus-Specific IgE in Atopic Dermatitis". J Allergy Clin Immunol. 78 (4 Pt 1): 583–9. doi:10.1016/0091-6749(86)90075-8. PMID   3771950.
  29. ↑ 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. 137 (6): 1788–1795.e9. doi:10.1016/j.jaci.2015.09.037. PMC   4889785 . PMID   26586040.
  30. ↑ Wollenberg, A.; Barbarot, S.; Bieber, T.; Christen-Zaech, S.; Deleuran, M.; Fink-Wagner, A.; Gieler, U.; Girolomoni, G.; Lau, S.; Muraro, A.; Czarnecka-Operacz, M. (May 2018). "Consensus-based European guidelines for treatment of atopic eczema (atopic dermatitis) in adults and children: part I". Journal of the European Academy of Dermatology and Venereology. 32 (5): 657–682. doi: 10.1111/jdv.14891 . PMID   29676534.
  31. ↑ Reddel, Helen K.; Bateman, Eric D.; Becker, Allan; Boulet, Louis-Philippe; Cruz, Alvaro A.; Drazen, Jeffrey M.; Haahtela, Tari; Hurd, Suzanne S.; Inoue, Hiromasa; de Jongste, Johan C.; Lemanske, Robert F. (September 2015). "A summary of the new GINA strategy: a roadmap to asthma control". European Respiratory Journal. 46 (3): 622–639. doi:10.1183/13993003.00853-2015. ISSN   0903-1936. PMC   4554554 . PMID   26206872.
  32. ↑ Klimek, Ludger; Bachert, Claus; Pfaar, Oliver; Becker, Sven; Bieber, Thomas; Brehler, Randolf; Buhl, Roland; Casper, Ingrid; Chaker, Adam; Czech, Wolfgang; Fischer, Jörg (2020-02-12). "Correction to "ARIA guideline 2019: treatment of allergic rhinitis in the German health system"". Allergo Journal International. 29 (2): 63–65. doi:10.1007/s40629-019-00115-4. ISSN   2197-0378. S2CID   211089322.
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