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Adjust with 2016 review. The role of diet in the cause and treatment of AD is very controversial. Pediatricians and allergologists are convinced of the causative role of food in the onset of AD, while dermatologists are convinced of the contrary
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According to the [[hygiene hypothesis]], when children are brought up exposed to allergens in the environment at a young age, their immune system is more likely to tolerate them, while children brought up in a modern "sanitary" environment are less likely to be exposed to those allergens at a young age, and, when they are finally exposed, develop allergies. There is some support for this hypothesis with respect to AD.<ref>{{Cite journal|last=Bieber|first=Thomas|date=2008-04-03|title=Atopic Dermatitis|url=http://dx.doi.org/10.1056/NEJMra074081|journal=New England Journal of Medicine|volume=358|issue=14|pages=1483–1494|doi=10.1056/NEJMra074081|issn=0028-4793|pmid=18385500}}</ref> Those exposed to dogs while growing up have a lower risk of atopic dermatitis.<ref>{{cite journal|last=Pelucchi|first=C |author2=Galeone, C |author3=Bach, JF |author4=La Vecchia, C |author5=Chatenoud, L |title=Pet exposure and risk of atopic dermatitis at the pediatric age: a meta-analysis of birth cohort studies.|journal=The Journal of Allergy and Clinical Immunology|date=September 2013|volume=132|issue=3|pages=616–622.e7|doi=10.1016/j.jaci.2013.04.009|pmid=23711545}}</ref> There is also support from epidemiological studies for a protective role for [[helminths]] against AD.<ref name="epid">{{cite journal|last=Flohr|first=C|author2=Mann, J|title=New insights into the epidemiology of childhood atopic dermatitis|journal=Allergy|date=January 2014|volume=69|issue=1|pages=3–16|doi=10.1111/all.12270|url=http://onlinelibrary.wiley.com/doi/10.1111/all.12270/pdf|format=PDF|pmid=24417229}}</ref> Likewise children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurised milk.<ref name="epid" />
According to the [[hygiene hypothesis]], when children are brought up exposed to allergens in the environment at a young age, their immune system is more likely to tolerate them, while children brought up in a modern "sanitary" environment are less likely to be exposed to those allergens at a young age, and, when they are finally exposed, develop allergies. There is some support for this hypothesis with respect to AD.<ref>{{Cite journal|last=Bieber|first=Thomas|date=2008-04-03|title=Atopic Dermatitis|url=http://dx.doi.org/10.1056/NEJMra074081|journal=New England Journal of Medicine|volume=358|issue=14|pages=1483–1494|doi=10.1056/NEJMra074081|issn=0028-4793|pmid=18385500}}</ref> Those exposed to dogs while growing up have a lower risk of atopic dermatitis.<ref>{{cite journal|last=Pelucchi|first=C |author2=Galeone, C |author3=Bach, JF |author4=La Vecchia, C |author5=Chatenoud, L |title=Pet exposure and risk of atopic dermatitis at the pediatric age: a meta-analysis of birth cohort studies.|journal=The Journal of Allergy and Clinical Immunology|date=September 2013|volume=132|issue=3|pages=616–622.e7|doi=10.1016/j.jaci.2013.04.009|pmid=23711545}}</ref> There is also support from epidemiological studies for a protective role for [[helminths]] against AD.<ref name="epid">{{cite journal|last=Flohr|first=C|author2=Mann, J|title=New insights into the epidemiology of childhood atopic dermatitis|journal=Allergy|date=January 2014|volume=69|issue=1|pages=3–16|doi=10.1111/all.12270|url=http://onlinelibrary.wiley.com/doi/10.1111/all.12270/pdf|format=PDF|pmid=24417229}}</ref> Likewise children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurised milk.<ref name="epid" />


==== Sensitization to food or environmental allergens ====
==== Food or environmental allergens ====
Exposure to allergens, either from food or the environment, can exacerbate existing atopic dermatitis, but they are not considered a direct causative factor.<ref>{{Cite journal|last=Williams|first=Hywel|last2=Flohr|first2=Carsten|date=2006-07-01|title=How epidemiology has challenged 3 prevailing concepts about atopic dermatitis|url=https://www.ncbi.nlm.nih.gov/pubmed/16815157|journal=The Journal of Allergy and Clinical Immunology|volume=118|issue=1|pages=209–213|doi=10.1016/j.jaci.2006.04.043|issn=0091-6749|pmid=16815157}}</ref> Exposure to dust mites, for example, is believed to contribute to one's risk of developing AD.<ref>{{cite journal|last=Fuiano |first=N |author2=Incorvaia, C |title=Dissecting the causes of atopic dermatitis in children: less foods, more mites. |journal=Allergology International |date=June 2012 |volume=61 |issue=2 |pages=231–43 |doi=10.2332/allergolint.11-RA-0371 |pmid=22361514 |url=http://ai.jsaweb.jp/pdf/061020231.pdf |format=PDF }}{{dead link|date=October 2016 |bot=InternetArchiveBot |fix-attempted=yes }}</ref> A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for fast foods.<ref name="epid" /> Atopic dermatitis sometimes appears associated with [[celiac disease]] and [[non-celiac gluten sensitivity]].<ref name="FasanoSapone2015">{{cite journal|vauthors=Fasano A, Sapone A, Zevallos V, Schuppan D|title=Nonceliac gluten sensitivity|journal=Gastroenterology|volume=148|issue=6|pages=1195–204|date=May 2015|pmid=25583468|doi=10.1053/j.gastro.2014.12.049|type=Review|quote=Many patients with celiac disease also have atopic disorders. Thirty percent of patients’ allergies with GI symptoms and mucosal lesions, but negative results from serologic (TG2 antibodies) or genetic tests (DQ2 or DQ8 genotype) for celiac disease, had reduced GI and atopic symptoms when they were placed on GFDs. These findings indicated that their symptoms were related to gluten ingestion. ''GFDs = [[Gluten free diet]]''}}</ref><ref name="MansuetoSeidita2014">{{cite journal|vauthors=Mansueto P, Seidita A, D'Alcamo A, Carroccio A|title=Non-celiac gluten sensitivity: literature review|date=2014|journal=J Am Coll Nutr|volume=33|issue=1|pages=39–54|doi=10.1080/07315724.2014.869996|pmid= 24533607|type=Review}}</ref>
In a small percentage of cases, atopic dermatitis is caused by sensitization to foods.<ref name=diMauroBernardin2016>{{cite journal| author=di Mauro G, Bernardini R, Barberi S, Capuano A, Correra A, De' Angelis GL et al.| title=Prevention of food and airway allergy: consensus of the Italian Society of Preventive and Social Paediatrics, the Italian Society of Paediatric Allergy and Immunology, and Italian Society of Pediatrics. | journal=World Allergy Organ J | year= 2016 | volume= 9 | issue= | pages= 28 | pmid=27583103 | doi=10.1186/s40413-016-0111-6 | pmc=4989298 | type=Review }} </ref> Also, exposure to allergens, either from food or the environment, can exacerbate existing atopic dermatitis.<ref>{{Cite journal|last=Williams|first=Hywel|last2=Flohr|first2=Carsten|date=2006-07-01|title=How epidemiology has challenged 3 prevailing concepts about atopic dermatitis|url=https://www.ncbi.nlm.nih.gov/pubmed/16815157|journal=The Journal of Allergy and Clinical Immunology|volume=118|issue=1|pages=209–213|doi=10.1016/j.jaci.2006.04.043|issn=0091-6749|pmid=16815157}}</ref> Exposure to dust mites, for example, is believed to contribute to one's risk of developing AD.<ref>{{cite journal|last=Fuiano |first=N |author2=Incorvaia, C |title=Dissecting the causes of atopic dermatitis in children: less foods, more mites. |journal=Allergology International |date=June 2012 |volume=61 |issue=2 |pages=231–43 |doi=10.2332/allergolint.11-RA-0371 |pmid=22361514 |url=http://ai.jsaweb.jp/pdf/061020231.pdf |format=PDF }}{{dead link|date=October 2016 |bot=InternetArchiveBot |fix-attempted=yes }}</ref> A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for fast foods.<ref name="epid" /> Atopic dermatitis sometimes appears associated with [[celiac disease]] and [[non-celiac gluten sensitivity]], and the improvement with a [[gluten-free diet]] indicates that [[gluten]] is a causative agent in these cases.<ref name="FasanoSapone2015">{{cite journal|vauthors=Fasano A, Sapone A, Zevallos V, Schuppan D|title=Nonceliac gluten sensitivity|journal=Gastroenterology|volume=148|issue=6|pages=1195–204|date=May 2015|pmid=25583468|doi=10.1053/j.gastro.2014.12.049|type=Review|quote=Many patients with celiac disease also have atopic disorders. Thirty percent of patients’ allergies with GI symptoms and mucosal lesions, but negative results from serologic (TG2 antibodies) or genetic tests (DQ2 or DQ8 genotype) for celiac disease, had reduced GI and atopic symptoms when they were placed on GFDs. These findings indicated that their symptoms were related to gluten ingestion. ''GFDs = [[Gluten free diet]]''}}</ref><ref name="MansuetoSeidita2014">{{cite journal|vauthors=Mansueto P, Seidita A, D'Alcamo A, Carroccio A|title=Non-celiac gluten sensitivity: literature review|date=2014|journal=J Am Coll Nutr|volume=33|issue=1|pages=39–54|doi=10.1080/07315724.2014.869996|pmid= 24533607|type=Review}}</ref>


==== Hard water ====
==== Hard water ====

Revision as of 11:42, 1 April 2017

Atopic dermatitis
SpecialtyDermatology Edit this on Wikidata

Atopic dermatitis (AD), also known as atopic eczema, is a 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 often thicken over time.[1] The condition typically starts in childhood with changing severity over the years.[1][2] In children under one year of age much of the body may be affected. As children get older, the back of the knees and front of the elbows are the most common areas affected. In adults the hands and feet are the most commonly affected areas.[2] Scratching worsens symptoms and affected people have an increased risk of skin infections. Many people with atopic dermatitis develop hay fever or asthma.[1]

The cause is unknown but believed to involve genetics, immune system dysfunction, environmental exposures, and difficulties with the permeability of the skin.[1][2] If one identical twin is affected, there is an 85% chance the other also has the condition.[3] Those who live in cities and dry climates are more commonly affected. Exposure to certain chemicals or frequent hand washing makes symptoms worse. While emotional stress may make the symptoms worse it is not a cause. The disorder is not contagious.[1] The diagnosis is typically based on the signs and symptoms. Other diseases that must be excluded before making a diagnosis include contact dermatitis, psoriasis, and seborrheic dermatitis.[2]

Treatment involves avoiding things that make the condition worse, daily bathing with application of a moisturising cream afterwards, applying steroid creams when flares occur, and medications to help with itchiness.[2] Things that commonly make it worse include wool clothing, soaps, perfumes, chlorine, dust, and cigarette smoke. Phototherapy may be useful in some people. Steroid pills or creams based on calcineurin inhibitors may occasionally be used if other measures are not effective.[1][4] Antibiotics (either by mouth or topically) may be needed if a bacterial infection develops.[2] Dietary changes are only needed if food allergies are suspected.[1]

Atopic dermatitis affects about 20% of people at some point in their lives.[1][5] It is more common in younger children.[2] Males and females are equally affected.[1] Many people outgrow the condition.[2] Atopic dermatitis is sometimes called eczema, a term that also refers to a larger group of skin conditions.[1] Other names include "infantile eczema", "flexural eczema", "prurigo Besnier", "allergic eczema", and "neurodermatitis".[6]

Signs and symptoms

Pattern of atopic eczema varies with age

People with AD often have dry and scaly skin that spans the entire body, except perhaps the diaper area, and intensely itchy red, splotchy, raised lesions to form in the bends of the arms or legs, face, and neck.[7][8][9][10][11]

AD commonly occurs on the eyelids where signs such as Dennie-Morgan infraorbital fold, infra-auricular fissure, periorbital pigmentation can be seen.[12] Post-inflammatory hyperpigmentation on the neck gives the classic 'dirty neck' appearance. Lichenification, excoriation and erosion or crusting on the trunk may indicate secondary infection. Flexural distribution with ill-defined edges with or without hyperlinearily on the wrist, finger knuckles, ankle, feet and hand are also commonly seen.[13]

Causes

Genetic

Atopy

Many people with AD have a family history of atopy. Atopy is an immediate-onset allergic reaction (type 1 hypersensitivity reaction) that manifests as asthma, food allergies, AD or hay fever.[7][8]

Filaggrin (FLG)

Mutations in the gene for the production of filaggrin strongly increased the risk for developing atopic dermatitis.[14] Most importantly two mutations were found that affect approximately 5% of people in Western Europe that may disrupt the production of filaggrin. Filaggrin is a protein that plays an important role in the retention of water in the stratum corneum. People who have these mutations often have dry skin.[15] Filaggrin also plays an important role in keeping the skin surface slightly acidic, hence giving it anti-microbial effects. It breaks down into trans-urocanic acid, which keeps the pH low.[16]

Environmental

Hygiene hypothesis

According to the hygiene hypothesis, when children are brought up exposed to allergens in the environment at a young age, their immune system is more likely to tolerate them, while children brought up in a modern "sanitary" environment are less likely to be exposed to those allergens at a young age, and, when they are finally exposed, develop allergies. There is some support for this hypothesis with respect to AD.[17] Those exposed to dogs while growing up have a lower risk of atopic dermatitis.[18] There is also support from epidemiological studies for a protective role for helminths against AD.[19] Likewise children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurised milk.[19]

Food or environmental allergens

In a small percentage of cases, atopic dermatitis is caused by sensitization to foods.[20] Also, exposure to allergens, either from food or the environment, can exacerbate existing atopic dermatitis.[21] Exposure to dust mites, for example, is believed to contribute to one's risk of developing AD.[22] A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for fast foods.[19] Atopic dermatitis sometimes appears associated with celiac disease and non-celiac gluten sensitivity, and the improvement with a gluten-free diet indicates that gluten is a causative agent in these cases.[23][24]

Hard water

Atopic dermatitis in children may be linked to the level of calcium carbonate or "hardness" of household water.[25][26] So far these findings have been supported in the United Kingdom, Spain, Japan, and Belgium.[27][28]

Diagnosis

Atopic dermatitis is typically diagnosed clinically, meaning it is diagnosed based on signs and symptoms alone, without special testing.[29] Several different forms of criteria developed for research have also been validated to aid in diagnosis.[30] Of these, the UK Diagnostic Criteria, based on the work of Hanifin and Rajka, has been the most widely validated.[31][30]

UK Diagnostic criteria for Atopic Dermatitis[31]
Patient must have itchy skin (pruritus), or evidence of rubbing or scratching, plus 3 or more of the following:
Skin creases are involved (flexural dermatitis of fronts of ankles, antecubital fossae, popliteal fossae, skin around eyes, or neck, (or cheeks for children under 10)
History of asthma or allergic rhinitis (or family history of these conditions if patient is a child ≤4 years old)
Symptoms began before age 2 (can only be applied to patients ≥4 years old)
History of dry skin (within the past year)
Dermatitis is visible on flexural surfaces (patients ≥age 4) or on the cheeks, forehead, and extensor surfaces (patients<age 4)

Treatments

There is no known cure for AD, although treatments may reduce the severity and frequency of flares.[7]

Lifestyle

Applying moisturisers may prevent the skin from drying out and decrease the need for other medications.[32] Affected persons often report that improvement of skin hydration parallels with improvement in AD symptoms.[7]

Health professionals often recommend that persons with AD bathe regularly in lukewarm baths, especially in salt water, to moisten their skin.[8][33] Avoiding woollen clothing is usually good for those with AD. Likewise silk, silver-coated clothing may help.[33] Dilute bleach baths have also been reported effective at managing AD.[33]

Diet

Vitamin D is an effective treatment for AD.[34]

Studies have investigated the role of long chain polyunsaturated fatty acids (LCPUFA) supplementation and LCPUFA status in the prevention and treatment of atopic diseases, but the results are controversial. It remains unclear if the nutritional intake of n-3 fatty acids has a clear preventive or therapeutic role, or if n-6 fatty acids consumption promotes atopic diseases.[35]

Several probiotics seem to have a positive effect with a roughly 20% reduction in the rate of atopic dermatitis.[36] The best evidence is for multiple strains of bacteria.[37]

In people with celiac disease or non-celiac gluten sensitivity, a gluten free diet improves their symptoms and prevents the occurrence of new outbreaks.[23][24]

Medication

Topical corticosteroids, such as hydrocortisone have proven themselves effective in managing AD.[7][8] If topical corticosteroids and moisturisers fail, short-term treatment with topical calcineurin inhibitors like tacrolimus or pimecrolimus may be tried, although they are usually avoided as they can increase the risk of developing skin cancer or lymphoma.[7][38] Alternatively systemic immunosuppressants may be tried such as ciclosporin, methotrexate, interferon gamma-1b, mycophenolate mofetil and azathioprine.[7][39] Antidepressants and naltrexone may be used to control pruritus (itchiness).[40] In 2017, the biologic agent dupilumab was approved to treat moderate-to-severe eczema.[41].

Light

A more novel form of treatment involves exposure to broad or narrow-band ultraviolet (UV) light. UV radiation exposure has been found to have a localized immunomodulatory effect on affected tissues and may be used to decrease the severity and frequency of flares.[42][43] In particular, the usage of UVA1 is more effective in treating acute flares, whereas narrow-band UVB is more effective in long-term management scenarios.[44] However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.[45]

Epidemiology

Since the beginning of the twentieth century, many mucosal inflammatory disorders have become more common; atopic eczema (AE) is a classic example of such a disease. It now affects 15–30% of children and 2–10% of adults in developed countries and in the United States has nearly tripled in the past thirty to forty years.[8][46] Over 15 million American adults and children have atopic dermatitis.[47]

Research

Evidence suggests that IL-4 is central in the pathogenesis of AD.[48] Therefore, there is a rationale for targeting IL-4 with anti-IL-4 inhibitors.[49] People with atopic dermatitis are more likely to have Staphylococcus aureus living on them.[50] The role this plays in pathogenesis is yet to be determined.

References

  1. ^ a b c d e f g h i j "Handout on Health: Atopic Dermatitis (A type of eczema)". National Institute of Arthritis and Musculoskeletal and Skin Diseases. May 2013. Retrieved 19 June 2015.
  2. ^ a b c d e f g h Tollefson, MM; Bruckner, AL; SECTION ON, DERMATOLOGY; SECTION ON, DERMATOLOGY (December 2014). "Atopic dermatitis: skin-directed management". Pediatrics. 134 (6): e1735-44. doi:10.1542/peds.2014-2812. PMID 25422009.
  3. ^ Williams, Hywel (2009). Evidence-Based Dermatology. John Wiley & Sons. p. 128. ISBN 9781444300178.
  4. ^ Carr, WW (Aug 2013). "Topical calcineurin inhibitors for atopic dermatitis: review and treatment recommendations". Paediatric drugs. 15 (4): 303–10. doi:10.1007/s40272-013-0013-9. PMC 3715696. PMID 23549982.
  5. ^ Thomsen, SF (2014). "Atopic dermatitis: natural history, diagnosis, and treatment". ISRN allergy. 2014: 354250. doi:10.1155/2014/354250. PMC 4004110. PMID 25006501.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  6. ^ Williams, Hywel C. (2000). The epidemiology of atopic dermatitis. New York: Cambridge University Press. p. 10. ISBN 9780521570756.
  7. ^ a b c d e f g Berke, R; Singh, A; Guralnick, M (July 2012). "Atopic dermatitis: an overview" (PDF). American Family Physician. 86 (1): 35–42. PMID 22962911.
  8. ^ a b c d e Kim, BS (21 January 2014). Fritsch, P; Vinson, RP; Perry, V; Quirk, CM; James, WD (eds.). "Atopic Dermatitis". Medscape Reference. WebMD. Retrieved 3 March 2014.
  9. ^ Brehler, R (2009). "Atopic Dermatitis". In Lang, F (ed.). Encyclopedia of molecular mechanisms of diseases. Berlin: Springer. ISBN 978-3-540-67136-7.
  10. ^ Baron, SE; Cohen, SN; Archer, CB (May 2012). "Guidance on the diagnosis and clinical management of atopic eczema" (PDF). Clinical and Experimental Dermatology. 37: 7–12. doi:10.1111/j.1365-2230.2012.04336.x. PMID 22486763.
  11. ^ Schmitt, J; Langan, S; Deckert, S; Svensson, A; von Kobyletzki, L; Thomas, K; Spuls, P; Harmonising Outcome Measures for Atopic Dermatitis (HOME) Initiative (December 2013). "Assessment of clinical signs of atopic dermatitis: a systematic review and recommendation". The Journal of Allergy and Clinical Immunology. 132 (6): 1337–47. doi:10.1016/j.jaci.2013.07.008. PMID 24035157.
  12. ^ "The infra-auricular fissure: A bedside marker of disease severity in patients with atopic dermatitis - Journal of the American Academy of Dermatology". www.jaad.org. Retrieved 2016-03-20.
  13. ^ Lau, Chu-Pak (2006-01-01). Problem-Based Medical Case Management. Hong Kong University Press. ISBN 9789622097759.
  14. ^ Irvine, Alan D.; McLean, W. H. Irwin; Leung, Donald Y. M. (2011-10-06). "Filaggrin mutations associated with skin and allergic diseases". The New England Journal of Medicine. 365 (14): 1315–1327. doi:10.1056/NEJMra1011040. ISSN 1533-4406. PMID 21991953.
  15. ^ Palmer, CN; Irvine, AD; Terron-Kwiatkowski, A; Zhao, Y; Liao, H; Lee, SP; Goudie, DR; Sandilands, A; Campbell, LE; Smith, FJ; O'Regan, GM; Watson, RM; Cecil, JE; Bale, SJ; Compton, JG; DiGiovanna, JJ; Fleckman, P; Lewis-Jones, S; Arseculeratne, G; Sergeant, A; Munro, CS; El Houate, B; McElreavey, K; Halkjaer, LB; Bisgaard, H; Mukhopadhyay, S; McLean, WH (April 2006). "Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis". Nature Genetics. 38 (4): 441–6. doi:10.1038/ng1767. PMID 16550169.
  16. ^ Jungersted JM, Scheer H, Mempel M, et al. (2010). "Stratum corneum lipids, skin barrier function and filaggrin mutations in patients with atopic eczema". Allergy. 65: 911–918. doi:10.1111/j.1398-9995.2010.02326.x.
  17. ^ Bieber, Thomas (2008-04-03). "Atopic Dermatitis". New England Journal of Medicine. 358 (14): 1483–1494. doi:10.1056/NEJMra074081. ISSN 0028-4793. PMID 18385500.
  18. ^ Pelucchi, C; Galeone, C; Bach, JF; La Vecchia, C; Chatenoud, L (September 2013). "Pet exposure and risk of atopic dermatitis at the pediatric age: a meta-analysis of birth cohort studies". The Journal of Allergy and Clinical Immunology. 132 (3): 616–622.e7. doi:10.1016/j.jaci.2013.04.009. PMID 23711545.
  19. ^ a b c Flohr, C; Mann, J (January 2014). "New insights into the epidemiology of childhood atopic dermatitis" (PDF). Allergy. 69 (1): 3–16. doi:10.1111/all.12270. PMID 24417229.
  20. ^ di Mauro G, Bernardini R, Barberi S, Capuano A, Correra A, De' Angelis GL; et al. (2016). "Prevention of food and airway allergy: consensus of the Italian Society of Preventive and Social Paediatrics, the Italian Society of Paediatric Allergy and Immunology, and Italian Society of Pediatrics". World Allergy Organ J (Review). 9: 28. doi:10.1186/s40413-016-0111-6. PMC 4989298. PMID 27583103. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  21. ^ Williams, Hywel; Flohr, Carsten (2006-07-01). "How epidemiology has challenged 3 prevailing concepts about atopic dermatitis". The Journal of Allergy and Clinical Immunology. 118 (1): 209–213. doi:10.1016/j.jaci.2006.04.043. ISSN 0091-6749. PMID 16815157.
  22. ^ Fuiano, N; Incorvaia, C (June 2012). "Dissecting the causes of atopic dermatitis in children: less foods, more mites" (PDF). Allergology International. 61 (2): 231–43. doi:10.2332/allergolint.11-RA-0371. PMID 22361514.[permanent dead link]
  23. ^ a b Fasano A, Sapone A, Zevallos V, Schuppan D (May 2015). "Nonceliac gluten sensitivity". Gastroenterology (Review). 148 (6): 1195–204. doi:10.1053/j.gastro.2014.12.049. PMID 25583468. Many patients with celiac disease also have atopic disorders. Thirty percent of patients' allergies with GI symptoms and mucosal lesions, but negative results from serologic (TG2 antibodies) or genetic tests (DQ2 or DQ8 genotype) for celiac disease, had reduced GI and atopic symptoms when they were placed on GFDs. These findings indicated that their symptoms were related to gluten ingestion. GFDs = Gluten free diet
  24. ^ a b Mansueto P, Seidita A, D'Alcamo A, Carroccio A (2014). "Non-celiac gluten sensitivity: literature review". J Am Coll Nutr (Review). 33 (1): 39–54. doi:10.1080/07315724.2014.869996. PMID 24533607.
  25. ^ McNally, N. J.; Williams, H. C.; Phillips, D. R.; Smallman-Raynor, M.; Lewis, S.; Venn, A.; Britton, J. (1998-08-15). "Atopic eczema and domestic water hardness". Lancet (London, England). 352 (9127): 527–531. ISSN 0140-6736. PMID 9716057.
  26. ^ Chaumont, Agnès; Voisin, Catherine; Sardella, Antonia; Bernard, Alfred (2012-07-01). "Interactions between domestic water hardness, infant swimming and atopy in the development of childhood eczema". Environmental Research. 116: 52–57. doi:10.1016/j.envres.2012.04.013. ISSN 1096-0953. PMID 22591883.
  27. ^ Miyake, Yoshihiro; Yokoyama, Tetsuji; Yura, Akiko; Iki, Masayuki; Shimizu, Tadahiko (2004-01-01). "Ecological association of water hardness with prevalence of childhood atopic dermatitis in a Japanese urban area". Environmental Research. 94 (1): 33–37. ISSN 0013-9351. PMID 14643284.
  28. ^ Arnedo-Pena, Alberto; Bellido-Blasco, Juan; Puig-Barbera, Joan; Artero-Civera, Adrián; Campos-Cruañes, Joan Baptista; Pac-Sa, M. Rosario; Villamarín-Vázquez, Jose Luis; Felis-Dauder, Carlos (2007-07-01). "[Domestic water hardness and prevalence of atopic eczema in Castellon (Spain) school children]". Salud Publica De Mexico. 49 (4): 295–301. ISSN 0036-3634. PMID 17710278.
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