Atopic dermatitis

Atopic dermatitis

Atopic dermatitis of the inside crease of the elbow.
Classification and external resources
Specialty Dermatology
ICD-10 L20
ICD-9-CM 691.8
OMIM 603165
DiseasesDB 4113
MedlinePlus 000853
eMedicine emerg/130 derm/38 ped/2567 oph/479
MeSH D003876

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] It 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 they get older the back of the knees and front of the elbows are the most common area for the rash. In adults the hands and feet are most affected.[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 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 it 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 may occasionally be used if other measures are not effective.[1] 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][4] 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".[5]

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.[6][7][8][9][10]

AD commonly occurs on the eyelids where signs such as Dennie-Morgan infraorbital fold, infra-auricular fissure, periorbital pigmentation can be seen.[11] 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.[12]

Cause

The cause of AD is not known, although there is some evidence of genetic factors, and some evidence that growing up in a sanitary environment encourages AD.[7]

It seems to have a genetic component. Many people with AD have a family history of atopy. Atopy is an immediate-onset allergic reaction ( type 1 hypersensitivity reaction ) as asthma, food allergies, AD or hay fever.[6][7] In 2006 it was discovered that mutations in the gene for the production of filaggrin strongly increased the risk for developing atopic dermatitis. 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.[13] 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.[14]

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.

Those exposed to dogs while growing up have a lower risk of atopic dermatitis.[15] There is also support from epidemiological studies for a protective role for helminths against AD.[16] Likewise children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurised milk.[16] Exposure to dust mites is believed to contribute to one's risk of developing AD.[17]

A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for fast foods.[16]

Atopic dermatitis appears associated with celiac disease and non-celiac gluten sensitivity.[18][19]

Diagnosis

Patch test

An atopy patch test can be used to determine whether or not a specific allergen is the cause of the rash. The test involves applying a series of allergens to the skin surface and evaluating the results in one to three days.[20][21]

Treatments

There is no known cure for AD, although treatments may reduce the severity and frequency of flares.[6] Applying moisturisers may prevent the skin from drying out and decrease the need for other medications.[22] Affected persons often report that improvement of skin hydration parallels with improvement in AD symptoms.[6] Additionally topical corticosteroids, especially hydrocortisone have proven themselves effective in managing AD.[6][7] 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 cause skin cancer or lymphoma.[6][23] Alternatively systemic immunosuppressants may be tried such as ciclosporin, methotrexate, interferon gamma-1b, mycophenolate mofetil and azathioprine.[6][24] Antidepressants and naltrexone may be used to control pruritus (itchiness).[25]

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.[26][27] In particular, Meduri et al. have suggested that the usage of UVA1 is more effective in treating acute flares, whereas narrow-band UVB is more effective in long-term management scenarios.[28] However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.[29] Vitamin D has also proven itself an effective treatment for AD.[30] Evidence suggests that IL-4 is central in the pathogenesis of AD.[31] Therefore there is a rationale for targeting IL-4 with anti-IL-4 inhibitors.[32]

Health professionals often recommend that persons with AD bathe regularly in lukewarm baths, especially in salt water, to moisten their skin.[7][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]

Studies have investigated the role of long chain polyunsaturated fatty acids (LCPUFA) supplementation and LCPUFA status in the prevention and therapy 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.[34]

Several probiotics seem to have a positive effect with a roughly 20% reduction in the rate of atopic dermatitis.[35]

In people with celiac disease or non-celiac gluten sensitivity, a gluten free diet improves their symptoms and prevents the occurrence of new outbreaks.[18][19]

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.[7][36] Over 15 million American adults and children have atopic dermatitis.[37]

See also

References

  1. 1 2 3 4 5 6 7 8 9 10 "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. 1 2 3 4 5 6 7 8 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. ↑ Thomsen, SF (2014). "Atopic dermatitis: natural history, diagnosis, and treatment.". ISRN allergy 2014: 354250. doi:10.1155/2014/354250. PMID 25006501.
  5. ↑ Williams, Hywel C. (2000). The epidemiology of atopic dermatitis. New York: Cambridge University Press. p. 10. ISBN 9780521570756.
  6. 1 2 3 4 5 6 7 Berke, R; Singh, A; Guralnick, M (July 2012). "Atopic dermatitis: an overview" (PDF). American Family Physician 86 (1): 35–42. PMID 22962911.
  7. 1 2 3 4 5 6 Kim, BS (21 January 2014). Fritsch, P; Vinson, RP; Perry, V; Quirk, CM; James, WD, ed. "Atopic Dermatitis". Medscape Reference. WebMD. Retrieved 3 March 2014.
  8. ↑ Brehler, R (2009). "Atopic Dermatitis". In Lang, F. Encyclopedia of molecular mechanisms of diseases. Berlin: Springer. ISBN 978-3-540-67136-7.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ "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.
  12. ↑ Lau, Chu-Pak (2006-01-01). Problem-Based Medical Case Management. Hong Kong University Press. ISBN 9789622097759.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. 1 2 3 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.
  17. ↑ 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.
  18. 1 2 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
  19. 1 2 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.
  20. ↑ Kerschenlohr K, Darsow U, Burgdorf WH, Ring J, Wollenberg A. (July 2004). "Lessons from atopy patch testing in atopic dermatitis". Curr Allergy Asthma Rep 4 (4): 285–9. doi:10.1007/s11882-004-0072-7. PMID 15175142.
  21. ↑ Jurakić Toncić R, Lipozencić J. (2010). "Role and Significance of Atopy Patch Test". Acta Dermatovenerol Croat 18 (1): 38–55. PMID 20361888.
  22. ↑ Varothai, S; Nitayavardhana, S; Kulthanan, K (Jun 2013). "Moisturizers for patients with atopic dermatitis." (PDF). Asian Pacific Journal of Allergy and Immunology 31 (2): 91–8. PMID 23859407.
  23. ↑ http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm051760.htm
  24. ↑ Yarbrough, KB; Neuhaus, KJ; Simpson, EL (March–April 2013). "The effects of treatment on itch in atopic dermatitis". Dermatologic Therapy 26 (2): 110–119. doi:10.1111/dth.12032. PMID 23551368.
  25. ↑ Kim, K (Nov 2012). "Neuroimmunological Mechanism of Pruritus in Atopic Dermatitis Focused on the Role of Serotonin." (PDF). Biomolecules & therapeutics 20 (6): 506–512. doi:10.4062/biomolther.2012.20.6.506. PMC 3762292. PMID 24009842.
  26. ↑ Tintle, S; Shemer, A; Suárez-Fariñas, M; Fujita, H; Gilleaudeau, P; Sullivan-Whalen, M; Johnson-Huang, L; Chiricozzi, A; Cardinale, I; Duan, S; Bowcock, A; Krueger, J. G.; Guttman-Yassky, E (2011). "Reversal of atopic dermatitis with narrow-band UVB phototherapy and biomarkers for therapeutic response". Journal of Allergy and Clinical Immunology 128 (3): 583–93.e1–4. doi:10.1016/j.jaci.2011.05.042. PMC 3448950. PMID 21762976.
  27. ↑ Beattie, P.E.; Finlan, L.E.; Kernohan, N.M.; Thomson, G.; Hupp, T.R.; Ibbotson, S.H. (2005). "The effect of ultraviolet (UV) A1, UVB and solar-simulated radiation on p53 activation and p21Waf1/Cip1". British Journal of Dermatology 152 (5): 1001–1008. doi:10.1111/j.1365-2133.2005.06557.x. PMID 15888160.
  28. ↑ Meduri, NB; Vandergriff, T; Rasmussen, H; Jacobe, H (2007). "Phototherapy in the management of atopic dermatitis: a systematic review". Photodermatology, Photoimmunology & Photomedicine 23 (4): 106–112. doi:10.1111/j.1600-0781.2007.00291.x. PMID 17598862.
  29. ↑ Jans, J; Garinis, GA; Schul, W; Van Oudenaren, A; Moorhouse, M; Smid, M; Sert, YG; Van Der Velde, A; Rijksen, Y; De Gruijl, FR; Van Der Spek, PJ; Yasui, A; Hoeijmakers, JHJ; Leenen, PJM; Van Der Horst, GTJ (2006). "Differential Role of Basal Keratinocytes in UV-Induced Immunosuppression and Skin Cancer". Molecular and Cellular Biology 26 (22): 8515–8526. doi:10.1128/MCB.00807-06. PMC 1636796. PMID 16966369.
  30. ↑ Samochocki, Z; Bogaczewicz, J; Jeziorkowska, R; Sysa-Jędrzejowska, A; Glińska, O; Karczmarewicz, E; McCauliffe, DP; Woźniacka, A (August 2013). "Vitamin D effects in atopic dermatitis.". Journal of the American Academy of Dermatology 69 (2): 238–44. doi:10.1016/j.jaad.2013.03.014. PMID 23643343.
  31. ↑ Bao, Lei; Shi, Vivian Y.; Chan, Lawrence S. (2013-02-01). "IL-4 up-regulates epidermal chemotactic, angiogenic, and pro-inflammatory genes and down-regulates antimicrobial genes in vivo and in vitro: relevant in the pathogenesis of atopic dermatitis". Cytokine 61 (2): 419–425. doi:10.1016/j.cyto.2012.10.031. ISSN 1096-0023. PMID 23207180.
  32. ↑ Di Lernia, Vito (2015-01-01). "Therapeutic strategies in extrinsic atopic dermatitis: focus on inhibition of IL-4 as a new pharmacological approach". Expert Opinion on Therapeutic Targets 19 (1): 87–96. doi:10.1517/14728222.2014.965682. ISSN 1744-7631. PMID 25283256.
  33. 1 2 3 Lio, PA (October 2013). "Non-pharmacologic therapies for atopic dermatitis". Current Allergy and Asthma Reports 13 (5): 528–538. doi:10.1007/s11882-013-0371-y. PMID 23881511.
  34. ↑ Lohner S, Decsi T. Role of Long-Chain Polyunsaturated Fatty Acids in the Prevention and Treatment of Atopic Diseases. In: Polyunsaturated Fatty Acids: Sources, Antioxidant Properties and Health Benefits (edited by: Angel Catalá). NOVA Publishers. 2013. Chapter 11, pp. 1-24. (ISBN 978-1-62948-151-7)
  35. ↑ Pelucchi C, Chatenoud L, Turati F, Galeone C, Moja L, Bach JF, La Vecchia C; Chatenoud; Turati; Galeone; Moja; Bach; La Vecchia (May 2012). "Probiotics supplementation during pregnancy or infancy for the prevention of atopic dermatitis: a meta-analysis". Epidemiology (Cambridge, Mass.) 23 (3): 402–414. doi:10.1097/EDE.0b013e31824d5da2. ISSN 1531-5487. PMID 22441545.
  36. ↑ Saito, Hirohisa (2005). "Much Atopy about the Skin: Genome-Wide Molecular Analysis of Atopic Eczema". International Archives of Allergy and Immunology 137 (4): 319–325. doi:10.1159/000086464. PMID 15970641.
  37. ↑ Atopic Dermatitis. (2015, January 1). Retrieved April 2, 2015, from http://www.uchospitals.edu/online-library/content=P01675

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