Atopic dermatitis: Wikis


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Atopic dermatitis
Classification and external resources

Atopic dermatitis
ICD-10 L20.
ICD-9 691.8
OMIM 603165
DiseasesDB 4113
eMedicine emerg/130 derm/38 ped/2567 oph/479
MeSH D003876

Atopic dermatitis (AD) (a type of eczema) is an inflammatory, chronically relapsing, non-contagious and pruritic skin disease.[1] It has been given names like "prurigo Besnier," "neurodermitis," "endogenous eczema," "flexural eczema," "infantile eczema," and "prurigo diathsique".[2]



A child with atopic dermatitis

The skin of a patient with atopic dermatitis reacts abnormally and easily to irritants, food, and environmental allergens and becomes red, flaky and very itchy. It also becomes vulnerable to surface infections caused by bacteria. The skin on the flexural surfaces of the joints (for example inner sides of elbows and knees) are the most commonly affected regions in people.

Atopic dermatitis often occurs together with other atopic diseases like hay fever, asthma and conjunctivitis. It is a familial and chronic disease and its symptoms can increase or disappear over time. Atopic dermatitis in older children and adults is often confused with psoriasis. Atopic dermatitis afflicts humans, particularly young children; it is also a well-characterized disease in domestic dogs.

Although there is no cure for atopic eczema, and its cause is not well understood, it can be treated very effectively in the short term through a combination of prevention (learning what triggers the allergic reactions) and drug therapy.


Since the beginning of the twentieth century, many mucosal inflammatory disorders have become dramatically more common; atopic eczema (AE) is a classic example of such a disease. It now affects 10-20% of children and 1-3% of adults in industrialized countries, and its prevalence in the United States alone has nearly tripled in the past thirty to forty years.[3]



Although it is an inherited disease, eczema is primarily aggravated by contact with or intake of allergens. It can also be influenced by other factors that affects the immune system such as stress or fatigue. Atopic eczema consists of chronic inflammation; it often occurs in people with a history of allergy disorders such as asthma or hay fever. There is no certain cause of atopic dermatitis.


Although it is such a common disease, relatively little is understood about the underlying causes of atopic eczema.[4] While AE is associated with allergic asthma and allergic rhinitis, the connection between the diseases has not been established.[4] Twin studies have consistently shown that the disease has a higher rate of concordance in identical as compared to fraternal twins, which also indicates that genetics plays a role in its development.[4] However, the rate of concordance between identical twins is far from 100%, and the changing frequency of the disease over time points to the environmental factors—nutrition or hygiene, for instance—that also play a role in disease susceptibility.[5]

Genomic research into the cause of multigenic diseases is still in its infancy: few genes have ever been identified that contribute to multigenic human disorders.[5] Researchers have attempted to do this in past whole-genome screens for AE and related diseases, but their results have been inconsistent. A few of the pertinent loci have been validated by replication in further studies (chromosome 2q, chromosome 6p, and chromosome 12q, for example),[6] but most have not been.

Associations with ATOD1, ATOD2, ATOD3, ATOD4, ATOD5 and ATOD6 have been identified.[7]

In a publication in Nature Genetics from April 6, 2009, Young-Ae Lee of the Max Delbrück Center for Molecular Medicine in Berlin and her colleagues report a strong association between atopic dermatitis and a common genetic variant, a new locus on chromosome 11, potentially associated with the gene C11orf30.[8]


Since there is no cure for atopic eczema, treatment should mainly involve discovering the triggers of allergic reactions and learning to avoid them.

Diet: Originally controversial, the association of food allergy with atopic dermatitis has now been clearly demonstrated. Many common food allergens can trigger an allergic reaction: such as milk, nuts, cheese, tomatoes, wheat, yeast, soy, and corn. Many of these allergens are common ingredients in grocery store products (especially corn syrup, which is a sugar substitute). Specialty health food stores often carry products that do not contain common allergens. Breastfeeding is the best way to avoid these problems, but if that is unavailable, then hydrolyzed formulas are preferred to cow's milk.[9]
The use of organic dairy products by children and breastfeeding or pregnant mothers reduces the risk of atopic dermatitis in young children.[10]

Environment and Lifestyle: Since dust is a very common allergen and irritant, adults with atopic eczema should likely avoid smoking, as well as the inhalation of dust in general. The dander from the fur of dogs and cats may also trigger an inflammatory response. It is a common misconception that simply removing an animal from a room will prevent an allergic reaction from occurring. A room must be completely free of animal dander in order to prevent an allergic reaction. Anger, stress, and lack of sleep are also factors that are known to aggravate eczema. Excessive heat (especially with humidity) and coldness are known to provoke outbreaks, as well as sudden and extreme temperature swings.

The Scratch Test: An allergy skin-patch or "scratch" test, given by an allergist, can often pinpoint the triggers of allergic reactions. Once the causes of the allergic reactions are discovered, the allergens should be eliminated from the diet, lifestyle, and/or environment. If the eczema is severe, it may take some time (days to weeks depending on the severity) for the body's immune system to begin to settle down after the irritants are withdrawn.


The primary treatment involves prevention, includes avoiding or minimizing contact with (or intake of) known allergens. Once that has been established, topical treatments can be used. Topical treatments focus on reducing both the dryness and inflammation of the skin.

To combat the severe dryness associated with eczema, a high-quality, dermatologist approved moisturizer should be used daily. Moisturizers should not have any ingredients that may further aggravate the condition. Moisturizers are especially effective if applied within 5–10 minutes after bathing. A doctor might also prescribe lotion containing sodium hyaluronate to improve skin dryness.[11]

Most commercial soaps wash away all the oils produced by the skin that normally serve to prevent drying. Using a soap substitute such as aqueous cream helps keep the skin moisturized. A non-soap cleanser can be purchased usually at a local drug store. Showers should be kept short and at a lukewarm/moderate temperature.

If moisturizers on their own don't help and the eczema is severe, a doctor may prescribe topical corticosteroid ointments, creams, or injections. Corticosteroids have traditionally been considered the most effective method of treating severe eczema. Disadvantages of using steroid creams include stretch marks and thinning of the skin. Higher-potency steroid creams must not be used on the face or other areas where the skin is naturally thin; usually a lower-potency steroid is prescribed for sensitive areas. The use of the Finger tip unit may be helpful in guiding how much topical cream is required to cover different areas. If the eczema is especially severe, a doctor may prescribe prednisone or administer a shot of cortisone or triamcinolone In some countries over-the-counter hydrocortisone can be purchased at the local drugstore, for treatment of mild eczema.

If complications include infections (often of Staphylococcus aureus), antibiotics may be employed.

The immunosuppressants tacrolimus and pimecrolimus can be used as a topical preparation in the treatment of severe atopic dermatitis instead of or in addition to traditional steroid creams. There can be unpleasant side effects in some patients such as intense stinging or burning, which mostly get better after the first week of treatment.[12] However, the risk of developing skin cancer from the use of these drugs[13] (especially when combined to UV exposure, such as sunrays) was not ignored by the FDA, which issued a "black box warning"[14].

A more novel form of treatment involves exposure to broad or narrow-band ultraviolet 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.[15] 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.[16] However, UV radiation has also been implicated in various types of skin cancer,[17] and thus UV treatment is not without risk.

If ultraviolet light therapy is employed, initial exposure should be no longer than 5–10 minutes, depending on skin type. UV therapy should only be moderate, and special care should be taken to avoid sunburn (sunburn will only aggravate the eczema). It does not necessarily have to be administered in a hospital, it can be done at a tanning salon or in natural sunlight, so as long as it's done under the direction and supervision of a dermatologist.

A study in April 2009 showed that bathing in a dilute household bleach solution (1/2 cup or 120 ml of ordinary household chlorine bleach (sodium hypochlorite) to a bathtub full of water) in combination with nasal application of mupirocin can be beneficial in patients with clinical signs of secondary bacterial infections.[18]. It is believed that the antibacterial effect of these agents prevents the skin's colonization by staphylococcus aureus which can cause infections in an existing rash when the skin is broken by scratching; which in turn increases the itching, leading to more scratching and inflammation. If a bath is not available, swab onto reddened skin a dilute solution of 4.5 ml household bleach in 750 ml water. The skin must be moisturised with the patient's preferred moisturiser or oil after the antibacterial swabbing or bath.

In severe cases that do not respond to other treatments, oral immunosuppressant medications are sometimes prescribed, such as ciclosporin, azothioprine and methotrexate, however these treatments require patients to take regular blood tests as they can have significant side effects on the kidneys and liver.

Alternative treatments

Oil from oenothera, commonly known as Evening Primrose, can in some cases, alleviate the symptoms of eczema. "Primrose Oil and vitamin B6 (pyridoxine) have helped infants with dermatitis"


Four small and low-quality randomized clinical trials have found beneficial effects from a Traditional Chinese medicine herbal formulation called Zemaphyte, which is no longer manufactured.[20] A randomized clinical trial published in 2007 found that another Chinese herbal formulation increased quality of life and reduced topical corticosteroid use.[21]

Alternative medicines may (illegally) contain corticosteroids which are standard treatments for atopic dermatitis, raising a question of whether these illicit substances cause the effects;[22] however, a 2006 study did not find corticosteroids in a PentaHerbs concoction which had shown beneficial effects.[23]

Future research

It was less than ten years ago that the researchers discovered the first mouse model to spontaneously developed AE-like lesions, the inbred NC/Nga mouse.[24] These models have been used for tests that would have been impossible in humans, like the administration of Mycobacterium vaccae for the possible prevention of AE-like lesions.[25]

See also


  1. ^ De Benedetto A et al. Atopic dermatitis: a disease caused by innate immune defects? J Invest Dermatol. 2009;129:14-30.
  2. ^ Abels C, Proksch E. Therapy of atopic dermatitis. Hautarzt. 2006;57:711-23.
  3. ^ Saito H (2005). "Much atopy about the skin: genome-wide molecular analysis of atopic eczema". Int. Arch. Allergy Immunol. 137 (4): 319–25. doi:10.1159/000086464. PMID 15970641. 
  4. ^ a b c Klüken H, Wienker T, Bieber T (2003). "Atopic eczema/dermatitis syndrome - a genetically complex disease. New advances in discovering the genetic contribution". Allergy 58 (1): 5–12. doi:10.1034/j.1398-9995.2003.02162.x. PMID 12580800. 
  5. ^ a b Schreiber S, Rosenstiel P, Albrecht M, Hampe J, Krawczak M (2005). "Genetics of Crohn disease, an archetypal inflammatory barrier disease". Nat. Rev. Genet. 6 (5): 376–88. doi:10.1038/nrg1607. PMID 15861209. 
  6. ^ Palmer LJ, Cookson WO (2000). "Genomic approaches to understanding asthma". Genome Res. 10 (9): 1280–7. doi:10.1101/gr.143400. PMID 10984446. 
  7. ^ "OMIM - DERMATITIS, ATOPIC". Retrieved 2008-09-19. 
  8. ^ Esparza-Gordillo; Weidinger, S; Fölster-Holst, R; Bauerfeind, A; Ruschendorf, F; Patone, G; Rohde, K; Marenholz, I et al. (2009). "A common variant on chromosome 11q13 is associated with atopic dermatitis.". Nature Genetics. 41 (5): 596–601. doi:10.1038/ng.347. PMID 19349984. 
  9. ^ van Odijk J, Kull I, Borres MP, et al. (2003). "Breastfeeding and allergic disease: a multidisciplinary review of the literature (1966-2001) on the mode of early feeding in infancy and its impact on later atopic manifestations". Allergy 58 (9): 833–43. doi:10.1034/j.1398-9995.2003.00264.x. PMID 12911410. 
  10. ^ KOALA Birth Cohort Study, University of Maastricht, the Netherlands (Dutch language only)
  11. ^ One brand of sodium hyaluronate lotion is Hylira. Information on sodium hyaluronate lotion is available here.
  12. ^ Jasek, W, ed (2007) (in German). Austria-Codex (62 ed.). Vienna. pp. 2720, 6770. ISBN 3-85200-181-4. 
  13. ^ Wooltorton E (2005). "Eczema drugs tacrolimus (Protopic) and pimecrolimus (Elidel): cancer concerns.". CMAJ 172 (9): 1179–80. doi:10.1503/cmaj.050373. PMID 15817641. 
  14. ^ Food and Drug Administration (United States) (2005-03-10). "Safety information on Protopic (tacrolimus), Elidel (pimecrolimus)". Retrieved 2009-10-21. 
  15. ^ Beattie PE, Finlan LE, Kernohan NM, Thomson G, Hupp TR, Ibbotson SH (2005). "The effect of ultraviolet (UV) A1, UVB and solar-simulated radiation on p53 activation and p21". Br. J. Dermatol. 152 (5): 1001–8. doi:10.1111/j.1365-2133.2005.06557.x. PMID 15888160. 
  16. ^ Meduri NB, Vandergriff T, Rasmussen H, Jacobe H (2007). "Phototherapy in the management of atopic dermatitis: a systematic review". Photodermatol Photoimmunol Photomed 23 (4): 106–12. doi:10.1111/j.1600-0781.2007.00291.x. PMID 17598862. 
  17. ^ Jans J, Garinis GA, Schul W, et al. (2006). "Differential role of basal keratinocytes in UV-induced immunosuppression and skin cancer". Mol. Cell. Biol. 26 (22): 8515–26. doi:10.1128/MCB.00807-06. PMID 16966369. 
  18. ^ Jennifer T. Huang, MD, Melissa Abrams, MD, Brook Tlougan, MD, Alfred Rademaker, PhD and Amy S. Paller, MD (2009). "Treatment of Staphylococcus aureus Colonization in Atopic Dermatitis Decreases Disease Severity". Pediatrics 123 (5): e808–14. doi:10.1542/peds.2008-2217. PMID 19403473. 
  19. ^ title="Prescription for Nutritional Healing A Practical Reference To Drug-free Remedies Using Vitamins, Minerals, Herbs and Food supplements" href="/w/index.php?title=Atopic_dermatitis James F. Balch, M.D. and Phyllis A. Balch, C.N.C., 1997, p. 228.
  20. ^ Zhang W, Leonard T, Bath-Hextall F, et al. (2005). "Chinese herbal medicine for atopic eczema". Cochrane Database Syst Rev (2): CD002291. doi:10.1002/14651858.CD002291.pub3. PMID 15846635. 
  21. ^ Hon KL, Leung TF, Ng PC, et al. (August 2007). "Efficacy and tolerability of a Chinese herbal medicine concoction for treatment of atopic dermatitis: a randomized, double-blind, placebo-controlled study". Br. J. Dermatol. 157 (2): 357–63. doi:10.1111/j.1365-2133.2007.07941.x. PMID 17501956. 
  22. ^ Ramsay HM, Goddard W, Gill S, Moss C (2003). "Herbal creams used for atopic eczema in Birmingham, UK illegally contain potent corticosteroids". Arch. Dis. Child. 88 (12): 1056–7. doi:10.1136/adc.88.12.1056. PMID 14670768. PMC 1719403. 
  23. ^ Hon KL, Lee VW, Leung TF, et al. (November 2006). "Corticosteroids are not present in a traditional Chinese medicine formulation for atopic dermatitis in children". Ann. Acad. Med. Singap. 35 (11): 759–63. PMID 17160188. 
  24. ^ Gutermuth J, Ollert M, Ring J, Behrendt H, Jakob T (2004). "Mouse models of atopic eczema critically evaluated". Int. Arch. Allergy Immunol. 135 (3): 262–76. doi:10.1159/000082099. PMID 15542938. 
  25. ^ Arkwright PD, Fujisawa C, Tanaka A, Matsuda H (2005). "Mycobacterium vaccae reduces scratching behavior but not the rash in NC mice with eczema: a randomized, blinded, placebo-controlled trial". J. Invest. Dermatol. 124 (1): 140–3. doi:10.1111/j.0022-202X.2004.23561.x. PMID 15654967. 

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