Eczema

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Eczema
Classification and external resources
Dermatitis.jpg
Typical, mild dermatitis
ICD-10L20-L30
ICD-9692
OMIM603165
MedlinePlus000853
eMedicineDerm/38 Ped/2567
MeSHD004485
 
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Eczema
Classification and external resources
Dermatitis.jpg
Typical, mild dermatitis
ICD-10L20-L30
ICD-9692
OMIM603165
MedlinePlus000853
eMedicineDerm/38 Ped/2567
MeSHD004485

Eczema (from Greek: ἔκζεμα ēkzema, "to boil over") also known as atopic dermatitis[1] is a form of chronic inflammation of the skin.[2]

The term eczema is broadly applied to a range of persistent skin conditions. These include dryness and recurring skin rashes that are characterized by one or more of these symptoms: redness, skin edema (swelling), itching and dryness, crusting, flaking, blistering, cracking, oozing, or bleeding. Areas of temporary skin discoloration may appear and are sometimes due to healed injuries. Scratching open a healing lesion may result in scarring and may enlarge the rash.

The word eczema comes from Greek, meaning "to boil over". Dermatitis comes from the Greek word for skin – and both terms refer to the same skin condition. In some languages, dermatitis and eczema are synonymous, while in other languages dermatitis implies an acute condition and "eczema" a chronic one.[3] The two conditions are often classified together.

Classification[edit]

More severe eczema
A patch of eczema that has been scratched

The term eczema refers to a set of clinical characteristics. Classification of the underlying diseases has been haphazard and unsystematic, with many synonyms used to describe the same condition. A type of eczema may be described by location (e.g., hand eczema), by specific appearance (eczema craquele or discoid), or by possible cause (varicose eczema). Further adding to the confusion, many sources use the term eczema for the most common type of eczema (atopic dermatitis) interchangeably.

The European Academy of Allergology and Clinical Immunology (EAACI) published a position paper in 2001 which simplifies the nomenclature of allergy-related diseases including atopic and allergic contact eczemas.[4] Non-allergic eczemas are not affected by this proposal.

Common[edit]

Less common[edit]

Cause[edit]

Complex eczema treated with a combination of antifungal and corticosteroid creams concurrently.

The cause of eczema is unknown but is presumed to be a combination of genetic and environmental factors.[5]

The hygiene hypothesis postulates that the cause of asthma, eczema, and other allergic diseases is an unusually clean environment. It is supported by epidemiologic studies for asthma.[6] The hypothesis states that exposure to bacteria and other immune system modulators is important during development, and missing out on this exposure increases risk for asthma and allergy.

While it has been suggested that eczema may sometimes be an allergic reaction to the excrement from house dust mites,[7] with up to 5% of people showing antibodies to the mites,[8] the overall role this plays awaits further corroboration.[9]

Researchers have compared the prevalence of eczema in people who also suffer from celiac disease to eczema prevalence in control subjects, and have found that eczema occurs about three times more frequently in celiac disease patients and about two times more frequently in relatives of celiac patients, potentially indicating a genetic link between the two conditions.[10][11]

The failure of the body to metabolize linoleic acid into y-linoleic acid (GLA) was thought to be a possible cause of eczema, however the largest and best reported studies into the efficacy of GLA supplements in the treatment of eczema failed to show any benefit.[12]

Diagnosis[edit]

Diagnosis of eczema is based mostly on history and physical examination. However, in uncertain cases, skin biopsy may be useful.[citation needed]

Prevention[edit]

People with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.[13]

Management[edit]

There is no known cure for eczema; therefore, treatments aim to control the symptoms by reducing inflammation and relieving itching.

Medications[edit]

Corticosteroids[edit]

Corticosteroids are highly effective in controlling or suppressing symptoms in most cases.[14] For mild-moderate eczema a weak steroid may be used (e.g. hydrocortisone), while in more severe cases a higher-potency steroid (e.g. clobetasol propionate) may be used. In severe cases, oral or injectable corticosteroids may be used. While these usually bring about rapid improvements, they have greater side effects.

Adverse effects[edit]
Lower arm of a 47-year-old female showing skin damage due to topical steroid use

Prolonged use of topical corticosteroids is thought to increase the risk of side effects, the most common of which is the skin becoming thin and fragile (atrophy).[15] Because of this, if used on the face or other delicate skin, only a low-strength steroid should be used. Additionally, high-strength steroids used over large areas, or under occlusion, may be significantly absorbed into the body, causing hypothalamic-pituitary-adrenal axis suppression (HPA axis suppression).[16] Finally by their immunosuppressive action they can, if used without antibiotics or antifungal drugs, lead to some skin infections (fungal or bacterial). Care must be taken to avoid the eyes, as topical corticosteroids applied to the eye can cause glaucoma [17] or cataracts.

Because of the risks associated with this type of drug, a steroid of an appropriate strength should be sparingly applied only to control an episode of eczema. Once the desired response has been achieved, it should be discontinued and replaced with emollients as maintenance therapy. Corticosteroids are generally considered safe to use in the short- to medium-term for controlling eczema, with no significant side effects differing from treatment with non-steroidal ointment.[18]

Some recent research claims that topically applied corticosteroids did not significantly increase the risk of skin thinning, stretch marks or HPA axis suppression (and where such suppression did occur, it was mild and reversible where the corticosteroids were used for limited periods of time). Further, skin conditions are often under-treated because of fears of side effects. This has led some researchers to suggest that the usual dosage instructions should be changed from "Use sparingly" to "Apply enough to cover affected areas", and that specific dosage directions using "fingertip units" or FTUs be provided, along with photos to illustrate FTUs.[19] However, caution must always be used as long-term use, prolonged widespread coverage, or use with occlusion, can create side effects that are permanent and resistant to treatment.[20]

Immunosuppressants[edit]

Tacrolimus 0.1%

Topical immunosuppressants like pimecrolimus and tacrolimus effectively suppress the immune system in the affected area, and appear to yield better results in some populations. The U.S. Food and Drug Administration has issued a public health advisory about the possible risk of lymph node or skin cancer from use of these products,[21] but many professional medical organizations disagree with the FDA's findings;

When eczema is severe and does not respond to other forms of treatment, systemic immunosuppressants are sometimes used. These dampen the immune system and can result in improvements to the person's eczema. However, immunosuppressants can cause side effects. Some require regular blood tests and be closely monitored. In the UK, the most commonly used immunosuppressants for eczema are ciclosporin, azathioprine and methotrexate.

Itch relief[edit]

Anti-itch drugs, often antihistamine, and dermasil may reduce the itch during a flare up of eczema, and the reduced scratching in turn reduces damage and irritation to the skin (the "itch cycle").[citation needed] However, in some cases, significant benefit may be due to the sedative side effects of these drugs, rather than their specific antihistamine effect. Thus sedating antihistamines such as promethazine (Phenergan) or diphenhydramine (Benadryl) may be more effective at preventing night time scratching than the newer, nonsedating antihistamines.[26]

Capsaicin applied to the skin acts as a counter irritant (see gate control theory of nerve signal transmission).

Hydrocortisone applied to the skin aids in temporary itch relief.

Temporary yet significant and fast-acting relief can be found by cooling the skin via water (swimming, cool water bath or wet washcloth), air (direct output of an air conditioning vent), or careful use of an ice pack (wrapped in soft smooth cloth, e.g., pillow case, to protect skin from damage).

Moisturizers[edit]

Eczema can be exacerbated by dryness of the skin. Moisturizing is one of the most important self-care treatments for eczema. Keeping the affected area moistened can promote skin healing and relief of symptoms. Soaps and detergents should not be used on affected skin because they can strip natural skin oils and lead to excessive dryness.

Moistening agents are called emollients. In general, it is best to match thicker ointments to the driest, flakiest skin. Light emollients may not have any effect on severely dry skin. Moisturizing gloves (gloves which keep emollients in contact with skin on the hands) can be worn while sleeping. Generally, twice-daily applications of emollients work best. Ointments, with less water content, stay on the skin longer and need fewer applications, but they can be greasy and inconvenient. Steroids may also be mixed in with ointments.

For unbroken skin, direct application of waterproof tape with or without an emollient or prescription ointment can improve moisture levels and skin integrity which allows the skin to heal. This treatment regimen can also help prevent the skin from cracking, as well as put a stop to the itch cycle. The end result is reduced lichenification (the roughening of skin from repeated scratching). Taping works best on skin away from joints.

There is a disagreement whether baths are desirable or a necessary evil. For example, the Mayo Clinic advises against daily baths to avoid skin drying.[27] On the other hand, the American Academy of Dermatology claims "it is a common misconception that bathing dries the skin and should be kept to a bare minimum" and recommends bathing to hydrate skin. They even suggest up to 3 short baths a day for people with severe eczema. According to them, a moisturizer should be applied within 3 minutes to trap the moisture from bath in the skin.[28]

Ceramides, which are the major lipid constituent of the stratum corneum, have been used in the treatment of eczema.[29][30][31] They are often one of the ingredients of modern moisturizers.[32]

The terms "hypoallergenic" and "doctor tested" are not regulated,[33] and no research has been done showing that products labeled "hypoallergenic" are in fact less problematic than any others.

Lifestyle[edit]

Various measures may reduce the amount of mite antigens, in particular swapping carpets for hard surfaces.[34] However it is not clear whether such measures actually help with eczema. A controlled study suggested that a number of environmental factors such as air exchange rates, relative humidity and room temperature (but not the level of house dust mites) might have an effect on the condition.[35]

Patients can also wear clothing designed specifically to manage the itching, scratching and peeling associated with eczema.[36]

Light therapy[edit]

Light therapy (or deep penetrating light therapy) using ultraviolet light can help control eczema.[37] UVA is mostly used, but UVB and Narrow Band UVB are also used. Overexposure to ultraviolet light carries its own risks, particularly potential skin cancer from exposure.[38]

When light therapy alone is found to be ineffective, the treatment is performed with the application (or ingestion) of a substance called psoralen. This PUVA (Psoralen + UVA) combination therapy is termed photo-chemotherapy. Psoralens make the skin more sensitive to UV light, thus allowing lower doses of UVA to be used. However, the increased sensitivity to UV light also puts the patient at greater risk for skin cancer.[39]

Dietary[edit]

There has not yet been adequate evaluation of the effects of altering the diet to reduce eczema.[40][41] There is some evidence that infants with eczema and an established egg allergy may have a reduction in symptoms if eggs are eliminated from their diets.[40] Benefits have not been shown for other elimination diets, but more research is needed to show whether dietary changes may help.[40][41] Establishing there is in fact a food allergy before dietary change could avoid unnecessary major lifestyle changes.[40] Those with eczema may be especially prone to misdiagnosis of food allergies.[42][43]

Dietary supplements are commonly used by people with eczema.[44] Probiotics are live microorganisms taken orally, such as the Lactobacillus bacteria found in yogurt. They are not effective for treating eczema in older populations, but some research points to some strains of beneficial microorganisms having the ability to prevent the triad of allergies, eczema and asthma, although in rare cases some species of probiotic bacteria have a very small risk of infection in those with poor immune system response.[45][46] Exposure to probiotics in infancy may shape the immune system to resist eczema.[47] Certain strains of probiotics are more effectual than others, and the timing of administration is also important.[47]

Borage oil has not shown benefits for eczema, and has mild transient adverse effects (predominantly gastrointestinal).[48] Evening primrose oil has not shown benefits for eczema, and has mild transient adverse effects (predominantly gastrointestinal).[48] There is some evidence to suggest prolonged use may cause inflammation, thrombosis, and immunosuppression, and it may increase bleeding risk in people using warfarin.[48] There is no evidence for zinc, selenium, vitamin D, vitamin E, pyridoxine (vitamin B6), sea buckthorn oil, hempseed oil, sunflower oil, or fish oil.[44]

Alternative therapies[edit]

A number of alternative therapies are used for eczema including:

Behavioural approach[edit]

In the 1980s, Swedish dermatologist Peter Noren developed a behavioural approach to the treatment of long term atopic eczema. This approach has been further developed by dermatologist Richard Staughton and psychiatrist Christopher Bridgett at the Chelsea and Westminster Hospital in London.[56][57] Patients undergo a six-week monitored program involving scratch habit reversal and self-awareness of scratching levels. For long-term eczema sufferers, scratching can become habitual. Sometimes scratching becomes a reflex, resulting in scratching without conscious awareness, rather than from the feeling of itchiness itself. The habit reversal program is done in conjunction with the standard applied emollient/corticosteroid treatments so that the skin can heal. It also reduces future scratching, as well as reduces the likelihood of further flareups. The behavioural approach can give an eczema sufferer some control over the degree of severity of eczema.

Epidemiology[edit]

Globally eczema affected approximately 230 million people as of 2010 (3.5% of the population).[58] The lifetime clinician-recorded prevalence of eczema has been seen to peak in infancy, with female predominance of eczema presentations occurring during the reproductive period of 15–49 years.[59] Although little data on the trend of eczema prevalence over time exists prior to the Second World War (1939–45), the prevalence of eczema has been found to have increased substantially in the latter half of the 20th Century, with eczema in school-aged children being found to increase between the late 1940s and 2000.[60] A review of epidemiological data in the UK has also found an inexorable rise in the prevalence of eczema over time.[61] Further recent increases in the incidence and lifetime prevalence of eczema in England have also been reported, such that an estimated 5,773,700 or about one in every nine people have been diagnosed with the disease by a clinician at some point in their lives.[62]

History[edit]

from ancient Greek ἔκζεμα ékzema,[63]
from ἐκζέ-ειν ekzé-ein,
from ἐκ ek "out" + ζέ-ειν zé-ein "to boil"

(OED)

The term "atopic dermatitis" was coined in 1933 by Wise and Sulzberger.[64]

Research[edit]

Other than direct treatments of the symptoms, no cure is presently known for most types of dermatitis; even cortisone treatments and immunomodulation may often have only minor effects on what may be a complex problem. Even though the effects of eczema are no longer active the person diagnosed is still subject to relapse. The condition is often related to family history of allergies.

Damage from the enzymatic activity of allergens is usually prevented by the body's own protease inhibitors, such as, LEKTI, produced from the gene SPINK5. Mutations in this gene are known to cause Netherton's syndrome, which is a congenital erythroderma. These patients nearly always develop atopic disease, including hay fever, food allergy, urticaria and asthma. Such evidence supports the hypothesis that skin damage from allergens may be the cause of eczema, and may provide a venue for further treatment.[65]

Another study identified a gene that the researchers believe to be the cause of inherited eczema and some related disorders. The gene produces the protein filaggrin, the lack of which causes dry skin and impaired skin barrier function.[66]

A recent study indicated that two specific chemicals found in the blood are connected to the itching sensations associated with eczema. The chemicals are Brain-derived neurotrophic factor (BDNF) and Substance P.[67]

In a genome-wide study published on Dec 25, 2011 in Nature Genetics, researchers reported discovery of three new genetic variants associated with eczema. They are OVOL1, ACTL9 and IL4-KIF3A.[68]

Eczema has increased dramatically in England as a study showed a 42% rise in diagnosis of the condition between 2001 and 2005, by which time it was estimated to affect 5.7 million adults and children. A paper in the Journal of the Royal Society of Medicine says Eczema is thought to be a trigger for other allergic conditions. GP records show over 9 million patients were used by researchers to assess how many people have the skin disorder.[69]

References[edit]

  1. ^ Bershad, SV (2011 Nov 1). "In the clinic. Atopic dermatitis (eczema).". Annals of internal medicine 155 (9): ITC51–15; quiz ITC516. doi:10.1059/0003-4819-155-9-201111010-01005. PMID 22041966. 
  2. ^ Armstrong, A; Johnson (19 May 2011). "Conquering Eczema!" (Video, Text). UCDMC Dermatology. Retrieved 3 July 2013. 
  3. ^ Johannes Ring; Bernhard Przybilla; Thomas Ruzicka (2006). Handbook of atopic eczema. Birkhäuser. p. 4. ISBN 978-3-540-23133-2. Retrieved 4 May 2010. 
  4. ^ Johansson SG, Hourihane JO, Bousquet J, et al. (September 2001). "A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force". Allergy 56 (9): 813–24. doi:10.1034/j.1398-9995.2001.t01-1-00001.x. PMID 11551246. 
  5. ^ "Atopic dermatitis". National Institute of Health. Retrieved 27 September 2011. 
  6. ^ Bufford, JD; Gern JE (May 2005). "The hygiene hypothesis revisited". Immunology and Allergy Clinics of North America 25 (2): 247–262. doi:10.1016/j.iac.2005.03.005. PMID 15878454. 
  7. ^ Carswell F, Thompson S (1986). "Does natural sensitisation in eczema occur through the skin?". Lancet 2 (8497): 13–5. doi:10.1016/S0140-6736(86)92560-2. PMID 2873316. 
  8. ^ Henszel Ł, Kuźna-Grygiel W (2006). "[House dust mites in the etiology of allergic diseases]". Annales Academiae Medicae Stetinensis (in Polish) 52 (2): 123–7. PMID 17633128. 
  9. ^ Atopic Dermatitis at eMedicine
  10. ^ Caproni, M; Bonciolini, V; D'Errico, A; Antiga, E; Fabbri, P. "Celiac Disease and Dermatologic Manifestations: Many Skin Clue to Unfold Gluten-Sensitive Enteropathy". Gastroenterol. Res. Pract. (Hindawi Publishing Corporation) 2012. doi:10.1155/2012/952753. PMID 22693492. 
  11. ^ Ciacci, C; Cavallaro R, Iovino P, Sabbatini F, Palumbo A, Amoruso D, Tortora R, Mazzacca G. (June 2004). "Allergy prevalence in adult celiac disease". J. Allergy Clin. Immunol. 113 (6): 1199–203. doi:10.1016/j.jaci.2004.03.012. PMID 15208605. 
  12. ^ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC292973/.  Missing or empty |title= (help)
  13. ^ "CDC Smallpox | Smallpox (Vaccinia) Vaccine Contraindications (Info for Clinicians)". Emergency.cdc.gov. 2007-02-07. Retrieved 2010-02-07. 
  14. ^ Hoare C, Li Wan Po A, Williams H (2000). "Systematic review of treatments for atopic eczema". Health Technology Assessment 4 (37): 1–191. PMID 11134919. 
  15. ^ Atherton DJ (October 2003). "Topical corticosteroids in atopic dermatitis". BMJ 327 (7421): 942–3. doi:10.1136/bmj.327.7421.942. PMC 259155. PMID 14576221. 
  16. ^ Lee NP, Arriola ER (1999). "Topical corticosteroids: back to basics". The Western Journal of Medicine 171 (5-6): 351–3. PMC 1308757. PMID 10639873. 
  17. ^ "neomycin and polymyxin b sulfates and bacitracin zinc with hydrocortisone acetate (Neomycin sulfate and Polymyxin B Sulfate, Bacitracin zinc and Hydrocortisone Acetate) ointment -- Warnings". U.S. Food and Drug Administration. 
  18. ^ Van Der Meer JB, Glazenburg EJ, Mulder PG, Eggink HF, Coenraads PJ (June 1999). "The management of moderate to severe atopic dermatitis in adults with topical fluticasone propionate. The Netherlands Adult Atopic DermatitisStudy Group". British Journal of Dermatology 140 (6): 1114–21. PMID 10354080. 
  19. ^ Bewley A; Dermatology Working, Group (May 2008). "Expert consensus: time for a change in the way we advise our patients to use topical corticosteroids". The British Journal of Dermatology 158 (5): 917–20. doi:10.1111/j.1365-2133.2008.08479.x. PMID 18294314. 
  20. ^ Ting P, Barankin B (December 2006). "Atrophic patches". Can Fam Physician (College of Family Physicians of Canada) 52 (12): 1547, 1551–2. PMC 1783752. PMID 17279233. 
  21. ^ "FDA Issues Public Health Advisory Informing Health Care Providers of Safety Concerns Associated with the Use of Two Eczema Drugs, Elidel and Protopic". FDA. March 10, 2005. Archived from the original on 2007-09-17. Retrieved 2007-10-16. 
  22. ^ N H Cox and Catherine H Smith (December 2002). "Advice to dermatologists re topical tacrolimus" (DOC). Therapy Guidelines Committee. British Association of Dermatologists. 
  23. ^ "Pimecrolimus cream for atopic dermatitis". Drug and Therapeutics Bulletin 41 (5): 33–6. May 2003. doi:10.1136/dtb.2003.41533. PMID 12789846. 
  24. ^ "Microsoft Word - package insert and med guide June 2009.doc" (PDF). Retrieved 2011-03-27. 
  25. ^ Martins, Gladys Aires; Arruda, Lucia (2004). "Tratamento sistêmico da psoríase - Parte I: metotrexato e acitretina". Anais Brasileiros de Dermatologia 79. doi:10.1590/S0365-05962004000300002. 
  26. ^ http://www.cks.nhs.uk/eczema_atopic/evidence/supporting_evidence/antihistamines | Retrieved 14 November 2011
  27. ^ "Atopic dermatitis (eczema) - Prevention at Mayoclinic's website". Retrieved 2011-10-10. 
  28. ^ "Daily Skin Care Essential to Control Atopic Dermatitis article at American Academy of Dermatology's EczemaNet website". Retrieved 2009-03-24. 
  29. ^ Coderch L, López O, de la Maza A, Parra JL (2003). "Ceramides and skin function". American Journal of Clinical Dermatology 4 (2): 107–29. doi:10.2165/00128071-200304020-00004. PMID 12553851. 
  30. ^ Bouwstra JA, Ponec M (December 2006). "The skin barrier in healthy and diseased state". Biochimica et Biophysica Acta 1758 (12): 2080–95. doi:10.1016/j.bbamem.2006.06.021. PMID 16945325. 
  31. ^ Choi MJ, Maibach HI (2005). "Role of ceramides in barrier function of healthy and diseased skin". American Journal of Clinical Dermatology 6 (4): 215–23. doi:10.2165/00128071-200506040-00002. PMID 16060709. 
  32. ^ "New Skin-healing Chemicals". Science Daily. August 30, 2007. Retrieved 2007-10-06. 
  33. ^ Murphy LA, White IR, Rastogi SC (May 2004). "Is hypoallergenic a credible term?". Clinical and Experimental Dermatology 29 (3): 325–7. doi:10.1111/j.1365-2230.2004.01521.x. PMID 15115531. 
  34. ^ Mihrshahi S, Marks G, Vanlaar C, Tovey E, Peat J (2002). "Predictors of high house dust mite allergen concentrations in residential homes in Sydney". Allergy 57 (2): 137–42. doi:10.1034/j.1398-9995.2002.5720999.x. PMID 11929416. 
  35. ^ Beck HI, Bjerring P, Harving H (1989). "Atopic dermatitis and the indoor climate. The effect from preventive measures". Acta Dermato-venereologica 69 (2): 162–5. PMID 2564236. 
  36. ^ Ricci G, Patrizi A, Bellini F, Medri M (2006). "Use of textiles in atopic dermatitis: care of atopic dermatitis". Current Problems in Dermatology 33: 127–43. doi:10.1159/000093940. PMID 16766885. 
  37. ^ Polderman MC, Wintzen M, le Cessie S, Pavel S (2005). "UVA-1 cold light therapy in the treatment of atopic dermatitis: 61 patients treated in the Leiden University Medical Center". Photodermatology, photoimmunology & photomedicine 21 (2): 93–6. doi:10.1111/j.1600-0781.2005.00150.x. PMID 15752127. 
  38. ^ Stöppler MC (31 May 2007). "Psoriasis PUVA Treatment Can Increase Melanoma Risk". MedicineNet. Retrieved 2007-10-17. 
  39. ^ Stern RS; Puva Follow Up, Study (May 2001). "The risk of melanoma in association with long-term exposure to PUVA". Journal of the American Academy of Dermatology 44 (5): 755–61. doi:10.1067/mjd.2001.114576. PMID 11312420. 
  40. ^ a b c d Bath-Hextall, F; Delamere, FM; Williams, HC (2008 Jan 23). "Dietary exclusions for established atopic eczema.". Cochrane database of systematic reviews (Online) (1): CD005203. doi:10.1002/14651858.CD005203.pub2. PMID 18254073. 
  41. ^ a b Institute for Quality and Efficiency in Health Care. "Eczema: Can eliminating particular foods help?". Informed Health Online. Institute for Quality and Efficiency in Health Care. Retrieved 24 June 2013. 
  42. ^ "Food allergies commonly misdiagnosed, especially among eczema patients" (Press release). National Jewish Medical and Research Center. 16 March 2009. Retrieved 2009-03-20. 
  43. ^ Atkins D (March 2008). "Food allergy: diagnosis and management". Primary Care 35 (1): 119–40, vii. doi:10.1016/j.pop.2007.09.003. PMID 18206721. 
  44. ^ a b Bath-Hextall, FJ; Jenkinson, C; Humphreys, R; Williams, HC (2012 Feb 15). "Dietary supplements for established atopic eczema.". Cochrane database of systematic reviews (Online) 2: CD005205. doi:10.1002/14651858.CD005205.pub3. PMID 22336810. 
  45. ^ Boyle RJ, Bath-Hextall FJ, Leonardi-Bee J, Murrell DF, Tang ML (2008). "Probiotics for treating eczema". In Boyle, Robert John. Cochrane Database of Systematic Reviews (Online) (4): CD006135. doi:10.1002/14651858.CD006135.pub2. PMID 18843705. 
  46. ^ Flohr C, Pascoe D, Williams HC (February 2005). "Atopic dermatitis and the 'hygiene hypothesis': too clean to be true?". The British Journal of Dermatology 152 (2): 202–16. doi:10.1111/j.1365-2133.2004.06436.x. PMID 15727630. 
  47. ^ a b Kalliomaki, M.; Antoine, J.-M.; Herz, U.; Rijkers, G. T.; Wells, J. M.; Mercenier, A. (2010). "Guidance for Substantiating the Evidence for Beneficial Effects of Probiotics: Prevention and Management of Allergic Diseases by Probiotics". Journal of Nutrition 140 (3): 713S–21S. doi:10.3945/jn.109.113761. PMID 20130079. 
  48. ^ a b c Bamford, JT; Ray, S; Musekiwa, A; van Gool, C; Humphreys, R; Ernst, E (2013 Apr 30). "Oral evening primrose oil and borage oil for eczema.". Cochrane database of systematic reviews (Online) 4: CD004416. doi:10.1002/14651858.CD004416.pub2. PMID 23633319. 
  49. ^ "Sulfur". University of Maryland Medical Center. 4/1/2002. Retrieved 2007-10-15. 
  50. ^ "Complementary Therapies". American Academy of Dermatology. Retrieved 2008-08-01. 
  51. ^ "Treating Childhood Eczema With Acupuncture and Chinese Herbs". Acupuncturetoday.com. 2011-10-04. Retrieved 2013-08-01. 
  52. ^ "Chinese medicine 'eases eczema'". BBC News. 13 March 2008. 
  53. ^ Armstrong NC, Ernst E (August 1999). "The treatment of eczema with Chinese herbs: a systematic review of randomized clinical trials". British Journal of Clinical Pharmacology 48 (2): 262–4. doi:10.1046/j.1365-2125.1999.00004.x. PMC 2014284. PMID 10417508. 
  54. ^ Bamford, JT; Ray, S; Musekiwa, A; van Gool, C; Humphreys, R; Ernst, E (2013 Apr 30). "Oral evening primrose oil and borage oil for eczema.". The Cochrane database of systematic reviews 4: CD004416. doi:10.1002/14651858.CD004416.pub2. PMID 23633319. 
  55. ^ Eldred DC, Tuchin PJ (November 1999). "Treatment of acute atopic eczema by chiropractic care. A case study". Australasian Chiropractic & Osteopathy 8 (3): 96–101. PMC 2051093. PMID 17987197. 
  56. ^ Bridgett, C. (2000). "Psychodermatology and Atopic Skin Disease in London 1989–1999 – Helping Patients to Help Themselves". Dermatology and Psychosomatics / Dermatologie und Psychosomatik 1: 183. doi:10.1159/000057975. 
  57. ^ Bridgett C (2004). "Psychocutaneous medicine". Journal of cosmetic dermatology 3 (2): 116. doi:10.1111/j.1473-2130.2004.00047.x. PMID 17147570. 
  58. ^ Vos, T (2012 Dec 15). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010.". Lancet 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMID 23245607. 
  59. ^ Osman M, Hansell AL, Simpson CR, Hollowell J, Helms PJ (February 2007). "Gender-specific presentations for asthma, allergic rhinitis and eczema in primary care". Primary Care Respiratory Journal 16 (1): 28–35. doi:10.3132/pcrj.2007.00006. PMID 17297524. 
  60. ^ Taylor B, Wadsworth J, Wadsworth M, Peckham C (December 1984). "Changes in the reported prevalence of childhood eczema since the 1939–45 war". Lancet 2 (8414): 1255–7. doi:10.1016/S0140-6736(84)92805-8. PMID 6150286. 
  61. ^ Gupta R, Sheikh A, Strachan DP, Anderson HR (April 2004). "Burden of allergic disease in the UK: secondary analyses of national databases". Clinical and Experimental Allergy 34 (4): 520–6. doi:10.1111/j.1365-2222.2004.1935.x. PMID 15080802. 
  62. ^ Simpson CR, Newton J, Hippisley-Cox J, Sheikh A (March 2009). "Trends in the epidemiology and prescribing of medication for eczema in England". Journal of the Royal Society of Medicine 102 (3): 108–17. doi:10.1258/jrsm.2009.080211. PMC 2746851. PMID 19297652. 
  63. ^ Henry George Liddell, Robert Scott. "Ekzema". A Greek-English Lexicon. Tufts University: Perseus. 
  64. ^ Textbook of Atopic Dermatitis. Taylor & Francis. p. 1. ISBN 9780203091449. 
  65. ^ Walley AJ, Chavanas S, Moffatt MF, et al. (2001). "Gene polymorphism in Netherton and common atopic disease". Nat. Genet. 29 (2): 175–8. doi:10.1038/ng728. PMID 11544479. 
  66. ^ Palmer CN et al. (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. 
  67. ^ "'Blood chemicals link' to eczema – Scientists have identified two blood chemicals linked to itchy eczema, offering new treatment possibilities.". BBC News. 26 August 2007. Retrieved 2007-10-16. 
  68. ^ Paternoster et al. (2011). "Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis". Nature Genetics. doi:10.1038/ng.1017. 
  69. ^ Wilkinson Emma (23 March 2009). "Eczema cases rise dramatically". BBC News. 

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