| Atopic eczema |
| Classification and external resources |
Atopic eczema
|
| ICD-10 |
L20 |
| ICD-9 |
691.8 |
| OMIM |
603165 |
| MedlinePlus |
000853 |
| eMedicine |
emerg/130 derm/38 ped/2567 oph/479 |
| MeSH |
D003876 |
Atopic eczema also known as atopic dermatitis[1] is a type of eczema, an inflammatory, relapsing, non-contagious and pruritic (itchy) skin disorder.[2] It has been given names like "prurigo Besnier," "neurodermitis," "endogenous eczema," "flexural eczema," "infantile eczema," and "prurigo diathésique".[3]
Contents
- 1 Signs and symptoms
- 2 Cause
- 2.1 Genetics
- 2.2 Allergies
- 2.3 Histamine intolerance
- 3 Treatments
- 3.1 Corticosteroids
- 3.2 Immunosuppressants
- 3.3 Immunotherapy
- 3.4 Emollient creams
- 3.5 UV light therapy
- 4 Epidemiology
- 5 See also
- 6 References
- 7 External links
Signs and symptoms[edit]
Atopic dermatitis of the anterior flextural crease of the elbow.
Pattern of atopic eczema varies with age
The skin of a patient with atopic dermatitis reacts abnormally and easily to irritants, food and environmental allergens and becomes very itchy, which leads to scratching, redness, and flaky skin. It is sometimes called "the itch that rashes" because the itchiness precedes the rash, and scratching the itchy skin may cause the rash.[4] 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 allergic 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, and is also a well-documented 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.
Atopic dermatitis most often begins in childhood before age 5 and may persist into adulthood. For some, it flares periodically and then subsides for a time, even up to several years.[5] Yet, it is estimated that 75% of the cases of atopic dermatitis improve by the time children reach adolescence, whereas 25% continue to have difficulties with the condition through adulthood.[6]
Although atopic dermatitis can theoretically affect any part of the body, it tends to be more frequent on the hands and feet, on the ankles, wrists, face, neck and upper chest. Atopic dermatitis can also affect the skin around the eyes, including the eyelids.[7]
In most patients, the usual symptoms that occur with this type of dermatitis are aggravated by a Staphylococcus aureus infection, dry skin, stress, low humidity and sweating, dust or sand or cigarette smoke. Also, the condition can be worsened by having long and hot baths or showers, solvents, cleaners or detergents and wool fabrics or clothing.
Atopic dermatitis is also known as infantile eczema, when it occurs in infants. Infantile eczema may continue into childhood and adolescence and it often involves an oozing, crusting rash mainly on the scalp and face, although it can occur anywhere on the body.[8] The appearance of the rash tends to modify, becoming dryer in childhood and then scaly or thickened in adolescence while the itching is persistent.
Approximately 50% of the patients who develop the condition display symptoms before the age of 1, and 80% display symptoms within the first 5 years of life.[6]
Symptoms may vary from person to person but they are usually present as a red, inflamed, and itchy rash and can quickly develop into raised and painful bumps.[9] The first sign of atopic dermatitis is the red to brownish-gray colored patches that are usually very itchy. Itching may become more intense during the night. The skin may present small and raised bumps which may be crusting or oozing if scratched, which will also worsen the itch. The skin tends to be more sensitive and may thicken, crack or scale.
When appearing in the area next to the eyes, scratching can cause redness and swelling around them and sometimes, rubbing or scratching in this area causes patchy loss of eyebrow hair and eyelashes.[5]
The symptoms of atopic dermatitis vary with the age of the patients. Usually, in infants, the condition causes red, scaly, oozy and crusty cheeks and the symptoms may also appear on their legs, neck and arms. Symptoms clear in about half of these children by the time they are 2 or 3 years old.[10] In older children, the symptoms include dry and thick, scaly skin with a very persistent itch, which is more severe than in infants. Adolescents are more likely to develop thick, leathery and dull-looking lesions on their face, neck, hands, feet, fingers or toes.
Cause[edit]
The exact cause of atopic dermatitis is currently unknown.[11]
Genetics[edit]
There is evidence suggesting that atopic dermatitis is genetically inherited.[12] People of all races can get eczema.
In 2006 is 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]
Allergies[edit]
Those exposed to dogs while growing up have a lower risk of atopic dermatitis.[14]
Food allergy do not cause atopic eczema but sensitivity to certain foods is often mistaken for the cause of eczema because of its links to diet. Many dermatologists and physicians test for food allergies in their office. The test is often done as a pin or needle prick. A drop of food extract is placed on the skin, and a small prick in the epidermis is made. A wheal indicates a positive result.
Histamine intolerance[edit]
A subset of people afflicted with atopic dermatitis are affected by exogenous sources of histamine,[15] meaning histamine from outside the body, because histamine causes itching and discomfort. 33% of atopic eczematics significantly improve their symptoms after following a histamine-free diet. This diet excludes various foods high in histamine content including cheeses, hard cured sausages, alcohol, and other fermented foods.[15] Other histamine-free diets also exclude fish, shellfish, tomatoes, spinach, and eggplant as well. Fish is known to succumb to bacterial degradation quickly thus forming high amounts of histamine in the fish which can cause Scombroid poisoning.
Treatments[edit]
There is no known cure for eczema. While these do not cure atopic eczema, these treatments are recommend by dermatologist and general practitioners to calm down flare ups.
Corticosteroids[edit]
Topical corticosteroids or injections maybe useful. They work by interfering with the body's natural inflammation response. Corticosteroids have traditionally been considered the most effective method of temporarily calming eczema. However the skin will relapse into a flare up so far as causative agents are not removed. Disadvantages of using steroid creams include stretch marks and thinning of the skin; further mitigating epidermal barrier function and increasing the sensitivity to contact allergens. If complications include infections (often of Staphylococcus aureus), antibiotics may be employed. Higher-potency steroid creams should never ever 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 is recommended in guiding how much topical cream is required to cover different areas. If the eczema is not responding prednisone or administer a shot of cortisone may help.
Immunosuppressants[edit]
The immunosuppressants tacrolimus and pimecrolimus are used as a "last line defense" topical preparation in the treatment of severe atopic dermatitis instead of, or in addition to traditional corticosteroid creams. In severe cases that do not respond to other treatments, oral immunosuppressant medications are sometimes prescribed, such as ciclosporin, azathioprine and methotrexate. Common unpleasant side effects in some patients include intense stinging, itching or burning.[16] Serious side effect include malfunction of important organs (which is why these treatments require patients to take regular blood tests as they can have significant side effects on the kidneys and liver) and developing skin cancer from the use of these drugs[17] (especially when combined to UV exposure, such as sun rays). These side effects have been clearly demonstrated and have not been ignored by the FDA, which issued a "black box warning."[18]
Immunotherapy[edit]
Immunotherapy against specific antigens has been found to be useful in both children and adults.[19]
Emollient creams[edit]
Applying moisturizer may prevent the skin from drying out and decrease the need for other medications.[20]
UV light therapy[edit]
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.[21][22] 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.[23] However, UV radiation has also been implicated in various types of skin cancer,[24] and thus UV treatment is not without risk.
Epidemiology[edit]
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 10–20% of children and 1–3% of adults in developed countries, and in the United States has nearly tripled in the past thirty to forty years.[25]
Atopic eczema is a common disease which tends to affect both males and females in the same proportion. It is estimated that this condition accounts for about 20% of all dermatologic referrals. The prevalence of atopic dermatitis is however quite difficult to establish since the diagnostic criteria are not applied universally and are not standard, but it is thought to vary roughly between 10% and 30%. Most of the population-based studies report that at least 80% of the atopic dermatitis populations have mild eczema.[26]
Atopic eczema occurs most often in infants and children, and its onset decreases substantially with age, and it is highly unlikely to develop in patients who are older than 30 years.[27] The condition appears to primarily affect individuals who live in urban areas and in climates with low humidity. However, specialists claim that there is a genetic factor which may play an important role in the development of atopic dermatitis.
See also[edit]
- SCORAD
- List of cutaneous conditions caused by mutations in keratins
References[edit]
- ^ Williams, Hywel (2009). Evidence-Based Dermatology. John Wiley & Sons. p. 128. ISBN 9781444300178.
- ^ De Benedetto, A; Agnihothri, R; McGirt, LY; Bankova, LG; Beck, LA (2009). "Atopic dermatitis: a disease caused by innate immune defects?". The Journal of investigative dermatology 129 (1): 14–30. doi:10.1038/jid.2008.259. PMID 19078985.
- ^ Abels, C; Proksch, E (2006). "Therapy of atopic dermatitis". Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete 57 (8): 711–725. doi:10.1007/s00105-006-1176-x. PMID 16816954.
- ^ A.D.A.M. Editorial Board (2012-11-20). "Atopic dermatitis". PubMed Health. Retrieved 14 March 2013
- ^ a b "Atopic dermatitis (eczema)". Archived from the original on 3 June 2010. Retrieved June 16, 2010.
- ^ a b "Atopic Dermatitis – Symptoms, Diagnosis". Archived from the original on 19 June 2010. Retrieved June 16, 2010.
- ^ "Factors that worsen atopic dermatitis". Archived from the original on 3 June 2010. Retrieved June 16, 2010.
- ^ "Infantile eczema". Archived from the original on 3 June 2010. Retrieved June 16, 2010.
- ^ "Dermatitis Atopic Eczema". Archived from the original on 7 June 2010. Retrieved June 16, 2010.
- ^ "Signs and Symptoms". Archived from the original on 19 June 2010. Retrieved June 16, 2010.
- ^ Article at the Mayo Clinic
- ^ Article at the New Zealand Dermatological Society
- ^ Palmer, C.N., Irvine, A.D., Terron-Kwiatkowski, A. et al. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat. Genet. 2006 Apr. 38(4): 441-6. PMID 16550169
- ^ Pelucchi, C.; Galeone, C.; Bach, JF.; La Vecchia, C.; Chatenoud, L. (Sep 2013). "Pet exposure and risk of atopic dermatitis at the pediatric age: a meta-analysis of birth cohort studies.". J Allergy Clin Immunol 132 (3): 616–622.e7. doi:10.1016/j.jaci.2013.04.009. PMID 23711545.
- ^ a b atopic dermatitis. pp. 52–56. doi:10.2340/00015555-0565. [dead link]
- ^ Jasek, W, ed. (2007). Austria-Codex (in German) (62 ed.). Vienna. pp. 2720, 6770. ISBN 978-3-85200-181-4. "Elidel Creme; Protopic Salbe"
- ^ Wooltorton, E. (2005). "Eczema drugs tacrolimus (Protopic) and pimecrolimus (Elidel): cancer concerns". Canadian Medical Association Journal 172 (9): 1179–1180. doi:10.1503/cmaj.050373. PMC 557066. PMID 15817641.
- ^ Food and Drug Administration (United States) (2005-03-10). "Safety information on Protopic (tacrolimus), Elidel (pimecrolimus)". Archived from the original on 4 November 2009. Retrieved 2009-10-21.
- ^ Bae, JM; Choi, YY; Park, CO; Chung, KY; Lee, KH (2013 Jul). "Efficacy of allergen-specific immunotherapy for atopic dermatitis: a systematic review and meta-analysis of randomized controlled trials.". The Journal of allergy and clinical immunology 132 (1): 110–7. PMID 23647790.
- ^ Varothai, S (2013). "Moisturizers for patients with atopic dermatitis.". Asian Pac J Allergy Immunol. PMID 23859407.
- ^ 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 JG, Guttman-Yassky E. Reversal of atopic dermatitis with narrow-band UVB phototherapy and biomarkers for therapeutic response. J Allergy Clin Immunol. 2011 Sep;128(3):583-93.e1-4. Epub 2011 Jul 16. PMID 21762976 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/pubmed/21762976
- ^ 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.
- ^ Meduri, N. Bhavani; Vandergriff, Travis; Rasmussen, Heather; Jacobe, Heidi (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.
- ^ Jans, J.; Garinis, G. A.; Schul, W.; Van Oudenaren, A.; Moorhouse, M.; Smid, M.; Sert, Y.-G.; Van Der Velde, A.; Rijksen, Y. et al. (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.
- ^ 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.
- ^ "Eczema". Retrieved June 16, 2010.
- ^ "How common is atopic dermatitis?". Archived from the original on 22 June 2010. Retrieved June 16, 2010.
External links[edit]
- NIH Handout on Health: Atopic Dermatitis
|
Health science – Medicine – Allergic conditions
|
|
| Respiratory system |
- Allergic rhinitis
- Asthma
- Hypersensitivity pneumonitis
- Eosinophilic pneumonia
- Churg-Strauss syndrome
- Allergic bronchopulmonary aspergillosis
- Farmer's lung
- Laboratory animal allergy
|
|
| Skin |
- Angioedema
- Urticaria
- Atopic dermatitis
- Allergic contact dermatitis
- Hypersensitivity vasculitis
|
|
| Blood and immune system |
|
|
| Circulatory system |
|
|
| Digestive system |
- Coeliac disease
- Eosinophilic gastroenteritis
- Eosinophilic esophagitis
- Food allergy
- Milk intolerance
|
|
| Nervous system |
|
|
| Genitourinary system |
- Acute interstitial nephritis
|
|
| Other conditions |
- Drug allergy
- Allergic conjunctivitis
- Latex allergy
|
|
|
|
cell/phys/auag/auab/comp, igrc
|
|
|
|
|
|
|
Dermatitis and eczema (L20–L30, 690–693,698)
|
|
| Atopic dermatitis |
|
|
| Seborrheic dermatitis |
- Pityriasis simplex capillitii
- Cradle cap
|
|
Contact dermatitis
(allergic, irritant) |
- plants: Urushiol-induced contact dermatitis
- African blackwood dermatitis
- Tulip fingers
- other: Abietic acid dermatitis
- Diaper rash
- Airbag dermatitis
- Baboon syndrome
- Contact stomatitis
- Protein contact dermatitis
|
|
| Eczema |
- Autoimmune estrogen dermatitis
- Autoimmune progesterone dermatitis
- Breast eczema
- Ear eczema
- Eyelid dermatitis
- Hand eczema
- Chronic vesiculobullous hand eczema
- Hyperkeratotic hand dermatitis
- Autosensitization dermatitis/Id reaction
- Candidid
- Dermatophytid
- Molluscum dermatitis
- Circumostomy eczema
- Dyshidrosis
- Juvenile plantar dermatosis
- Nummular eczema
- Nutritional deficiency eczema
- Sulzberger–Garbe syndrome
- Xerotic eczema
|
|
Pruritus/Itch/
Prurigo |
- Lichen simplex chronicus/Prurigo nodularis
- by location: Pruritus ani
- Pruritus scroti
- Pruritus vulvae
- Scalp pruritus
- Drug-induced pruritus
- Hydroxyethyl starch-induced pruritus
- Senile pruritus
- Aquagenic pruritus
- Adult blaschkitis
- due to liver disease
- Biliary pruritus
- Cholestatic pruritus
- Prion pruritus
- Prurigo pigmentosa
- Prurigo simplex
- Puncta pruritica
- Uremic pruritus
|
|
| Other/ungrouped |
- substances taken internally: Bromoderma
- Fixed drug reaction
- Nummular dermatitis
- Pityriasis alba
- Papuloerythroderma of Ofuji
|
|
|
|
|
noco (i/b/d/q/u/r/p/m/k/v/f)/cong/tumr (n/e/d), sysi/epon
|
proc, drug (D2/3/4/5/8/11)
|
|
|
|
|
Immune disorders: hypersensitivity and autoimmune diseases (279.5–6)
|
|
Type I/allergy/atopy
(IgE) |
|
Foreign
|
Atopic dermatitis · Allergic urticaria · Hay fever · Allergic asthma · Anaphylaxis · Food allergy (Milk, Egg, Peanut, Tree nut, Seafood, Soy, Wheat), Penicillin allergy
|
|
|
Autoimmune
|
none
|
|
|
Type II/ADCC
(IgM, IgG) |
|
Foreign
|
Pernicious anemia · Hemolytic disease of the newborn
|
|
|
Autoimmune
|
|
Cytotoxic
|
Autoimmune hemolytic anemia · Idiopathic thrombocytopenic purpura · Bullous pemphigoid · Pemphigus vulgaris · Rheumatic fever · Goodpasture's syndrome
|
|
|
"Type 5"/receptor
|
Graves' disease · Myasthenia gravis
|
|
|
|
Type III
(Immune complex) |
|
Foreign
|
Henoch–Schönlein purpura · Hypersensitivity vasculitis · Reactive arthritis · Farmer's lung · Post-streptococcal glomerulonephritis · Serum sickness · Arthus reaction
|
|
|
Autoimmune
|
Systemic lupus erythematosus · Subacute bacterial endocarditis · Rheumatoid arthritis
|
|
|
Type IV/cell-mediated
(T-cells) |
|
Foreign
|
Allergic contact dermatitis · Mantoux test
|
|
|
Autoimmune
|
Diabetes mellitus type 1 · Hashimoto's thyroiditis · Guillain–Barré syndrome · Multiple sclerosis · Coeliac disease · Giant-cell arteritis
|
|
|
GVHD
|
Transfusion-associated graft versus host disease
|
|
|
Unknown/
multiple |
|
Foreign
|
Hypersensitivity pneumonitis (Allergic bronchopulmonary aspergillosis) · Transplant rejection · Latex allergy (I+IV)
|
|
|
Autoimmune
|
Sjögren's syndrome · Autoimmune hepatitis · Autoimmune polyendocrine syndrome (APS1, APS2) · Autoimmune adrenalitis · Systemic autoimmune disease
|
|
|
|
|
cell/phys/auag/auab/comp, igrc
|
|
|
|
|
|
