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Atopic eczema

MedGen UID:
41502
Concept ID:
C0011615
Disease or Syndrome
Synonyms: Atopic Dermatitis; Atopic Eczema; Atopic Neurodermatitis; Dermatitis, Atopic; Disseminated Neurodermatitis; Eczema, Atopic; Neurodermatitis, Atopic; Neurodermatitis, Disseminated
SNOMED CT: AD - Atopic dermatitis (24079001); Atopic neurodermatitis (200775004); Constitutional eczema (24079001); Atopic dermatitis (24079001); Atopic eczema (24079001); Allergic eczema (24079001); Allergic dermatitis (24079001); Disseminated neurodermatitis (24079001)
 
Related gene: FLG
 
HPO: HP:0001047
Monarch Initiative: MONDO:0004980
OMIM®: 603165
OMIM® Phenotypic series: PS603165

Definition

Atopic dermatitis (ATOD), also known as eczema, is a common chronic pruritic inflammatory skin disease with a strong genetic component. Onset typically occurs during the first 2 years of life (review by Soderhall et al., 2007). Genetic Heterogeneity of Atopic Dermatitis Many inflammatory diseases, such as atopic eczema, are genetically complex, with multiple alleles at several loci thought to be involved in their pathogenesis. Several susceptibility loci for atopic dermatitis have been identified: ATOD1 on chromosome 3q21, ATOD2 (605803) on chromosome 1q21, ATOD3 (605804) on chromosome 20p, ATOD4 (605805) on chromosome 17q25.3, ATOD5 (603165) on chromosome 13q12-q14, ATOD6 (605845) on chromosome 5q31-q33, ATOD7 (613064) on chromosome 11q13.5, ATOD8 (613518) on chromosome 4q22.1, and ATOD9 (613519) on chromosome 3p24. [from OMIM]

Conditions with this feature

Follicular atrophoderma and basal cell epitheliomata
MedGen UID:
87539
Concept ID:
C0346104
Neoplastic Process
Bazex-Dupre-Christol syndrome (BDCS) is an X-linked dominant disorder characterized by a triad of congenital hypotrichosis, follicular atrophoderma affecting the dorsa of the hands and feet, the face, and extensor surfaces of the elbows or knees, and the development of basal cell neoplasms, including basal cell nevi and basal cell carcinomas from the second decade onward (Yung and Newton-Bishop, 2005). Rombo syndrome (180730) has similar features, but shows autosomal dominant inheritance.
Deletion of long arm of chromosome 18
MedGen UID:
96605
Concept ID:
C0432443
Disease or Syndrome
Monosomy 18q is a partial deletion of the long arm of chromosome 18 characterized by highly variable phenotype, most commonly including hypotonia, developmental delay, short stature, growth hormone deficiency, hearing loss and external ear anomalies, intellectual disability, palatal defects, dysmorphic facial features, skeletal anomalies (foot deformities, tapering fingers, scoliosis) and mood disorders.
Floating-Harbor syndrome
MedGen UID:
152667
Concept ID:
C0729582
Disease or Syndrome
Floating-Harbor syndrome (FHS) is characterized by typical craniofacial features; low birth weight, normal head circumference, and short stature; bone age delay that normalizes between ages six and 12 years; skeletal anomalies (brachydactyly, clubbing, clinodactyly, short thumbs, prominent joints, clavicular abnormalities); severe receptive and expressive language impairment; hypernasality and high-pitched voice; and intellectual disability that is typically mild to moderate. Difficulties with temperament and behavior that are present in many children tend to improve in adulthood. Other features can include hyperopia and/or strabismus, conductive hearing loss, seizures, gastroesophageal reflux, renal anomalies (e.g., hydronephrosis / renal pelviectasis, cysts, and/or agenesis), and genital anomalies (e.g., hypospadias and/or undescended testes).
Cardio-facio-cutaneous syndrome
MedGen UID:
266149
Concept ID:
C1275081
Disease or Syndrome
Cardiofaciocutaneous (CFC) syndrome is characterized by cardiac abnormalities (pulmonic stenosis and other valve dysplasias, septal defects, hypertrophic cardiomyopathy, rhythm disturbances), distinctive craniofacial appearance, and cutaneous abnormalities (including xerosis, hyperkeratosis, ichthyosis, keratosis pilaris, ulerythema ophryogenes, eczema, pigmented moles, hemangiomas, and palmoplantar hyperkeratosis). The hair is typically sparse, curly, fine or thick, woolly or brittle; eyelashes and eyebrows may be absent or sparse. Nails may be dystrophic or fast growing. Some form of neurologic and/or cognitive delay (ranging from mild to severe) is seen in all affected individuals. Neoplasia, mostly acute lymphoblastic leukemia, has been reported in some individuals.
Intellectual disability-obesity-prognathism-eye and skin anomalies syndrome
MedGen UID:
376145
Concept ID:
C1847522
Disease or Syndrome
A rare genetic syndromic intellectual disability disorder with characteristics of mild to profound intellectual disability, delayed speech, obesity, ocular anomalies (blepharophimosis, blepharoptosis, hyperopic astigmatism, decreased visual acuity, strabismus, abducens nerve palsy, and/or accommodative esotropia), and dermal manifestations, such as chronic atopic dermatitis. Associated craniofacial dysmorphism includes macrocephaly, maxillary hypoplasia, mandibular prognathism and crowding of teeth.
Intellectual disability, microcephaly, growth retardation, joint contractures, and facial dysmorphism
MedGen UID:
342889
Concept ID:
C1853480
Disease or Syndrome
Dermatitis, atopic
MedGen UID:
350353
Concept ID:
C1864155
Disease or Syndrome
Cleft lip/palate-ectodermal dysplasia syndrome
MedGen UID:
444067
Concept ID:
C2931488
Disease or Syndrome
Zlotogora-Ogur syndrome is an ectodermal dysplasia syndrome with characteristics of hair, skin and teeth anomalies, facial dysmorphism with cleft lip and palate, cutaneous syndactyly and, in some cases, intellectual disability.The prevalence is unknown but to date, less than 50 cases have been described in the literature. Caused by mutations in the gene PVRL1 (11q23-q24) which encodes nectin-1, the principal receptor used by alpha-herpesviruses to mediate entry into human cells. Transmission is autosomal recessive.
Arthrogryposis, Perthes disease, and upward gaze palsy
MedGen UID:
481939
Concept ID:
C3280309
Disease or Syndrome
Aicardi-Goutieres syndrome 7
MedGen UID:
854829
Concept ID:
C3888244
Disease or Syndrome
Most characteristically, Aicardi-Goutières syndrome (AGS) manifests as an early-onset encephalopathy that usually, but not always, results in severe intellectual and physical disability. A subgroup of infants with AGS present at birth with abnormal neurologic findings, hepatosplenomegaly, elevated liver enzymes, and thrombocytopenia, a picture highly suggestive of congenital infection. Otherwise, most affected infants present at variable times after the first few weeks of life, frequently after a period of apparently normal development. Typically, they demonstrate the subacute onset of a severe encephalopathy characterized by extreme irritability, intermittent sterile pyrexias, loss of skills, and slowing of head growth. Over time, as many as 40% develop chilblain skin lesions on the fingers, toes, and ears. It is becoming apparent that atypical, sometimes milder, cases of AGS exist, and thus the true extent of the phenotype associated with pathogenic variants in the AGS-related genes is not yet known.
Even-plus syndrome
MedGen UID:
904613
Concept ID:
C4225180
Disease or Syndrome
EVEN-plus syndrome (EVPLS) is characterized by prenatal-onset short stature, vertebral and epiphyseal changes, microtia, midface hypoplasia with flat nose and triangular nares, cardiac malformations, and other findings including anal atresia, hypodontia, and aplasia cutis. The features overlap those reported in patients with CODAS syndrome (600373; Royer-Bertrand et al., 2015).
Immunodeficiency 11b with atopic dermatitis
MedGen UID:
1627819
Concept ID:
C4539957
Disease or Syndrome
IMD11B is an autosomal dominant disorder of immune dysfunction characterized by onset of moderate to severe atopic dermatitis in early childhood. Some patients may have recurrent infections and other variable immune abnormalities. Laboratory studies show defects in T-cell activation, increased IgE, and eosinophilia (summary by Ma et al., 2017).
Combined immunodeficiency due to DOCK8 deficiency
MedGen UID:
1648410
Concept ID:
C4722305
Disease or Syndrome
Hyper-IgE syndrome-2 with recurrent infections (HIES2) is an autosomal recessive immunologic disorder characterized by recurrent staphylococcal infections of the skin and respiratory tract, eczema, elevated serum immunoglobulin E, and hypereosinophilia. It is distinguished from autosomal dominant HIES1 (147060) by the lack of connective tissue and skeletal involvement (Renner et al., 2004). For a discussion of genetic heterogeneity of hyper-IgE syndrome, see 147060. See also TYK2 deficiency (611521), a clinically distinct disease entity that includes characteristic features of both autosomal recessive HIES2 and mendelian susceptibility to mycobacterial disease (MSMD; 209950) (Minegishi et al., 2006).
Peeling skin syndrome 6
MedGen UID:
1648406
Concept ID:
C4748093
Disease or Syndrome
Peeling skin syndrome-6 (PSS6) is characterized by generalized ichthyotic dry skin and bullous peeling lesions on the trunk and limbs at sites of minor trauma. There is residual hyperpigmentation in areas of healing, but no scarring. Skin symptoms are exacerbated by warmth and humidity; however, the disorder improves markedly with age (Bolling et al., 2018; Mohamad et al., 2018). For a discussion of genetic heterogeneity of peeling skin syndrome, see PSS1 (270300).
Hyper-IgE recurrent infection syndrome 3, autosomal recessive
MedGen UID:
1648483
Concept ID:
C4748969
Disease or Syndrome
Hyper-IgE syndrome-3 with recurrent infections (HIES3) is an autosomal recessive immunologic disorder characterized by childhood onset of atopic dermatitis, skin infections particularly with Staphylococcus aureus, recurrent sinopulmonary infections, and increased serum IgE and IgG. Patients are susceptible to bacterial and fungal infections, including chronic mucocutaneous candidiasis. Immunologic workup shows impaired differentiation of CD4+ T cells into T-helper 17 cells, decreased memory B cells, and often decreased NK cells (summary by Beziat et al., 2018). For a discussion of genetic heterogeneity of hyper-IgE syndrome, see HIES1 (147060).
Noonan syndrome 12
MedGen UID:
1684730
Concept ID:
C5231432
Disease or Syndrome
Noonan syndrome (NS) is characterized by characteristic facies, short stature, congenital heart defect, and developmental delay of variable degree. Other findings can include broad or webbed neck, unusual chest shape with superior pectus carinatum and inferior pectus excavatum, cryptorchidism, varied coagulation defects, lymphatic dysplasias, and ocular abnormalities. Although birth length is usually normal, final adult height approaches the lower limit of normal. Congenital heart disease occurs in 50%-80% of individuals. Pulmonary valve stenosis, often with dysplasia, is the most common heart defect and is found in 20%-50% of individuals. Hypertrophic cardiomyopathy, found in 20%-30% of individuals, may be present at birth or develop in infancy or childhood. Other structural defects include atrial and ventricular septal defects, branch pulmonary artery stenosis, and tetralogy of Fallot. Up to one fourth of affected individuals have mild intellectual disability, and language impairments in general are more common in NS than in the general population.
T-cell lymphopenia, infantile, with or without nail dystrophy, autosomal dominant
MedGen UID:
1712366
Concept ID:
C5394133
Disease or Syndrome
Infantile T-cell lymphopenia with or without nail dystrophy (TLIND) is an autosomal dominant disorder characterized by decreased numbers of T cells, particularly cytotoxic CD8+ T cells, usually apparent from infancy. Patients are often identified through newborn screening with the finding of low levels of T-cell receptor excision circles (TRECs). Affected individuals tend to be more susceptible to recurrent infections, mainly respiratory viral infections. However, the severity is highly variable, and patients usually improve with age later in childhood and as adults, even if CD8+ T cells remain decreased compared to normal. Additional features may include a small thymic shadow, indicative of impaired thymic development, skin abnormalities, such as atopic dermatitis, and nail dystrophy. As rare patients may develop more serious infections, affected individuals should be monitored. Bone marrow transplantation is not curative (summary by Bosticardo et al., 2019).
Hyper-IgE recurrent infection syndrome 5, autosomal recessive
MedGen UID:
1716052
Concept ID:
C5394550
Disease or Syndrome
Hyper-IgE syndrome-5 with recurrent infections (HEIS5) is an autosomal recessive immunologic disorder characterized by onset of recurrent sinopulmonary and deep skin infections in early childhood. The infections are mostly caused by bacteria, including H. influenza and Staphylococcus aureus. Additional features include atopic dermatitis, impaired inflammatory responses during infection, increased serum IgE, and increased IL6 (147620) (summary by Spencer et al., 2019). For a discussion of genetic heterogeneity of hyper-IgE syndrome, see HIES1 (147060).
Autoinflammation, immune dysregulation, and eosinophilia
MedGen UID:
1750270
Concept ID:
C5436572
Disease or Syndrome
Autoinflammation, immune dysregulation, and eosinophilia (AIIDE) is an autosomal dominant disorder characterized by onset of severe atopic dermatitis and chronic gastrointestinal inflammation, mainly involving the colon, in infancy or early childhood. Affected individuals tend to have asthma and food or environmental allergies, as well as poor overall growth with short stature. Severe liver involvement has also been reported (Takeichi et al., 2021). Laboratory studies show increased eosinophils with normal or increased IgE levels, as well as evidence of a hyperactive immune state, including increased erythrocyte sedimentation rate and C-reactive protein. Treatment with JAK inhibitors, such as ruxolitinib and tofacitinib, results in dramatic clinical improvement (summary by Gruber et al., 2020).
Cleft palate, proliferative retinopathy, and developmental delay
MedGen UID:
1765503
Concept ID:
C5436739
Disease or Syndrome
Cleft palate, proliferative retinopathy, and developmental delay (CPPRDD) is characterized by motor and speech delay, with intellectual disability ranging from mild to severe. Brain imaging shows ventriculomegaly as well as other malformations (Harel et al., 2019).
VISS syndrome
MedGen UID:
1794165
Concept ID:
C5561955
Disease or Syndrome
VISS syndrome is a generalized connective tissue disorder characterized by early-onset thoracic aortic aneurysm and other connective tissue findings, such as aneurysm and tortuosity of other arteries, joint hypermobility, skin laxity, and hernias, as well as craniofacial dysmorphic features, structural cardiac defects, skeletal anomalies, and motor developmental delay (Van Gucht et al., 2021). Immune dysregulation has been observed in some patients (Ziegler et al., 2021).
Neurodevelopmental disorder with hypotonia and dysmorphic facies
MedGen UID:
1794184
Concept ID:
C5561974
Disease or Syndrome
Neurodevelopmental disorder with hypotonia and dysmorphic facies (NEDHYDF) is characterized by global developmental delay and hypotonia apparent from birth. Affected individuals have variably impaired intellectual development, often with speech delay and delayed walking. Seizures are generally not observed, although some patients may have single seizures or late-onset epilepsy. Most patients have prominent dysmorphic facial features. Additional features may include congenital cardiac defects (without arrhythmia), nonspecific renal anomalies, joint contractures or joint hyperextensibility, dry skin, and cryptorchidism. There is significant phenotypic variability in both the neurologic and extraneurologic manifestations (summary by Tan et al., 2022).
Intellectual disability and myopathy syndrome
MedGen UID:
1808193
Concept ID:
C5676904
Disease or Syndrome
Intellectual disability and myopathy syndrome (IDMYS) is an autosomal recessive developmental disorder characterized by global developmental delay with mildly impaired intellectual development, hypotonia, muscle weakness and fatigue, and white matter abnormalities on brain imaging. Variable additional features may include sensorineural hearing loss, dysmorphic facies, and progressive heart disease (summary by Smeland et al., 2019).
Hyper-IgE recurrent infection syndrome 4A, autosomal dominant
MedGen UID:
1809613
Concept ID:
C5676920
Disease or Syndrome
Hyper-IgE syndrome-4A with recurrent infections (HIES4A) is an autosomal dominant immunologic disorder characterized by recurrent, mainly sinopulmonary infections associated with increased serum IgE. The phenotype is variable, even within families. Some patients have onset of symptoms in early childhood and develop complications, including bronchiectasis or hemoptysis, whereas others have later onset of less severe infections. Immunologic workup usually shows normal leukocyte levels, although some patients may demonstrate alterations in lymphocyte subsets, including T cells. Affected individuals also have variable skeletal abnormalities, including high-arched palate, hyperextensible joints, scoliosis, and bone fractures. The IL6ST mutations are loss-of-function, although the truncated mutant proteins are expressed and interfere with the wildtype protein in a dominant-negative manner by disrupting IL6 (147620) and IL11 (147681) signaling (summary by Beziat et al., 2020). For a discussion of genetic heterogeneity of hyper-IgE syndrome, see HIES1 (147060).
Hatipoglu immunodeficiency syndrome
MedGen UID:
1841075
Concept ID:
C5830439
Disease or Syndrome
Hatipoglu immunodeficiency syndrome (HATIS) is an autosomal recessive immunologic disorder characterized by childhood onset of failure to thrive, skin manifestations, pancytopenia, and susceptibility to recurrent infections (Harapas et al., 2022).
Autoinflammatory disease, systemic, with vasculitis
MedGen UID:
1841161
Concept ID:
C5830525
Disease or Syndrome
Systemic autoinflammatory disease with vasculitis (SAIDV) is an autosomal dominant disorder that manifests soon after birth with features such as purpuric skin rash, fever, hepatosplenomegaly, and elevated C-reactive protein (CRP; 123260). Laboratory studies may show leukocytosis, thrombocytopenia, and autoantibodies. A subset of patients develop progressive liver involvement that may result in fibrosis. Other systemic features, such as periorbital edema, conjunctivitis, infections, abdominal pain, and arthralgia are usually observed. Mutations occur de novo. De Jesus et al. (2023) referred to this disorder as LAVLI (LYN kinase-associated vasculopathy and liver fibrosis).

Professional guidelines

PubMed

Wollenberg A, Kinberger M, Arents B, Aszodi N, Avila Valle G, Barbarot S, Bieber T, Brough HA, Calzavara Pinton P, Christen-Zäch S, Deleuran M, Dittmann M, Dressler C, Fink-Wagner AH, Fosse N, Gáspár K, Gerbens L, Gieler U, Girolomoni G, Gregoriou S, Mortz CG, Nast A, Nygaard U, Redding M, Rehbinder EM, Ring J, Rossi M, Serra-Baldrich E, Simon D, Szalai ZZ, Szepietowski JC, Torrelo A, Werfel T, Flohr C
J Eur Acad Dermatol Venereol 2022 Nov;36(11):1904-1926. Epub 2022 Sep 3 doi: 10.1111/jdv.18429. PMID: 36056736
Wollenberg A, Kinberger M, Arents B, Aszodi N, Avila Valle G, Barbarot S, Bieber T, Brough HA, Calzavara Pinton P, Christen-Zäch S, Deleuran M, Dittmann M, Dressler C, Fink-Wagner AH, Fosse N, Gáspár K, Gerbens L, Gieler U, Girolomoni G, Gregoriou S, Mortz CG, Nast A, Nygaard U, Redding M, Rehbinder EM, Ring J, Rossi M, Serra-Baldrich E, Simon D, Szalai ZZ, Szepietowski JC, Torrelo A, Werfel T, Flohr C
J Eur Acad Dermatol Venereol 2022 Sep;36(9):1409-1431. doi: 10.1111/jdv.18345. PMID: 35980214
Frazier W, Bhardwaj N
Am Fam Physician 2020 May 15;101(10):590-598. PMID: 32412211

Curated

UK NICE Clinical Guideline CG57, Atopic eczema in under 12s: diagnosis and management, 2023

UK NICE Guideline NG190, Secondary bacterial infection of eczema and other common skin conditions: antimicrobial prescribing, 2021

Recent clinical studies

Etiology

Lau HX, Lee JW, Yap QV, Chan YH, Samuel M, Loo EXL
Pediatr Allergy Immunol 2023 Aug;34(8):e14010. doi: 10.1111/pai.14010. PMID: 37622263
El-Heis S, D'Angelo S, Curtis EM, Healy E, Moon RJ, Crozier SR, Inskip H, Cooper C, Harvey NC, Godfrey KM; MAVIDOS Trial Group
Br J Dermatol 2022 Nov;187(5):659-666. Epub 2022 Aug 3 doi: 10.1111/bjd.21721. PMID: 35763390Free PMC Article
Ascott A, Mansfield KE, Schonmann Y, Mulick A, Abuabara K, Roberts A, Smeeth L, Langan SM
Br J Dermatol 2021 May;184(5):871-879. Epub 2020 Dec 1 doi: 10.1111/bjd.19597. PMID: 33090454
Ingram JR
BMJ 2018 May 23;361:k2064. doi: 10.1136/bmj.k2064. PMID: 29794003
Hoare C, Li Wan Po A, Williams H
Health Technol Assess 2000;4(37):1-191. PMID: 11134919Free PMC Article

Diagnosis

Williams HC, Chalmers J
Acta Derm Venereol 2020 Jun 9;100(12):adv00166. doi: 10.2340/00015555-3516. PMID: 32419030Free PMC Article
Elsner P, Agner T
J Eur Acad Dermatol Venereol 2020 Jan;34 Suppl 1:13-21. doi: 10.1111/jdv.16062. PMID: 31860736
Roenneberg S, Biedermann T
J Eur Acad Dermatol Venereol 2018 Jun;32(6):889-898. Epub 2018 Jan 17 doi: 10.1111/jdv.14761. PMID: 29247481
Avena-Woods C
Am J Manag Care 2017 Jun;23(8 Suppl):S115-S123. PMID: 28978208
Hoare C, Li Wan Po A, Williams H
Health Technol Assess 2000;4(37):1-191. PMID: 11134919Free PMC Article

Therapy

Flohr C, Rosala-Hallas A, Jones AP, Beattie P, Baron S, Browne F, Brown SJ, Gach JE, Greenblatt D, Hearn R, Hilger E, Esdaile B, Cork MJ, Howard E, Lovgren ML, August S, Ashoor F, Williamson PR, McPherson T, O'Kane D, Ravenscroft J, Shaw L, Sinha MD, Spowart C, Taams LS, Thomas BR, Wan M, Sach TH, Irvine AD; TREAT Trial Investigators
Br J Dermatol 2023 Nov 16;189(6):674-684. doi: 10.1093/bjd/ljad281. PMID: 37722926
El-Heis S, D'Angelo S, Curtis EM, Healy E, Moon RJ, Crozier SR, Inskip H, Cooper C, Harvey NC, Godfrey KM; MAVIDOS Trial Group
Br J Dermatol 2022 Nov;187(5):659-666. Epub 2022 Aug 3 doi: 10.1111/bjd.21721. PMID: 35763390Free PMC Article
Williams HC, Chalmers J
Acta Derm Venereol 2020 Jun 9;100(12):adv00166. doi: 10.2340/00015555-3516. PMID: 32419030Free PMC Article
Cury Martins J, Martins C, Aoki V, Gois AF, Ishii HA, da Silva EM
Cochrane Database Syst Rev 2015 Jul 1;2015(7):CD009864. doi: 10.1002/14651858.CD009864.pub2. PMID: 26132597Free PMC Article
Hoare C, Li Wan Po A, Williams H
Health Technol Assess 2000;4(37):1-191. PMID: 11134919Free PMC Article

Prognosis

Williams HC, Chalmers J
Acta Derm Venereol 2020 Jun 9;100(12):adv00166. doi: 10.2340/00015555-3516. PMID: 32419030Free PMC Article
Roenneberg S, Biedermann T
J Eur Acad Dermatol Venereol 2018 Jun;32(6):889-898. Epub 2018 Jan 17 doi: 10.1111/jdv.14761. PMID: 29247481
Rożalski M, Rudnicka L, Samochocki Z
Acta Dermatovenerol Croat 2016 Jun;24(2):110-5. PMID: 27477170
Brown SJ
Clin Med (Lond) 2016 Feb;16(1):66-9. doi: 10.7861/clinmedicine.16-1-66. PMID: 26833520Free PMC Article
Cury Martins J, Martins C, Aoki V, Gois AF, Ishii HA, da Silva EM
Cochrane Database Syst Rev 2015 Jul 1;2015(7):CD009864. doi: 10.1002/14651858.CD009864.pub2. PMID: 26132597Free PMC Article

Clinical prediction guides

Wang Q, Liu L, Gao S, Su S
Int Arch Allergy Immunol 2023;184(2):132-141. Epub 2022 Nov 2 doi: 10.1159/000527007. PMID: 36323240
El-Heis S, D'Angelo S, Curtis EM, Healy E, Moon RJ, Crozier SR, Inskip H, Cooper C, Harvey NC, Godfrey KM; MAVIDOS Trial Group
Br J Dermatol 2022 Nov;187(5):659-666. Epub 2022 Aug 3 doi: 10.1111/bjd.21721. PMID: 35763390Free PMC Article
Simpson E, Bissonnette R, Eichenfield LF, Guttman-Yassky E, King B, Silverberg JI, Beck LA, Bieber T, Reich K, Kabashima K, Seyger M, Siegfried E, Stingl G, Feldman SR, Menter A, van de Kerkhof P, Yosipovitch G, Paul C, Martel P, Dubost-Brama A, Armstrong J, Chavda R, Frey S, Joubert Y, Milutinovic M, Parneix A, Teixeira HD, Lin CY, Sun L, Klekotka P, Nickoloff B, Dutronc Y, Mallbris L, Janes JM, DeLozier AM, Nunes FP, Paller AS
J Am Acad Dermatol 2020 Sep;83(3):839-846. Epub 2020 Apr 25 doi: 10.1016/j.jaad.2020.04.104. PMID: 32344071
Hoare C, Li Wan Po A, Williams H
Health Technol Assess 2000;4(37):1-191. PMID: 11134919Free PMC Article
Finlay AY, Khan GK
Clin Exp Dermatol 1994 May;19(3):210-6. doi: 10.1111/j.1365-2230.1994.tb01167.x. PMID: 8033378

Recent systematic reviews

Yepes-Nuñez JJ, Guyatt GH, Gómez-Escobar LG, Pérez-Herrera LC, Chu AWL, Ceccaci R, Acosta-Madiedo AS, Wen A, Moreno-López S, MacDonald M, Barrios M, Chu X, Islam N, Gao Y, Wong MM, Couban R, Garcia E, Chapman E, Oykhman P, Chen L, Winders T, Asiniwasis RN, Boguniewicz M, De Benedetto A, Ellison K, Frazier WT, Greenhawt M, Huynh J, Kim E, LeBovidge J, Lind ML, Lio P, Martin SA, O'Brien M, Ong PY, Silverberg JI, Spergel J, Wang J, Wheeler KE, Schneider L, Chu DK
J Allergy Clin Immunol 2023 Jan;151(1):147-158. Epub 2022 Sep 30 doi: 10.1016/j.jaci.2022.09.020. PMID: 36191689
Drucker AM, Morra DE, Prieto-Merino D, Ellis AG, Yiu ZZN, Rochwerg B, Di Giorgio S, Arents BWM, Burton T, Spuls PI, Schmitt J, Flohr C
JAMA Dermatol 2022 May 1;158(5):523-532. doi: 10.1001/jamadermatol.2022.0455. PMID: 35293977Free PMC Article
Musters AH, Mashayekhi S, Harvey J, Axon E, Lax SJ, Flohr C, Drucker AM, Gerbens L, Ferguson J, Ibbotson S, Dawe RS, Garritsen F, Brouwer M, Limpens J, Prescott LE, Boyle RJ, Spuls PI
Cochrane Database Syst Rev 2021 Oct 28;10(10):CD013870. doi: 10.1002/14651858.CD013870.pub2. PMID: 34709669Free PMC Article
Kramer MS, Kakuma R
Cochrane Database Syst Rev 2012 Aug 15;2012(8):CD003517. doi: 10.1002/14651858.CD003517.pub2. PMID: 22895934Free PMC Article
Hoare C, Li Wan Po A, Williams H
Health Technol Assess 2000;4(37):1-191. PMID: 11134919Free PMC Article

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    Curated

    • NICE, 2023
      UK NICE Clinical Guideline CG57, Atopic eczema in under 12s: diagnosis and management, 2023
    • NICE, 2021
      UK NICE Guideline NG190, Secondary bacterial infection of eczema and other common skin conditions: antimicrobial prescribing, 2021

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