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Eczema

MedGen UID:
3968
Concept ID:
C0013595
Disease or Syndrome
Synonym: Eczematous rash
SNOMED CT: Eczema (43116000)
 
HPO: HP:0000964

Definition

Eczema is a form of dermatitis that is characterized by scaly, pruritic, erythematous lesions located on flexural surfaces. [from HPO]

Conditions with this feature

Extramammary Paget disease
MedGen UID:
45280
Concept ID:
C0030186
Neoplastic Process
A rare skin tumor characterized by predominantly intraepithelial growth of an adenocarcinoma which may either arise primarily in the skin (primary extramammary Paget disease) or result from intraepithelial spread of a visceral carcinoma (secondary extramammary Paget disease). The lesion is typically located in the anogenital region, presenting as a scaly, oozing, pruritic or painful erythematous plaque often resembling eczema. It may exhibit an invasive component with a significant risk of lymph node metastasis.
Ichthyosis vulgaris
MedGen UID:
38217
Concept ID:
C0079584
Disease or Syndrome
The phenotypic characteristics of ichthyosis vulgaris include palmar hyperlinearity, keratosis pilaris, and a fine scale that is most prominent over the lower abdomen, arms, and legs. Marked presentation includes prominent scaling, whereas mild presentation consists of palmar hyperlinearity, keratosis pilaris, and, in some cases, fine scaling (summary by Smith et al., 2006).
T-lymphocyte deficiency
MedGen UID:
101814
Concept ID:
C0152094
Disease or Syndrome
T-cell immunodeficiency with thymic aplasia (TIDTA) is an autosomal recessive disorder that is often detected at birth through newborn SCID screening with the finding of decreased T-cell receptor excision circles (TRECs). Affected individuals have selective hypo- or aplasia of the thymus, which results in T-cell immunodeficiency due to impaired T-cell development and increased susceptibility to viral infections. The phenotype is similar to T-/B+/NK+ SCID. Some patients may die in childhood; thymus transplantation may be curative (summary by Du et al., 2019).
Granulomatous disease, chronic, X-linked
MedGen UID:
336165
Concept ID:
C1844376
Disease or Syndrome
Chronic granulomatous disease (CGD) is a primary immunodeficiency disorder of phagocytes (neutrophils, monocytes, macrophages, and eosinophils) resulting from impaired killing of bacteria and fungi. CGD is characterized by severe recurrent bacterial and fungal infections and dysregulated inflammatory responses resulting in granuloma formation and other inflammatory disorders such as colitis. Infections typically involve the lung (pneumonia), lymph nodes (lymphadenitis), liver (abscess), bone (osteomyelitis), and skin (abscesses or cellulitis). Granulomas typically involve the genitourinary system (bladder) and gastrointestinal tract (often the pylorus initially, and later the esophagus, jejunum, ileum, cecum, rectum, and perirectal area). Some males with X-linked CGD have McLeod neuroacanthocytosis syndrome as the result of a contiguous gene deletion. While CGD may present anytime from infancy to late adulthood, the vast majority of affected individuals are diagnosed before age five years. Use of antimicrobial prophylaxis and therapy has greatly improved overall survival.
Granulomatous disease, chronic, autosomal recessive, cytochrome b-positive, type 2
MedGen UID:
383869
Concept ID:
C1856245
Disease or Syndrome
Chronic granulomatous disease (CGD) is a primary immunodeficiency disorder of phagocytes (neutrophils, monocytes, macrophages, and eosinophils) resulting from impaired killing of bacteria and fungi. CGD is characterized by severe recurrent bacterial and fungal infections and dysregulated inflammatory responses resulting in granuloma formation and other inflammatory disorders such as colitis. Infections typically involve the lung (pneumonia), lymph nodes (lymphadenitis), liver (abscess), bone (osteomyelitis), and skin (abscesses or cellulitis). Granulomas typically involve the genitourinary system (bladder) and gastrointestinal tract (often the pylorus initially, and later the esophagus, jejunum, ileum, cecum, rectum, and perirectal area). Some males with X-linked CGD have McLeod neuroacanthocytosis syndrome as the result of a contiguous gene deletion. While CGD may present anytime from infancy to late adulthood, the vast majority of affected individuals are diagnosed before age five years. Use of antimicrobial prophylaxis and therapy has greatly improved overall survival.
Granulomatous disease, chronic, autosomal recessive, cytochrome b-positive, type 1
MedGen UID:
341102
Concept ID:
C1856251
Disease or Syndrome
Chronic granulomatous disease (CGD) is a primary immunodeficiency disorder of phagocytes (neutrophils, monocytes, macrophages, and eosinophils) resulting from impaired killing of bacteria and fungi. CGD is characterized by severe recurrent bacterial and fungal infections and dysregulated inflammatory responses resulting in granuloma formation and other inflammatory disorders such as colitis. Infections typically involve the lung (pneumonia), lymph nodes (lymphadenitis), liver (abscess), bone (osteomyelitis), and skin (abscesses or cellulitis). Granulomas typically involve the genitourinary system (bladder) and gastrointestinal tract (often the pylorus initially, and later the esophagus, jejunum, ileum, cecum, rectum, and perirectal area). Some males with X-linked CGD have McLeod neuroacanthocytosis syndrome as the result of a contiguous gene deletion. While CGD may present anytime from infancy to late adulthood, the vast majority of affected individuals are diagnosed before age five years. Use of antimicrobial prophylaxis and therapy has greatly improved overall survival.
Granulomatous disease, chronic, autosomal recessive, cytochrome b-negative
MedGen UID:
383872
Concept ID:
C1856255
Disease or Syndrome
Chronic granulomatous disease (CGD) is a primary immunodeficiency disorder of phagocytes (neutrophils, monocytes, macrophages, and eosinophils) resulting from impaired killing of bacteria and fungi. CGD is characterized by severe recurrent bacterial and fungal infections and dysregulated inflammatory responses resulting in granuloma formation and other inflammatory disorders such as colitis. Infections typically involve the lung (pneumonia), lymph nodes (lymphadenitis), liver (abscess), bone (osteomyelitis), and skin (abscesses or cellulitis). Granulomas typically involve the genitourinary system (bladder) and gastrointestinal tract (often the pylorus initially, and later the esophagus, jejunum, ileum, cecum, rectum, and perirectal area). Some males with X-linked CGD have McLeod neuroacanthocytosis syndrome as the result of a contiguous gene deletion. While CGD may present anytime from infancy to late adulthood, the vast majority of affected individuals are diagnosed before age five years. Use of antimicrobial prophylaxis and therapy has greatly improved overall survival.
Hypertrophic osteoarthropathy, primary, autosomal recessive, 1
MedGen UID:
1641972
Concept ID:
C4551679
Disease or Syndrome
Autosomal recessive primary hypertrophic osteoarthropathy-1 (PHOAR1) is a rare familial disorder characterized by digital clubbing, osteoarthropathy, and acroosteolysis, with variable features of pachydermia, delayed closure of the fontanels, and congenital heart disease (summary by Uppal et al., 2008; Radhakrishnan et al., 2020). Secondary hypertrophic osteoarthropathy, or pulmonary hypertrophic osteoarthropathy, is a different disorder characterized by digital clubbing secondary to acquired diseases, most commonly intrathoracic neoplasm (Uppal et al., 2008). Touraine et al. (1935) recognized pachydermoperiostosis as a familial disorder with 3 clinical presentations or forms: a complete form characterized by periostosis and pachydermia; an incomplete form with bone changes but without pachydermia; and a 'forme fruste' with pachydermia and minimal skeletal changes. Genetic Heterogeneity Autosomal recessive primary hypertrophic osteoarthropathy-2-enteropathy syndrome (PHOAR2E; 614441) is caused by mutation in the SLCO2A1 gene (601460) on chromosome 3q22. Families with an autosomal dominant form of primary hypertrophic osteoarthropathy have also been reported (PHOAD; 167100).
Hyper-IgE recurrent infection syndrome 1, autosomal dominant
MedGen UID:
1648470
Concept ID:
C4721531
Disease or Syndrome
STAT3 hyper IgE syndrome (STAT3-HIES) is a primary immune deficiency syndrome characterized by elevated serum IgE, eczema, and recurrent skin and respiratory tract infections, together with several nonimmune features. This disorder typically manifests in the newborn period with a rash (often diagnosed as eosinophilic pustulosis) that subsequently evolves into an eczematoid dermatitis. Recurrent staphylococcal skin boils and bacterial pneumonias usually manifest in the first years of life. Pneumatoceles and bronchiectasis often result from aberrant healing of pneumonias. Mucocutaneous candidiasis is common. Nonimmune features may include retained primary teeth, scoliosis, bone fractures following minimal trauma, joint hyperextensibility, and characteristic facial appearance, which typically emerges in adolescence. Vascular abnormalities have been described and include middle-sized artery tortuosity and aneurysms, with infrequent clinical sequelae of myocardial infarction and subarachnoid hemorrhage. Gastrointestinal (GI) manifestations include gastroesophageal reflux disease, esophageal dysmotility, and spontaneous intestinal perforations (some of which are associated with diverticuli). Fungal infections of the GI tract (typically histoplasmosis, Cryptococcus, and Coccidioides) also occur infrequently. Survival is typically into adulthood, with most individuals now living into or past the sixth decade. Most deaths are associated with gram-negative (Pseudomonas) or filamentous fungal pneumonias resulting in hemoptysis. Lymphomas occur at an increased frequency.
Agammaglobulinemia 9, autosomal recessive
MedGen UID:
1794269
Concept ID:
C5562059
Disease or Syndrome
Agammaglobulinemia-9 (AGM9) is an autosomal recessive primary immunodeficiency characterized by recurrent bacterial infections associated with agammaglobulinemia and absence of circulating B cells. Additional features include failure to thrive and skin involvement. The severity is variable: more severe cases may require hematopoietic stem cell transplantation, whereas others can be treated effectively with Ig replacement therapy (summary by Anzilotti et al., 2019). For a discussion of genetic heterogeneity of autosomal agammaglobulinemia, see AGM1 (601495).
Combined immunodeficiency due to ZAP70 deficiency
MedGen UID:
1809040
Concept ID:
C5575025
Disease or Syndrome
ZAP70-related combined immunodeficiency (ZAP70-related CID) is a cell-mediated immunodeficiency caused by abnormal T-cell receptor (TCR) signaling. Affected children usually present in the first year of life with recurrent bacterial, viral, and opportunistic infections, diarrhea, and failure to thrive. Severe lower-respiratory infections and oral candidiasis are common. Affected children usually do not survive past their second year without hematopoietic stem cell transplantation (HSCT).

Professional guidelines

PubMed

Frazier W, Bhardwaj N
Am Fam Physician 2020 May 15;101(10):590-598. PMID: 32412211
Cranendonk DR, Lavrijsen APM, Prins JM, Wiersinga WJ
Neth J Med 2017 Nov;75(9):366-378. PMID: 29219814
Eichenfield LF, Tom WL, Chamlin SL, Feldman SR, Hanifin JM, Simpson EL, Berger TG, Bergman JN, Cohen DE, Cooper KD, Cordoro KM, Davis DM, Krol A, Margolis DJ, Paller AS, Schwarzenberger K, Silverman RA, Williams HC, Elmets CA, Block J, Harrod CG, Smith Begolka W, Sidbury R
J Am Acad Dermatol 2014 Feb;70(2):338-51. Epub 2013 Nov 27 doi: 10.1016/j.jaad.2013.10.010. PMID: 24290431Free PMC Article

Curated

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

Recent clinical studies

Etiology

Napolitano M, Fabbrocini G, Martora F, Genco L, Noto M, Patruno C
Dermatol Ther 2022 Dec;35(12):e15901. Epub 2022 Oct 13 doi: 10.1111/dth.15901. PMID: 36200594Free PMC Article
Loh EW, Yew YW
Contact Dermatitis 2022 Oct;87(4):303-314. Epub 2022 May 2 doi: 10.1111/cod.14133. PMID: 35460528Free PMC Article
Kvam MS, Alfonso JH, Berents TL, Randem BG, Stylianou E
Tidsskr Nor Laegeforen 2019 Feb 12;139(3) Epub 2019 Feb 5 doi: 10.4045/tidsskr.18.0213. PMID: 30754949
Makrgeorgou A, Leonardi-Bee J, Bath-Hextall FJ, Murrell DF, Tang ML, Roberts A, Boyle RJ
Cochrane Database Syst Rev 2018 Nov 21;11(11):CD006135. doi: 10.1002/14651858.CD006135.pub3. PMID: 30480774Free PMC Article
Sohn A, Frankel A, Patel RV, Goldenberg G
Mt Sinai J Med 2011 Sep-Oct;78(5):730-9. doi: 10.1002/msj.20289. PMID: 21913202

Diagnosis

Napolitano M, Fabbrocini G, Martora F, Genco L, Noto M, Patruno C
Dermatol Ther 2022 Dec;35(12):e15901. Epub 2022 Oct 13 doi: 10.1111/dth.15901. PMID: 36200594Free PMC Article
Leung AKC, Lam JM, Leong KF, Leung AAM, Wong AHC, Hon KL
Recent Pat Inflamm Allergy Drug Discov 2020;14(2):146-155. doi: 10.2174/1872213X14666200810152246. PMID: 32778043
Elsner P, Agner T
J Eur Acad Dermatol Venereol 2020 Jan;34 Suppl 1:13-21. doi: 10.1111/jdv.16062. PMID: 31860736
Raveendran R
Immunol Allergy Clin North Am 2019 Nov;39(4):521-533. Epub 2019 Aug 31 doi: 10.1016/j.iac.2019.07.006. PMID: 31563186
Sohn A, Frankel A, Patel RV, Goldenberg G
Mt Sinai J Med 2011 Sep-Oct;78(5):730-9. doi: 10.1002/msj.20289. PMID: 21913202

Therapy

Sedeh FB, Henning MAS, Jemec GBE, Ibler KS
Acta Derm Venereol 2022 Aug 24;102:adv00764. doi: 10.2340/actadv.v102.2075. PMID: 35818735Free PMC Article
Simpson EL, Papp KA, Blauvelt A, Chu CY, Hong HC, Katoh N, Calimlim BM, Thyssen JP, Chiou AS, Bissonnette R, Stein Gold LF, Wegzyn C, Hu X, Liu M, Liu J, Tenorio AR, Chu AD, Guttman-Yassky E
JAMA Dermatol 2022 Apr 1;158(4):404-413. doi: 10.1001/jamadermatol.2022.0029. PMID: 35262646Free PMC Article
van Zuuren EJ, Fedorowicz Z, Christensen R, Lavrijsen A, Arents BWM
Cochrane Database Syst Rev 2017 Feb 6;2(2):CD012119. doi: 10.1002/14651858.CD012119.pub2. PMID: 28166390Free 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

Nocerino R, Bedogni G, Carucci L, Cosenza L, Cozzolino T, Paparo L, Palazzo S, Riva L, Verduci E, Berni Canani R
J Pediatr 2021 May;232:183-191.e3. Epub 2021 Jan 29 doi: 10.1016/j.jpeds.2021.01.059. PMID: 33524387
Agner T, Elsner P
J Eur Acad Dermatol Venereol 2020 Jan;34 Suppl 1:4-12. doi: 10.1111/jdv.16061. PMID: 31860734
Hartman-Adams H, Banvard C, Juckett G
Am Fam Physician 2014 Aug 15;90(4):229-35. PMID: 25250996
Hay RJ, Johns NE, Williams HC, Bolliger IW, Dellavalle RP, Margolis DJ, Marks R, Naldi L, Weinstock MA, Wulf SK, Michaud C, J L Murray C, Naghavi M
J Invest Dermatol 2014 Jun;134(6):1527-1534. Epub 2013 Oct 28 doi: 10.1038/jid.2013.446. PMID: 24166134
Strachan DP
BMJ 1989 Nov 18;299(6710):1259-60. doi: 10.1136/bmj.299.6710.1259. PMID: 2513902Free 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
Ali F, Vyas J, Finlay AY
Acta Derm Venereol 2020 Jun 9;100(12):adv00161. doi: 10.2340/00015555-3511. PMID: 32412644Free PMC Article
Biagini Myers JM, Schauberger E, He H, Martin LJ, Kroner J, Hill GM, Ryan PH, LeMasters GK, Bernstein DI, Lockey JE, Arshad SH, Kurukulaaratchy R, Khurana Hershey GK
J Allergy Clin Immunol 2019 May;143(5):1803-1810.e2. Epub 2018 Dec 13 doi: 10.1016/j.jaci.2018.09.037. PMID: 30554722Free PMC Article
Wollenberg A, Howell MD, Guttman-Yassky E, Silverberg JI, Kell C, Ranade K, Moate R, van der Merwe R
J Allergy Clin Immunol 2019 Jan;143(1):135-141. Epub 2018 Jun 12 doi: 10.1016/j.jaci.2018.05.029. PMID: 29906525
Makrgeorgou A, Leonardi-Bee J, Bath-Hextall FJ, Murrell DF, Tang ML, Roberts A, Boyle RJ
Cochrane Database Syst Rev 2018 Nov 21;11(11):CD006135. doi: 10.1002/14651858.CD006135.pub3. PMID: 30480774Free PMC Article

Recent systematic reviews

Loh EW, Yew YW
Contact Dermatitis 2022 Oct;87(4):303-314. Epub 2022 May 2 doi: 10.1111/cod.14133. PMID: 35460528Free PMC Article
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
Silverberg JI, Thyssen JP, Fahrbach K, Mickle K, Cappelleri JC, Romero W, Cameron MC, Myers DE, Clibborn C, DiBonaventura M
J Eur Acad Dermatol Venereol 2021 Sep;35(9):1797-1810. Epub 2021 Jun 12 doi: 10.1111/jdv.17351. PMID: 33991374Free PMC Article
Kussainova A, Kassym L, Akhmetova A, Glushkova N, Sabirov U, Adilgozhina S, Tuleutayeva R, Semenova Y
PLoS One 2020;15(11):e0241445. Epub 2020 Nov 10 doi: 10.1371/journal.pone.0241445. PMID: 33170870Free PMC Article
Vaughn AR, Branum A, Sivamani RK
Phytother Res 2016 Aug;30(8):1243-64. Epub 2016 May 23 doi: 10.1002/ptr.5640. PMID: 27213821

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    Clinical resources

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    • PubMed
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      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Curated

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

    Consumer resources

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