Eczema
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Lixia Ellis, M.D., Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]
Synonyms and keywords: Atopic dermatitis; Besnier prurigo; Neurodermatitis, atopic; Eczema, atopic
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]
Overview
Eczema, also known as atopic dermatitis, or [atopic eczema]], is a dermatologic problem which is commonly seen in children. It is a relapsing-remitting skin problem that is predominantly manifested as pruritus, with accompanied swelling, redness, and dryness of the skin. Flaking, cracking, oozing, blistering or bleeding may occur as a result of excessive scratching of the skin.
Historical Perspective
It was in the 20th century when eczema came into existence, and later on, concepts on this had evolved including major insights on the nature of the disease.
Classification
Eczema is classified according to location, appearance, or etiology.
Pathophysiology
The mechanism of disease of eczema involves a complex interplay of abnormalities of skin microbiomes, a dysfunction in the epidermal barrier, and an immune dysregulation. There are two main theories on the existence of atopic dermatitis, also known as atopic eczema – the inside-out hypothesis, and the outside-in hypothesis.
Causes
The etiology of eczema is multifactorial and complex. This involves aberrations in genetic component, adverse effect of certain medication and some environmental factors.
Differentiating Eczema from other Diseases
Eczema has various mimics with regards to the clinical presentation, severity, and course of disease. A strong clinical evaluation by the physician based on the presenting signs and symptoms is needed to come up with the correct diagnosis. Differential diagnoses of eczema include infectious disease, inflammatory disease, immunodeficiency problem, or a nutritional deficiency.
Epidemiology and Demographics
In the United States, eczema has a prevalence of 10.7% in children and 7.2% in adults. Eczema has more predilection in males.
Risk Factors
Risk factors of eczema include family history and FLG gene mutation.
Screening
Hanifin and Rajka criteria are the gold standard for diagnosing eczema.
Natural History, Complications, and Prognosis
Eczema has regarded as a medical condition with a natural history that occurs consistently. It is characterized as a disease with an early onset, mostly during the childhood period, and remits during the adolescence period. If left untreated, eczema can lead to viral, bacterial and fungal infections. Psychological problems could also arise brought about by constant itching.
Diagnosis
History and Symptoms
Family history, dietary habits, lifestyle habits, and allergies should be elicited whenever considering eczema as the primary diagnosis. This is important because eczema can be based on the patient‘s history and evolution and distribution of the skin lesion.
Physical Examination
Eczema is a [dermatologic disease]] and pruritus is the hallmark feature of this disease.
Laboratory Findings
Levels of IgE are associated with allergy, aside from parasitic infections, autoimmune diseases, and certain carcinomas.
Other Diagnostic Studies
No particular biomarker is reliable to diagnose eczema. However, the current practice is by using the laboratory levels of IgE, which when elevated, can also be associated with allergy, aside from parasitic infections, autoimmune diseases, and certain carcinomas.
Treatment
Medical Therapy
Topical corticosteroids are the mainline treatment for eczema. Different potencies of steroids are rendered specifically for the severity of eczema. Other drug treatments oftenly used for eczema include topical calcineurin inhibitors,crisaborole, antimicrobials, and antifungals.
Surgery
Surgical treatment is not commonly used as a means of management for eczema.
Primary Prevention
Primary prevention is the most effective means to avoid complications of eczema. Emolients and consumption of prebiotics and probiotics can prevent the occurrence of this condition.
Secondary Prevention
Prevention of further trans-epidermal water loss is the cornerstone of management of eczema. Since dysfunctional skin barriers could lead to water loss, daily replenishment of skin moisture is needed. This can be achieved through different modalities such as emollients, occlusives, and humectants.
Cost-Effectiveness of Therapy
The economic impact of eczema causes a burden to patients suffering from this disease. A recent study showed that an average of $274 ($199 indirect cost, and $75 direct cost) is spent by each patient for eczema.
Social Impact
Pruritus and constant scratching of the skin can significantly affect the social life of patient. Sleep disturbances, attention-deficit/hyperactivity disorder, headaches, daytime fatigue, and stunted growth are commonly seen in these patients and could lead to embarrassment and poor self-esteem.
Future or Investigational Therapies
Future trends will focus more on genetic studies in eczema.
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]
Overview
It was in the 20th century when eczema came into existence, and later on, concepts on this had evolved including major insights on the nature of the disease.[1]
Historical Perspectives
- It was in the 20th century when eczema came into existence, and later on, concepts on this had evolved including major insights on the nature of the disease.[1]
- Listed below is a summary of the history of eczema.
| Period | Highlights | Treatment |
|---|---|---|
| Ancient History |
Ebers Papyrus (1500 BCE)
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Hippocrates (400 BCE)
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Celsus (AD)
" certain degree of hardness of the skin with pustules, some humid and some dry " |
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Suetonius (AD)
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Avicenna (980-1037 CE)
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| Premodern Era |
Girolamo Mercurialis (1572) |
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Daniel Turner
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Jean-Louis Alibert (1806)
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Willan and Bateman (early 19th century)
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Pierre Rayer (1835)
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Ferdinand von Hebra (1860)
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Erasmus Wilson
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Ernest Besnier (1892)
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| Twentieth Century and Beyond | Von Pirquet (1906)
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Coca and Cooke (1923)
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Wise and Sulzberger (1933)
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Blackfan and Talbot (1916)
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Hanifin and Rajka (1980)
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References
- ↑ 1.0 1.1 1.2 Bhattacharya T, Strom MA, Lio PA (2016). “Historical Perspectives on Atopic Dermatitis: Eczema Through the Ages”. Pediatr Dermatol. 33 (4): 375–9. doi:10.1111/pde.12853. PMID 27086570.
- ↑ Ali FR, Finlayson AE (2013). “Pharaonic trichology: the Ebers Papyrus”. JAMA Dermatol. 149 (8): 920. doi:10.1001/jamadermatol.2013.4240. PMID 24026454.
- ↑ Tan EK, Millington GW, Levell NJ (2009). “Acupuncture in dermatology: an historical perspective”. Int J Dermatol. 48 (6): 648–52. doi:10.1111/j.1365-4632.2009.03899.x. PMID 19538380.
- ↑ Liddell K (2000). “Choosing a dermatological hero for the millennium. Hippocrates of Cos (460-377 BC)”. Clin Exp Dermatol. 25 (1): 86–8. doi:10.1046/j.1365-2230.2000.0580d.x. PMID 10671984.
- ↑ Hajar R (2013). “The air of history (part v) ibn sina (avicenna): the great physician and philosopher”. Heart Views. 14 (4): 196–201. doi:10.4103/1995-705X.126893. PMC 3970379. PMID 24696763.
- ↑ Khalili M, Wong RJ (2018). “Underserved Does Not Mean Undeserved: Unfurling the HCV Care in the Safety Net”. Dig Dis Sci. 63 (12): 3250–3252. doi:10.1007/s10620-018-5316-9. PMC 6436636. PMID 30311153.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]
Overview
Eczema is classified according to location, appearance, or etiology. We have more common causes of eczema, such as seborrheic dermatitis, and less common causes such as dyshidrosis.
Eczema Classification
- National Eczema Association classified eczema into different types.
- Table 1 enumerates the common types of eczema with their corresponding description.[1]
| Classification | Description |
|---|---|
| Atopic eczema | |
| Contact dermatitis |
|
| Seborrhoeic dermatitis |
|
Lesser Common Types of Eczema
- Table 2 highlights the lesser common types of eczema with their respective features.
| Classification | Description |
|---|---|
| Dyshidrosis (Dyshidrotic Eczema, Pompholyx, Vesicular Palmoplantar Dermatitis, or Housewife’s Eczema) |
|
| Nummular Dermatitis (Discoid Eczema) |
|
| Stasis Dermatitis (Venous Eczema, Gravitational Eczema, Varicose eczema) |
|
| Dermatitis herpetiformis (Duhring’s Disease) |
|
| Neurodermatitis (Localized Scratch Dermatitis, Lichen Simplex Chronicus) |
|
| Autoeczematization (Autosensitization) |
|
Source
“Dyshidrotic eczema – Symptoms and causes | National Eczema Association”.
References
- ↑ Johansson SG, Hourihane JO, Bousquet J; et al. (2001). “A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force”. Allergy. 56 (9): 813–24. PMID 11551246.
- ↑ Peters N, Peters AT (2019). “Atopic dermatitis”. Allergy Asthma Proc. 40 (6): 433–436. doi:10.2500/aap.2019.40.4265. PMID 31690388.
- ↑ Sampogna F, Linder D, Piaserico S, Altomare G, Bortune M, Calzavara-Pinton P; et al. (2014). “Quality of life assessment of patients with scalp dermatitis using the Italian version of the Scalpdex”. Acta Derm Venereol. 94 (4): 411–4. doi:10.2340/00015555-1731. PMID 24287710.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]
Overview
The mechanism of disease of eczema involves a complex interplay of abnormalities of skin microbiomes, a dysfunction in the epidermal barrier, and an immune dysregulation. [1] There are two main theories on the existence of atopic dermatitis, also known as atopic eczema – the inside-out hypothesis, and the outside-in hypothesis.
Pathophysiology
Immunological Dysregulation
- Affected skin involves the uptake of antigens and allergens by the epidermal dendritic cells, dermal dendritic cells, and Langerhan cells.
- Sensory nerves are activated by the released cytokines interleukins 4,13 and 31 (IL-4, IL-13, and IL-31), which are responsible for the pruritic sensation.
- As the event becomes chronic, an increased expression of keratinocyte and Th-cell-derived cytokines is achieved, with more pruritogens contributing to itch sensation. [1]
Genetic Inheritance
- There are 34 genetic loci which are thought to be associated with eczema.
- These regions contain several genes which have important immunological functions, such as T-cell activation, type-2 helper cell differentiation, and innate immunity. [2] [3][4]
Epithelium Barrier Dysfunction
- Multiple factors cause the disruption of epithelial barrier. These include:
- As a result, an interrupted normal skin barrier with elevated pH, high skin permeability, altered lipid composition, and decreased water retention is observed. [5] [6] [7] [8] [9] [10]
Hypotheses on Development of Eczema
- There are two main theories on the existence of atopic dermatitis, also known as atopic eczema – the inside-out hypothesis, and the outside-in hypothesis.[11]
- Inside-out hypothesis
- This hypothesis denotes that some allergic triggers weaken the skin barrier that leads to more introduction of allergens to the area, causing more inflammatory reaction.[11]
- Outside-in hypothesis
- This hypothesis suggests that an impairment of the skin barrier should occur first before the onset of atopic dermatitis.
- This involves the down-regulation of filaggrin genes (FLG) responsible for maintenance of the proper function of skin barrier.[11] [12]
References
- ↑ 1.0 1.1 Feld M, Garcia R, Buddenkotte J, Katayama S, Lewis K, Muirhead G; et al. (2016). “The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves”. J Allergy Clin Immunol. 138 (2): 500–508.e24. doi:10.1016/j.jaci.2016.02.020. PMID 27212086.
- ↑ Paternoster L, Standl M, Waage J, Baurecht H, Hotze M, Strachan DP; et al. (2015). “Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis”. Nat Genet. 47 (12): 1449–1456. doi:10.1038/ng.3424. PMC 4753676. PMID 26482879.
- ↑ Weidinger S, Willis-Owen SA, Kamatani Y, Baurecht H, Morar N, Liang L; et al. (2013). “A genome-wide association study of atopic dermatitis identifies loci with overlapping effects on asthma and psoriasis”. Hum Mol Genet. 22 (23): 4841–56. doi:10.1093/hmg/ddt317. PMC 3820131. PMID 23886662.
- ↑ Martin MJ, Estravís M, García-Sánchez A, Dávila I, Isidoro-García M, Sanz C (2020). “Genetics and Epigenetics of Atopic Dermatitis: An Updated Systematic Review”. Genes (Basel). 11 (4). doi:10.3390/genes11040442. PMC 7231115 Check
|pmc=value (help). PMID 32325630 Check|pmid=value (help). - ↑ Seidenari S, Giusti G (1995). “Objective assessment of the skin of children affected by atopic dermatitis: a study of pH, capacitance and TEWL in eczematous and clinically uninvolved skin”. Acta Derm Venereol. 75 (6): 429–33. doi:10.2340/0001555575429433. PMID 8651017.
- ↑ Jungersted JM, Scheer H, Mempel M, Baurecht H, Cifuentes L, Høgh JK; et al. (2010). “Stratum corneum lipids, skin barrier function and filaggrin mutations in patients with atopic eczema”. Allergy. 65 (7): 911–8. doi:10.1111/j.1398-9995.2010.02326.x. PMID 20132155.
- ↑ Tsakok T, Woolf R, Smith CH, Weidinger S, Flohr C (2019). “Atopic dermatitis: the skin barrier and beyond”. Br J Dermatol. 180 (3): 464–474. doi:10.1111/bjd.16934. PMID 29969827.
- ↑ Halling-Overgaard AS, Kezic S, Jakasa I, Engebretsen KA, Maibach H, Thyssen JP (2017). “Skin absorption through atopic dermatitis skin: a systematic review”. Br J Dermatol. 177 (1): 84–106. doi:10.1111/bjd.15065. PMID 27639188.
- ↑ Howell MD, Kim BE, Gao P, Grant AV, Boguniewicz M, Debenedetto A; et al. (2007). “Cytokine modulation of atopic dermatitis filaggrin skin expression”. J Allergy Clin Immunol. 120 (1): 150–5. doi:10.1016/j.jaci.2007.04.031. PMC 2669594. PMID 17512043.
- ↑ Baurecht H, Rühlemann MC, Rodríguez E, Thielking F, Harder I, Erkens AS; et al. (2018). “Epidermal lipid composition, barrier integrity, and eczematous inflammation are associated with skin microbiome configuration”. J Allergy Clin Immunol. 141 (5): 1668–1676.e16. doi:10.1016/j.jaci.2018.01.019. PMID 29421277.
- ↑ 11.0 11.1 11.2 Silverberg NB, Silverberg JI (2015). “Inside out or outside in: does atopic dermatitis disrupt barrier function or does disruption of barrier function trigger atopic dermatitis?”. Cutis. 96 (6): 359–61. PMID 26761930.
- ↑ Leung DY, Guttman-Yassky E (2014). “Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches”. J Allergy Clin Immunol. 134 (4): 769–79. doi:10.1016/j.jaci.2014.08.008. PMC 4186710. PMID 25282559.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]
Overview
The etiology of eczema is multifactorial and complex. This involves aberrations in genetic components, adverse effects of certain medications, and some environmental factors.
Etiology of Eczema
Genetic problem
- 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.
- Lack of filaggrin gene causes dry skin. [1]
Eczema as an Adverse Drug Reaction
- Eczema can also be brought about by some adverse effects of medications.
- Below is a list of commonly prescribed medications with eczema as the common adverse drug effect (Table 1).
| Medication |
|---|
| Cidofovir |
| Flurbiprofen |
| Olaparib |
| Siltuximab |
| Sorafenib |
| Tiagabine |
References
- ↑ Palmer CN, Irvine AD, Terron-Kwiatkowski A, Zhao Y, Liao H, Lee SP; et al. (2006). “Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis”. Nat Genet. 38 (4): 441–6. doi:10.1038/ng1767. PMID 16550169.
Differentiating Eczema from other Diseases
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]
Overview
Eczema has various mimics with regards to the clinical presentation, severity, and course of disease. A strong clinical evaluation by the physician based on the presenting signs and symptoms is needed to come up with the correct diagnosis. Differential diagnoses of eczema include infectious disease, inflammatory disease, immunodeficiency problem, or a nutritional deficiency.[1]
Differential Diagnosis
A strong clinical evaluation by the physician based on the presenting signs and symptoms is needed to come up with the correct diagnosis.
- Table 1 summarizes these medical conditions that can mimic the presentation of eczema, with their corresponding expected time of onset.
| Type | Medical Condition | Manifestations | Expected Time of Presentation |
|---|---|---|---|
| Inflammatory | Psoriasis |
|
Adolescence to adulthood. |
| Viral Exanthem | Infancy. | ||
| Contact Dermatitis | Infancy. | ||
| Neoplastic | Cutaneous T-cell Lymphoma | Adulthood. | |
| Immunodeficiency | Wiskott-Aldrich Syndrome |
|
Infancy. |
| Netherton syndrome |
|
Infancy. | |
| Hyper IgE syndrome |
|
Infancy. | |
| DOCK8 |
|
Infancy. | |
| Nutritional Deficiency | Zinc | Infancy to early childhood. | |
| Biotin | Infancy to early childhood. |
References
- ↑ 1.0 1.1 Raveendran R (2019). “Tips and Tricks for Controlling Eczema”. Immunol Allergy Clin North Am. 39 (4): 521–533. doi:10.1016/j.iac.2019.07.006. PMID 31563186.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
In the United States, eczema has a prevalence of 10.7% in children and 7.2% in adults. [1] [2] Eczema has more predilection in males. [3]
Eczema Epidemiology and Demographics
- A recent study showed that persistence of disease 8 years from the onset is noted in 20% of children.[4]
- Eczema has more predilection in males. [3]
- In the United States, eczema has a prevalence of 10.7% in children and 7.2% in adults. [1] [2]
- Prevalence of eczema has plateaued in high-income countries, with low- and middle-income countries still having increasing cases. [5]
References
- ↑ 1.0 1.1 Shaw TE, Currie GP, Koudelka CW, Simpson EL (2011). “Eczema prevalence in the United States: data from the 2003 National Survey of Children’s Health”. J Invest Dermatol. 131 (1): 67–73. doi:10.1038/jid.2010.251. PMC 3130508. PMID 20739951.
- ↑ 2.0 2.1 Silverberg JI, Garg NK, Paller AS, Fishbein AB, Zee PC (2015). “Sleep disturbances in adults with eczema are associated with impaired overall health: a US population-based study”. J Invest Dermatol. 135 (1): 56–66. doi:10.1038/jid.2014.325. PMID 25078665.
- ↑ 3.0 3.1 Hanifin JM, Reed ML, Eczema Prevalence and Impact Working Group (2007). “A population-based survey of eczema prevalence in the United States”. Dermatitis. 18 (2): 82–91. doi:10.2310/6620.2007.06034. PMID 17498413.
- ↑ Kim JP, Chao LX, Simpson EL, Silverberg JI (2016). “Persistence of atopic dermatitis (AD): A systematic review and meta-analysis”. J Am Acad Dermatol. 75 (4): 681–687.e11. doi:10.1016/j.jaad.2016.05.028. PMC 5216177. PMID 27544489.
- ↑ Baurecht H, Rühlemann MC, Rodríguez E, Thielking F, Harder I, Erkens AS; et al. (2018). “Epidermal lipid composition, barrier integrity, and eczematous inflammation are associated with skin microbiome configuration”. J Allergy Clin Immunol. 141 (5): 1668–1676.e16. doi:10.1016/j.jaci.2018.01.019. PMID 29421277.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
Risk factors of eczema include family history and FLG gene mutation.
Risk Factors
- Hereditary factors
- Genetics is the strongest identifiable factor associated with development of eczema. [1]
- Family history and FLG gene mutation. [2]
- 34 genetic loci have been identified based on genome-wide association studies that accounts for almost 20% of eczema inheritance. [3]
- The profilaggrin protein of the FLG gene maintains the intactness of the skin. [4]
- Peanut allergy, herpes virus, and contact dermatitis were found to be associated with FLG gene mutation.[5] [6]
- Environmental factors
References
- ↑ Feld M, Garcia R, Buddenkotte J, Katayama S, Lewis K, Muirhead G; et al. (2016). “The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves”. J Allergy Clin Immunol. 138 (2): 500–508.e24. doi:10.1016/j.jaci.2016.02.020. PMID 27212086.
- ↑ Sicherer SH, Leung DY (2009). “Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects in 2008”. J Allergy Clin Immunol. 123 (2): 319–27. doi:10.1016/j.jaci.2008.12.025. PMID 19203656.
- ↑ Paternoster L, Standl M, Waage J, Baurecht H, Hotze M, Strachan DP; et al. (2015). “Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis”. Nat Genet. 47 (12): 1449–1456. doi:10.1038/ng.3424. PMC 4753676. PMID 26482879.
- ↑ Sandilands A, Sutherland C, Irvine AD, McLean WH (2009). “Filaggrin in the frontline: role in skin barrier function and disease”. J Cell Sci. 122 (Pt 9): 1285–94. doi:10.1242/jcs.033969. PMC 2721001. PMID 19386895.
- ↑ Leung DY, Guttman-Yassky E (2014). “Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches”. J Allergy Clin Immunol. 134 (4): 769–79. doi:10.1016/j.jaci.2014.08.008. PMC 4186710. PMID 25282559.
- ↑ Irvine AD, McLean WH, Leung DY (2011). “Filaggrin mutations associated with skin and allergic diseases”. N Engl J Med. 365 (14): 1315–27. doi:10.1056/NEJMra1011040. PMID 21991953.
- ↑ Silverberg JI, Hanifin J, Simpson EL (2013). “Climatic factors are associated with childhood eczema prevalence in the United States”. J Invest Dermatol. 133 (7): 1752–9. doi:10.1038/jid.2013.19. PMC 3646081. PMID 23334343.
Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
Hanifin and Rajka criteria are the gold standard for diagnosing eczema. [1] [2]
Eczema screening
- Hanifin and Rajka criteria are the gold standard for diagnosing eczema.
- It should satisfy 3 out of 4 major criteria or 3 out of 23 minor criteria. [3]
References
- ↑ Eichenfield LF, Tom WL, Chamlin SL, Feldman SR, Hanifin JM, Simpson EL; et al. (2014). “Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis”. J Am Acad Dermatol. 70 (2): 338–51. doi:10.1016/j.jaad.2013.10.010. PMC 4410183. PMID 24290431.
- ↑ Schulte-Herbrüggen O, Fölster-Holst R, von Elstermann M, Augustin M, Hellweg R (2007). “Clinical relevance of nerve growth factor serum levels in patients with atopic dermatitis and psoriasis”. Int Arch Allergy Immunol. 144 (3): 211–6. doi:10.1159/000103994. PMID 17579279.
- ↑ Avena-Woods C (2017). “Overview of atopic dermatitis”. Am J Manag Care. 23 (8 Suppl): S115–S123. PMID 28978208.
Natural History, Complications, and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
Eczema has regarded as a medical condition with a natural history that occurs consistently. It is characterized as a disease with an early onset, mostly during the childhood period, and remits during the adolescence period. If eczema is left untreated, it can lead to viral, bacterial and fungal infections. Psychological problems could also arise brought about by constant itching.
Eczema Natural History, Complications, and Prognosis
Natural History
- Eczema has regarded as a medical condition with a natural history that occurs consistently.
- It is characterized as a disease with an early onset, mostly during the childhood period, and remits during the adolescence period. [1]
Comorbidities
- Individuals suffering from eczema often have comorbidities like asthma [2], allergic rhinitis [3], contact dermatitis [4], food allergy, [5] and atopy-associated eye diseases.[6]
- Peanut allergy is the most common form of food allergy associated with eczema. [5]
- The National Institute of Allergy and Infectious Diseases 2017 guidelines recommend that all infants suffering from severe eczema should undergo skin prick testing or peanut-specific IgE evaluation to assess for possible occurrence of peanut allergy and be prevented as early as possible. [7]
- Eczema is also associated with metabolic problems such as obesity. [8]
Complications
- Eczema can lead to viral, bacterial and fungal infections.
- Psychological problems could also arise brought about by constant itching.
- 92,642 children participants with eczema in a cross-sectional study were observed to have a two-fold increase in having an attention deficit hyperactivity disorder (ADHD). [9] [10]
- A higher incidence rate of anxiety disorders in adolescence is observed. These include generalized anxiety disorder and social anxiety disorder.
- The elderly people with eczema are the most commonly affected with depression. [11]
Prognosis
- In those patients who have an onset of eczema during their first two years of life, a higher remission rate is expected than those who have a later onset of disease. [12]
- Hand eczema has poor prognosis with accounted 44% manifestation of symptoms in a 15-year follow-up study. [13]
- In another study, complete healing was only observed among 19.3% of the patients after a 5-year follow-up. [14]
References
- ↑ Paternoster L, Savenije OEM, Heron J, Evans DM, Vonk JM, Brunekreef B; et al. (2018). “Identification of atopic dermatitis subgroups in children from 2 longitudinal birth cohorts”. J Allergy Clin Immunol. 141 (3): 964–971. doi:10.1016/j.jaci.2017.09.044. PMC 5840507. PMID 29129583.
- ↑ Holgate ST (2007). “The epithelium takes centre stage in asthma and atopic dermatitis”. Trends Immunol. 28 (6): 248–51. doi:10.1016/j.it.2007.04.007. PMID 17466594.
- ↑ Zheng T, Yu J, Oh MH, Zhu Z (2011). “The atopic march: progression from atopic dermatitis to allergic rhinitis and asthma”. Allergy Asthma Immunol Res. 3 (2): 67–73. doi:10.4168/aair.2011.3.2.67. PMC 3062798. PMID 21461244.
- ↑ de Groot AC (1990). “The frequency of contact allergy in atopic patients with dermatitis”. Contact Dermatitis. 22 (5): 273–7. doi:10.1111/j.1600-0536.1990.tb01595.x. PMID 2383986.
- ↑ 5.0 5.1 Jackson PG, Lessof MH, Baker RW, Ferrett J, MacDonald DM (1981). “Intestinal permeability in patients with eczema and food allergy”. Lancet. 1 (8233): 1285–6. doi:10.1016/s0140-6736(81)92459-4. PMID 6112605.
- ↑ Kulthanan K, Tuchinda P, Nitiyarom R, Chunharas A, Chantaphakul H, Aunhachoke K; et al. (2021). “Clinical practice guidelines for the diagnosis and management of atopic dermatitis”. Asian Pac J Allergy Immunol. 39 (3): 145–155. doi:10.12932/AP-010221-1050. PMID 34246205 Check
|pmid=value (help). - ↑ Togias A, Cooper SF, Acebal ML, Assa’ad A, Baker JR, Beck LA; et al. (2017). “Addendum Guidelines for the Prevention of Peanut Allergy in the United States: Report of the National Institute of Allergy and Infectious Diseases-Sponsored Expert Panel”. J Pediatr Nurs. 32: 91–98. doi:10.1016/j.pedn.2016.12.006. PMID 28137368.
- ↑ Silverberg JI, Kleiman E, Lev-Tov H, Silverberg NB, Durkin HG, Joks R; et al. (2011). “Association between obesity and atopic dermatitis in childhood: a case-control study”. J Allergy Clin Immunol. 127 (5): 1180–6.e1. doi:10.1016/j.jaci.2011.01.063. PMID 21411132.
- ↑ Yaghmaie P, Koudelka CW, Simpson EL (2013). “Mental health comorbidity in patients with atopic dermatitis”. J Allergy Clin Immunol. 131 (2): 428–33. doi:10.1016/j.jaci.2012.10.041. PMC 3565469. PMID 23245818.
- ↑ Buske-Kirschbaum A, Schmitt J, Plessow F, Romanos M, Weidinger S, Roessner V (2013). “Psychoendocrine and psychoneuroimmunological mechanisms in the comorbidity of atopic eczema and attention deficit/hyperactivity disorder”. Psychoneuroendocrinology. 38 (1): 12–23. doi:10.1016/j.psyneuen.2012.09.017. PMID 23141851.
- ↑ Nicholas MN, Gooderham MJ (2017). “Atopic Dermatitis, Depression, and Suicidality”. J Cutan Med Surg. 21 (3): 237–242. doi:10.1177/1203475416685078. PMID 28300443.
- ↑ Kim JP, Chao LX, Simpson EL, Silverberg JI (2016). “Persistence of atopic dermatitis (AD): A systematic review and meta-analysis”. J Am Acad Dermatol. 75 (4): 681–687.e11. doi:10.1016/j.jaad.2016.05.028. PMC 5216177. PMID 27544489.
- ↑ Meding B, Wrangsjö K, Järvholm B (2005). “Fifteen-year follow-up of hand eczema: persistence and consequences”. Br J Dermatol. 152 (5): 975–80. doi:10.1111/j.1365-2133.2005.06494.x. PMID 15888155.
- ↑ Olesen CM, Agner T, Ebbehøj NE, Carøe TK (2019). “Factors influencing prognosis for occupational hand eczema: new trends”. Br J Dermatol. 181 (6): 1280–1286. doi:10.1111/bjd.17870. PMID 30851194.
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