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{{Atopic dermatitis}} | {{Atopic dermatitis}} | ||
{{CMG}} | {{CMG}} {{AE}} {{S.S}} [[Ogechukwu Hannah Nnabude, MD]] | ||
== Overview == | |||
Atopic dermatitis is a [[chronic]] inflammatory skin disorder that occurs primarily in children, but also affects adults, usually with a personal or [[family history]] of [[atopy]] including [[asthma]], and [[allergic rhinitis]]. Atopic dermatitis presents usually with intense [[pruritus]] and is often associated with elevated levels of [[Immunoglobulin E|immunoglobulin E (IgE)]]. | ==Overview== | ||
Atopic dermatitis is a [[chronic]] [[inflammatory]] skin disorder that occurs primarily in children, but also affects adults, usually with a personal or [[family history]] of [[atopy]] including [[asthma]], and [[allergic rhinitis]]. [[Atopic dermatitis]] presents usually with intense [[pruritus]] and is often associated with elevated levels of [[Immunoglobulin E|immunoglobulin E (IgE)]]. | |||
==Historical Perspective== | ==Historical Perspective== | ||
The term | The term [[atopic dermatitis]] was first coined by Fred Wise and Marion Sulzberger, American [[Dermatologist|dermatologists]], in 1933, and the first widely used [[diagnostic criteria]] for [[atopic dermatitis]] was published by Jon Hanifin and Georg Rajka, in 1980. | ||
==Pathophysiology== | |||
[[Atopic dermatitis]] is a [[chronic]] [[inflammatory]] [[skin disorder]] with an [[Immunology|immunologic]] background and occurs in patients with a personal or [[family history]] of [[atopy]] (i.e. [[asthma]] or [[allergic rhinitis]]). It is caused by either skin barrier dysfunction or immune dysregulation of the [[Adaptive immunity|adaptive]] and [[innate immune response]] leading to an enhanced [[IgE]]-mediated, systemic [[Th2 response]]. The skin barrier is invaded by [[exogenous]] substances, including [[allergens]], [[irritants]] and [[microbes]]; and the tightly packed structure of the [[stratum corneum]] is further compromised. Systemically, a dysfunctional [[Innate immune system|innate]] and [[adaptive immune response]] causes further damage to the [[epidermis]]. | |||
==Causes== | ==Causes== | ||
Atopic dermatitis is the result of either skin barrier dysfunction or immune dysregulation due to [[Genetics|genetic]] defects. The most important genetic defect includes [[Mutation|mutations]] in the [[filaggrin]] gene (FLG). | |||
==Differentiating Atopic Dermatitis from other Diseases== | |||
[[Atopic dermatitis]] is a chronic [[inflammatory]] skin disorder, which is indistinguishable from other causes of dermatitis. [[Atopic dermatitis]] is usually associated with a personal or [[family history]] of [[atopic diseases]] including [[asthma]], allergic rhinitis and [[food allergy]]. The most common clinically similar dermatitis in infancy is [[seborrheic dermatitis]] which includes [[hyperkeratosis]] of the [[Scalp rash|scalp]], also found in [[atopic dermatitis]]. | |||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
It now affects 10-20% of children and 1-3% of adults in industrialized countries, and its [[prevalence]] there has more than doubled in the past thirty years.< | It now affects 10-20% of children and 1-3% of adults in industrialized countries, and its [[prevalence]] there has more than doubled in the past thirty years. [[Atopic dermatitis]] incidence is highest during [[infancy]] and early childhood. The majority of [[atopic dermatitis]] patients have onset of symptoms <5 years of age. The [[prevalence]] of atopic dermatitis is approximately 5,000-20,000 cases per 100,000 children worldwide. In 2003, the prevalence of [[atopic dermatitis]] was estimated to be 10,700 cases per 100,000 children in the [[United States]]. | ||
==Risk Factors== | |||
[[Atopic dermatitis]] is a multifactorial, [[chronic]] [[inflammatory]] skin disease as a result of interactions between various [[Genetics|genetic]], [[immune]] and environmental factors. The most important [[risk factor]] for the development of atopic dermatitis is a [[family history]] or personal history of [[atopy]] including [[asthma]], [[allergic rhinitis]], [[food allergy]]. | |||
==Screening== | |||
There is insufficient evidence to recommend routine screening for atopic dermatitis. | |||
==Natural History, Complications and Prognosis== | |||
The symptoms of atopic dermatitis usually start during the first few years of life, and present with [[symptoms]] such as intense [[pruritus]] and chronic and relapsing age dependent [[Eczema|eczematous]] lesions. Common [[complications]] of atopic dermatitis include super-infection with [[Staphylococcus aureus|staphylococcus ''aureus'']]'','' [[herpes simplex virus]], and [[molluscum contagiosum]]; [[Sleep disturbances|sleep problems]] due to intense [[pruritus]], [[ocular]] [[comorbidities]], and topical [[corticosteroids]] leading to [[striae]] formation. | |||
==Diagnosis== | ==Diagnosis== | ||
===Diagnostic Studies=== | ===Diagnostic Studies=== | ||
Due to the variable morphology, distribution of skin lesions and intermittent clinical features, it is very challenging to define the diagnosis of atopic dermatitis. Atopic dermatitis is primarily diagnosed based on the clinical presentation. Currently, the most used [[criteria]] worldwide is published by United Kingdom | Due to the variable [[morphology]], distribution of skin lesions, and intermittent clinical features, it is very challenging to define the diagnosis of atopic dermatitis. Atopic dermatitis is primarily diagnosed based on the [[clinical]] presentation. Currently, the most commonly used [[criteria]] worldwide is published by the United Kingdom Working Group and is based upon history, [[morphology]] and distribution of [[Eczema|eczematous]] lesions, and clinical features of atopic dermatitis. In [[patients]] with atopic dermatitis, to rule out other skin [[conditions]], a [[histologic]] examination of a [[skin biopsy]] and other [[laboratory]] tests (eg, [[Immunoglobulin E|serum immunoglobulin E]], [[KOH test|potassium hydroxide preparation]], patch testing, [[genetic testing]]) can be considered. | ||
===History and Symptoms=== | |||
The most common [[symptoms]] of atopic dermatitis include [[pruritus]], distribution of [[rash]] in age- specific patters and [[dry skin]]. Patients often have a personal or [[family history]] of [[asthma]] or [[allergic rhinitis]]. [[Patients]] with atopic dermatitis may report a positive history of [[cutaneous]] hyper-reactivity to diverse environmental stimuli and [[Atopy|atopic disorders]]. | |||
===Physical Examination=== | |||
Atopic dermatitis is a chronic or relapsing [[hypersensitive]] manifestation of the [[skin]]. Common [[physical examination]] findings of [[atopic dermatitis]] include [[pruritus]], [[Eczema|eczematous]] lesions, [[xerosis]] and [[lichenification]]. The lesions are usually age-specific and can be at various stages of development. The lesions can involve any area of the body in severe cases, but usually, it is uncommon to find lesions in the [[axillary]], [[gluteal]], or [[groin]] area. | |||
===Laboratory Findings=== | |||
The diagnosis of atopic dermatitis remains clinical as there is no reliable [[Biomarker|bio-marker]] that can differentiate [[atopic dermatitis]] from other skin diseases. | |||
===Other diagnostic studies=== | |||
There are no routinely diagnostic studies for [[atopic dermatitis]], but in selected patients to rule out other skin conditions, a [[histologic]] examination of a [[skin biopsy]] and other laboratory tests (eg, [[IgE|serum immunoglobulin E]], [[KOH test|potassium hydroxide preparation]], [[patch testing]], [[genetic testing]]) can be considered. | |||
==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
The mainstay of treatment for atopic dermatitis depends upon the severity of the disease and is treated with a combination of conservative and medical therapy. The goals of treatment include elimination of aggravating factors, skin barrier function repair, maintaining skin hydration and pharmacologic treatment of skin inflammation. Pharmacologic medical therapies for atopic dermatitis can be classified according to | The mainstay of treatment for [[atopic dermatitis]] depends upon the severity of the disease and is treated with a combination of conservative and medical therapy. The goals of treatment include the elimination of aggravating factors, skin barrier function repair, maintaining skin hydration, and pharmacologic treatment of skin [[inflammation]]. [[Pharmacological|Pharmacologic]] medical therapies for atopic dermatitis can be classified according to several severity scales( (i.e [[SCORAD]] index, the Eczema Area, and Severity Index (EASI), and the Patient-Oriented Eczema Measure POEM). | ||
===Primary Prevention=== | ===Primary Prevention=== | ||
Primary prevention applies to | Primary prevention applies to patients with a history of other [[atopic diseases]] and have not been diagnosed with [[atopic dermatitis]] yet. Its primary goal is to reduce the risk of developing [[atopic dermatitis]] in the future. Approaches to reduce the development of [[atopic dermatitis]] in children usually include the minimization of [[antibiotics]] administration in infants and infections in [[infants]]. | ||
== | |||
===Secondary prevention=== | |||
Secondary prevention involves protecting and restoring the epidermal skin barrier function including abstaining from using soap, cosmetics, dyes, fragrances, and detergents, washing new clothes before wearing them, avoiding frequent and sudden climate changes, using air humidifiers in winters, avoiding excessive exposure to [[UV radiation]] and using SPF sunscreens, regular application of emollients every 6 hours, and stress-reducing therapy | |||
===Financial costs=== | |||
There has been no discussion on the cost-effectiveness of therapy for [[atopic dermatitis]], however, in a retrospective study, the utilization of health care and treatment costs annually were higher for patients with atopic dermatitis than for controls without [[atopic dermatitis]] and was associated with the severity of the disease. | |||
===Future or Investigational Therapies=== | |||
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 [[tissue]]s, and may be used to decrease the severity and frequency of flares. 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. However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk. | |||
[[Category:Autoimmune diseases]] | [[Category:Autoimmune diseases]] | ||
[[Category:Dermatology]] | [[Category:Dermatology]] | ||
[[Category: | [[Category:Up-To-Date]] | ||
Latest revision as of 02:50, 21 October 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shalinder Singh, M.B.B.S.[2] Ogechukwu Hannah Nnabude, MD
Overview
Atopic dermatitis is a chronic inflammatory skin disorder that occurs primarily in children, but also affects adults, usually with a personal or family history of atopy including asthma, and allergic rhinitis. Atopic dermatitis presents usually with intense pruritus and is often associated with elevated levels of immunoglobulin E (IgE).
Historical Perspective
The term atopic dermatitis was first coined by Fred Wise and Marion Sulzberger, American dermatologists, in 1933, and the first widely used diagnostic criteria for atopic dermatitis was published by Jon Hanifin and Georg Rajka, in 1980.
Pathophysiology
Atopic dermatitis is a chronic inflammatory skin disorder with an immunologic background and occurs in patients with a personal or family history of atopy (i.e. asthma or allergic rhinitis). It is caused by either skin barrier dysfunction or immune dysregulation of the adaptive and innate immune response leading to an enhanced IgE-mediated, systemic Th2 response. The skin barrier is invaded by exogenous substances, including allergens, irritants and microbes; and the tightly packed structure of the stratum corneum is further compromised. Systemically, a dysfunctional innate and adaptive immune response causes further damage to the epidermis.
Causes
Atopic dermatitis is the result of either skin barrier dysfunction or immune dysregulation due to genetic defects. The most important genetic defect includes mutations in the filaggrin gene (FLG).
Differentiating Atopic Dermatitis from other Diseases
Atopic dermatitis is a chronic inflammatory skin disorder, which is indistinguishable from other causes of dermatitis. Atopic dermatitis is usually associated with a personal or family history of atopic diseases including asthma, allergic rhinitis and food allergy. The most common clinically similar dermatitis in infancy is seborrheic dermatitis which includes hyperkeratosis of the scalp, also found in atopic dermatitis.
Epidemiology and Demographics
It now affects 10-20% of children and 1-3% of adults in industrialized countries, and its prevalence there has more than doubled in the past thirty years. Atopic dermatitis incidence is highest during infancy and early childhood. The majority of atopic dermatitis patients have onset of symptoms <5 years of age. The prevalence of atopic dermatitis is approximately 5,000-20,000 cases per 100,000 children worldwide. In 2003, the prevalence of atopic dermatitis was estimated to be 10,700 cases per 100,000 children in the United States.
Risk Factors
Atopic dermatitis is a multifactorial, chronic inflammatory skin disease as a result of interactions between various genetic, immune and environmental factors. The most important risk factor for the development of atopic dermatitis is a family history or personal history of atopy including asthma, allergic rhinitis, food allergy.
Screening
There is insufficient evidence to recommend routine screening for atopic dermatitis.
Natural History, Complications and Prognosis
The symptoms of atopic dermatitis usually start during the first few years of life, and present with symptoms such as intense pruritus and chronic and relapsing age dependent eczematous lesions. Common complications of atopic dermatitis include super-infection with staphylococcus aureus, herpes simplex virus, and molluscum contagiosum; sleep problems due to intense pruritus, ocular comorbidities, and topical corticosteroids leading to striae formation.
Diagnosis
Diagnostic Studies
Due to the variable morphology, distribution of skin lesions, and intermittent clinical features, it is very challenging to define the diagnosis of atopic dermatitis. Atopic dermatitis is primarily diagnosed based on the clinical presentation. Currently, the most commonly used criteria worldwide is published by the United Kingdom Working Group and is based upon history, morphology and distribution of eczematous lesions, and clinical features of atopic dermatitis. In patients with atopic dermatitis, to rule out other skin conditions, a histologic examination of a skin biopsy and other laboratory tests (eg, serum immunoglobulin E, potassium hydroxide preparation, patch testing, genetic testing) can be considered.
History and Symptoms
The most common symptoms of atopic dermatitis include pruritus, distribution of rash in age- specific patters and dry skin. Patients often have a personal or family history of asthma or allergic rhinitis. Patients with atopic dermatitis may report a positive history of cutaneous hyper-reactivity to diverse environmental stimuli and atopic disorders.
Physical Examination
Atopic dermatitis is a chronic or relapsing hypersensitive manifestation of the skin. Common physical examination findings of atopic dermatitis include pruritus, eczematous lesions, xerosis and lichenification. The lesions are usually age-specific and can be at various stages of development. The lesions can involve any area of the body in severe cases, but usually, it is uncommon to find lesions in the axillary, gluteal, or groin area.
Laboratory Findings
The diagnosis of atopic dermatitis remains clinical as there is no reliable bio-marker that can differentiate atopic dermatitis from other skin diseases.
Other diagnostic studies
There are no routinely diagnostic studies for atopic dermatitis, but in selected patients to rule out other skin conditions, a histologic examination of a skin biopsy and other laboratory tests (eg, serum immunoglobulin E, potassium hydroxide preparation, patch testing, genetic testing) can be considered.
Treatment
Medical Therapy
The mainstay of treatment for atopic dermatitis depends upon the severity of the disease and is treated with a combination of conservative and medical therapy. The goals of treatment include the elimination of aggravating factors, skin barrier function repair, maintaining skin hydration, and pharmacologic treatment of skin inflammation. Pharmacologic medical therapies for atopic dermatitis can be classified according to several severity scales( (i.e SCORAD index, the Eczema Area, and Severity Index (EASI), and the Patient-Oriented Eczema Measure POEM).
Primary Prevention
Primary prevention applies to patients with a history of other atopic diseases and have not been diagnosed with atopic dermatitis yet. Its primary goal is to reduce the risk of developing atopic dermatitis in the future. Approaches to reduce the development of atopic dermatitis in children usually include the minimization of antibiotics administration in infants and infections in infants.
Secondary prevention
Secondary prevention involves protecting and restoring the epidermal skin barrier function including abstaining from using soap, cosmetics, dyes, fragrances, and detergents, washing new clothes before wearing them, avoiding frequent and sudden climate changes, using air humidifiers in winters, avoiding excessive exposure to UV radiation and using SPF sunscreens, regular application of emollients every 6 hours, and stress-reducing therapy
Financial costs
There has been no discussion on the cost-effectiveness of therapy for atopic dermatitis, however, in a retrospective study, the utilization of health care and treatment costs annually were higher for patients with atopic dermatitis than for controls without atopic dermatitis and was associated with the severity of the disease.
Future or Investigational Therapies
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. 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. However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.