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{{Xyz}}
{{CMG}}; {{AE}} {{S.S}}
{{CMG}}; {{AE}}


==Overview==
==Overview==
It is thought that Atopic dermatitis is caused by either skin barrier dysfunction or immune dysregulation.
The mainstay of treatment for atopic dermatitis depends upon the severity of the disease and is treated with 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.
 
 
 
==Pathogenesis===
 
It is understood that Atopic dermatitis is the result of skin barrier dysfunction or by immune dysregulation.<ref name="pmid21682749">{{cite journal |vauthors=Boguniewicz M, Leung DY |title=Atopic dermatitis: a disease of altered skin barrier and immune dysregulation |journal=Immunol. Rev. |volume=242 |issue=1 |pages=233–46 |date=July 2011 |pmid=21682749 |pmc=3122139 |doi=10.1111/j.1600-065X.2011.01027.x |url=}}</ref>
*Dysfunction of the skin barrier:
**Skin barrier abnormalities lead to the permeability of epidermis, causing entry of antigens or pathogens and leading to the production of inflammatory cytokines.
**The major factors to abnormal skin barrier include loss-of-function mutations in the filaggrin gene (FLG) causing Filaggrin deficiency<ref name="pmid19720210">{{cite journal |vauthors=Howell MD, Kim BE, Gao P, Grant AV, Boguniewicz M, DeBenedetto A, Schneider L, Beck LA, Barnes KC, Leung DY |title=Cytokine modulation of atopic dermatitis filaggrin skin expression |journal=J. Allergy Clin. Immunol. |volume=124 |issue=3 Suppl 2 |pages=R7–R12 |date=September 2009 |pmid=19720210 |doi=10.1016/j.jaci.2009.07.012 |url=}}</ref>, tight junction abnormalities<ref name="pmid21163515">{{cite journal |vauthors=De Benedetto A, Rafaels NM, McGirt LY, Ivanov AI, Georas SN, Cheadle C, Berger AE, Zhang K, Vidyasagar S, Yoshida T, Boguniewicz M, Hata T, Schneider LC, Hanifin JM, Gallo RL, Novak N, Weidinger S, Beaty TH, Leung DY, Barnes KC, Beck LA |title=Tight junction defects in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=127 |issue=3 |pages=773–86.e1–7 |date=March 2011 |pmid=21163515 |pmc=3049863 |doi=10.1016/j.jaci.2010.10.018 |url=}}</ref>,  more alkaline surface pH,<ref name="pmid18329087">{{cite journal |vauthors=Elias PM, Hatano Y, Williams ML |title=Basis for the barrier abnormality in atopic dermatitis: outside-inside-outside pathogenic mechanisms |journal=J. Allergy Clin. Immunol. |volume=121 |issue=6 |pages=1337–43 |date=June 2008 |pmid=18329087 |pmc=2706021 |doi=10.1016/j.jaci.2008.01.022 |url=}}</ref> microbial colonization, altered protease activity in the stratum corneum.<ref name="pmid16815133">{{cite journal |vauthors=Cork MJ, Robinson DA, Vasilopoulos Y, Ferguson A, Moustafa M, MacGowan A, Duff GW, Ward SJ, Tazi-Ahnini R |title=New perspectives on epidermal barrier dysfunction in atopic dermatitis: gene-environment interactions |journal=J. Allergy Clin. Immunol. |volume=118 |issue=1 |pages=3–21; quiz 22–3 |date=July 2006 |pmid=16815133 |doi=10.1016/j.jaci.2006.04.042 |url=}}</ref><ref name="pmid23374260">{{cite journal |vauthors=McAleer MA, Irvine AD |title=The multifunctional role of filaggrin in allergic skin disease |journal=J. Allergy Clin. Immunol. |volume=131 |issue=2 |pages=280–91 |date=February 2013 |pmid=23374260 |doi=10.1016/j.jaci.2012.12.668 |url=}}</ref><ref name="pmid22951058">{{cite journal |vauthors=Margolis DJ, Apter AJ, Gupta J, Hoffstad O, Papadopoulos M, Campbell LE, Sandilands A, McLean WH, Rebbeck TR, Mitra N |title=The persistence of atopic dermatitis and filaggrin (FLG) mutations in a US longitudinal cohort |journal=J. Allergy Clin. Immunol. |volume=130 |issue=4 |pages=912–7 |date=October 2012 |pmid=22951058 |pmc=3462287 |doi=10.1016/j.jaci.2012.07.008 |url=}}</ref><ref name="pmid22521249">{{cite journal |vauthors=Morizane S, Yamasaki K, Kajita A, Ikeda K, Zhan M, Aoyama Y, Gallo RL, Iwatsuki K |title=TH2 cytokines increase kallikrein 7 expression and function in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=130 |issue=1 |pages=259–61.e1 |date=July 2012 |pmid=22521249 |pmc=3387356 |doi=10.1016/j.jaci.2012.03.006 |url=}}</ref>
**It leads to increased trans-epidermal water loss, and decreased levels of ceramides and antimicrobial peptides.<ref name="pmid19494826">{{cite journal| author=Cork MJ, Danby SG, Vasilopoulos Y, Hadgraft J, Lane ME, Moustafa M et al.| title=Epidermal barrier dysfunction in atopic dermatitis. | journal=J Invest Dermatol | year= 2009 | volume= 129 | issue= 8 | pages= 1892-908 | pmid=19494826 | doi=10.1038/jid.2009.133 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19494826  }} </ref>
**Severe Atopic Dermatitis have been associated with higher levels of transepidermal water loss.<ref name="pmid21137118">{{cite journal |vauthors=Flohr C, England K, Radulovic S, McLean WH, Campbel LE, Barker J, Perkin M, Lack G |title=Filaggrin loss-of-function mutations are associated with  early-onset eczema, eczema severity and transepidermal  water loss at 3 months of age |journal=Br. J. Dermatol. |volume=163 |issue=6 |pages=1333–6 |date=December 2010 |pmid=21137118 |doi= |url=}}</ref>
 
 
 
Immune dysregulation:
*Innate immune response:
**Innate immune system recognizes microbes or pathogens through innate immune receptors known as pattern recognition receptors(PRR) which also includes Toll-like receptors(TLRs).
 
 
*Adaptive immune response:
 
*Thymic stromal lymphopoietin:
 
 
 
 
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==Pathogenesis===
 
It is understood that Atopic dermatitis is the result of skin barrier dysfunction or by immune dysregulation.<ref name="pmid21682749">{{cite journal |vauthors=Boguniewicz M, Leung DY |title=Atopic dermatitis: a disease of altered skin barrier and immune dysregulation |journal=Immunol. Rev. |volume=242 |issue=1 |pages=233–46 |date=July 2011 |pmid=21682749 |pmc=3122139 |doi=10.1111/j.1600-065X.2011.01027.x |url=}}</ref>
*Dysfunction of the skin barrier:
**Skin barrier abnormalities lead to the permeability of epidermis, causing entry of antigens or pathogens and leading to the production of inflammatory cytokines.
**The major factors to abnormal skin barrier include loss-of-function mutations in the filaggrin gene (FLG) causing Filaggrin deficiency<ref name="pmid19720210">{{cite journal |vauthors=Howell MD, Kim BE, Gao P, Grant AV, Boguniewicz M, DeBenedetto A, Schneider L, Beck LA, Barnes KC, Leung DY |title=Cytokine modulation of atopic dermatitis filaggrin skin expression |journal=J. Allergy Clin. Immunol. |volume=124 |issue=3 Suppl 2 |pages=R7–R12 |date=September 2009 |pmid=19720210 |doi=10.1016/j.jaci.2009.07.012 |url=}}</ref>, tight junction abnormalities<ref name="pmid21163515">{{cite journal |vauthors=De Benedetto A, Rafaels NM, McGirt LY, Ivanov AI, Georas SN, Cheadle C, Berger AE, Zhang K, Vidyasagar S, Yoshida T, Boguniewicz M, Hata T, Schneider LC, Hanifin JM, Gallo RL, Novak N, Weidinger S, Beaty TH, Leung DY, Barnes KC, Beck LA |title=Tight junction defects in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=127 |issue=3 |pages=773–86.e1–7 |date=March 2011 |pmid=21163515 |pmc=3049863 |doi=10.1016/j.jaci.2010.10.018 |url=}}</ref>,  more alkaline surface pH,<ref name="pmid18329087">{{cite journal |vauthors=Elias PM, Hatano Y, Williams ML |title=Basis for the barrier abnormality in atopic dermatitis: outside-inside-outside pathogenic mechanisms |journal=J. Allergy Clin. Immunol. |volume=121 |issue=6 |pages=1337–43 |date=June 2008 |pmid=18329087 |pmc=2706021 |doi=10.1016/j.jaci.2008.01.022 |url=}}</ref> microbial colonization, altered protease activity in the stratum corneum.<ref name="pmid16815133">{{cite journal |vauthors=Cork MJ, Robinson DA, Vasilopoulos Y, Ferguson A, Moustafa M, MacGowan A, Duff GW, Ward SJ, Tazi-Ahnini R |title=New perspectives on epidermal barrier dysfunction in atopic dermatitis: gene-environment interactions |journal=J. Allergy Clin. Immunol. |volume=118 |issue=1 |pages=3–21; quiz 22–3 |date=July 2006 |pmid=16815133 |doi=10.1016/j.jaci.2006.04.042 |url=}}</ref><ref name="pmid23374260">{{cite journal |vauthors=McAleer MA, Irvine AD |title=The multifunctional role of filaggrin in allergic skin disease |journal=J. Allergy Clin. Immunol. |volume=131 |issue=2 |pages=280–91 |date=February 2013 |pmid=23374260 |doi=10.1016/j.jaci.2012.12.668 |url=}}</ref><ref name="pmid22951058">{{cite journal |vauthors=Margolis DJ, Apter AJ, Gupta J, Hoffstad O, Papadopoulos M, Campbell LE, Sandilands A, McLean WH, Rebbeck TR, Mitra N |title=The persistence of atopic dermatitis and filaggrin (FLG) mutations in a US longitudinal cohort |journal=J. Allergy Clin. Immunol. |volume=130 |issue=4 |pages=912–7 |date=October 2012 |pmid=22951058 |pmc=3462287 |doi=10.1016/j.jaci.2012.07.008 |url=}}</ref><ref name="pmid22521249">{{cite journal |vauthors=Morizane S, Yamasaki K, Kajita A, Ikeda K, Zhan M, Aoyama Y, Gallo RL, Iwatsuki K |title=TH2 cytokines increase kallikrein 7 expression and function in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=130 |issue=1 |pages=259–61.e1 |date=July 2012 |pmid=22521249 |pmc=3387356 |doi=10.1016/j.jaci.2012.03.006 |url=}}</ref>
**It leads to increased trans-epidermal water loss, and decreased levels of ceramides and antimicrobial peptides.<ref name="pmid19494826">{{cite journal| author=Cork MJ, Danby SG, Vasilopoulos Y, Hadgraft J, Lane ME, Moustafa M et al.| title=Epidermal barrier dysfunction in atopic dermatitis. | journal=J Invest Dermatol | year= 2009 | volume= 129 | issue= 8 | pages= 1892-908 | pmid=19494826 | doi=10.1038/jid.2009.133 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19494826  }} </ref>
**Severe Atopic Dermatitis have been associated with higher levels of transepidermal water loss.<ref name="pmid21137118">{{cite journal |vauthors=Flohr C, England K, Radulovic S, McLean WH, Campbel LE, Barker J, Perkin M, Lack G |title=Filaggrin loss-of-function mutations are associated with  early-onset eczema, eczema severity and transepidermal  water loss at 3 months of age |journal=Br. J. Dermatol. |volume=163 |issue=6 |pages=1333–6 |date=December 2010 |pmid=21137118 |doi= |url=}}</ref>
 
 
 
Immune dysregulation:
*Innate immune response:
*Adaptive immune response:
*Thymic stromal lymphopoietin:
 
 
 
 
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
 
OR
 
Genes involved in the pathogenesis of [disease name] include:
*[Gene1]
*[Gene2]
*[Gene3]


OR
==Conservative Therapy==


The development of [disease name] is the result of multiple genetic mutations such as:
{| class="wikitable"
|+
!'''Elimination of exacerbating factors'''
!'''Maintaining skin hydration'''
!'''Controlling pruritus'''
|-
|
* Avoid trigger factors such as low humidity, overheating of skin
* Treating stress and anxiety
* Avoid exposure to solvents and detergents
* Treat skin infections such as ''Staphylococcus aureus'' and herpes simplex
|
* '''Emollients and moisturizers'''
** Thick creams, ointments (eg, petroleum jelly) with low/zero water content
** Immediately after 5-minute, lukewarm baths BID
* '''Bathing practices'''
** Warm soaking baths or showers using mild or soap-free cleansers
|
* Conservative
** Tepid baths
** Wet dressings (wet wraps)
** Moisturizers containing anti-pruritic ingredients such as phenol, menthol, and camphor


*[Mutation 1]
*
*[Mutation 2]
|}
*[Mutation 3]


==Associated Conditions==
==Medical Therapy==
Conditions associated with [disease name] include:
*Pharmacologic medical therapies for atopic dermatitis can be classified according to the several severity scales( (i.e SCORAD index, the eczema area and severity index [EASI], and the patient-oriented eczema measure [POEM]) which includes characteristics of the rash, questions about itch, sleep, impact on daily activities, and persistence of disease.
===Atopic dermatitis===


*[Condition 1]
* '''MIld atopic dermatitis''':
*[Condition 2]
** Topical corticosteroids and emollients - mainstay therapy
*[Condition 3]
*** '''Adult'''
**** Preferred regimen (1): [[drug name|desonide 0.05%]] top. q12h-q24h for 14-28 days
**** Preferred regimen (2): [[drug name|hydrocortisone 2.5% top.]] q12h-q24h for 14-28 days
**** Preferred regimen (3): fluocinolone acetonide [[drug name|0.01% top.]] q12h-q24h for 14-28 days
**** Alternative regimen (1) tacrolimus 0.1% top. q8h ('''0.03% for adults who do not tolerate the higher dose)'''
**** Alternative regimen (2): pimecrolimus 1% top. q8h
**** Alternative regimen (3) crisaborole 2% top.
*** '''Pediatric'''
**** Preferred regimen (1): [[drug name|desonide 0.05%]] top. q12h-q24h for 14-28 days
**** Preferred regimen (2): [[drug name|hydrocortisone 2.5% top.]] q12h-q24h for 14-28 days
**** Preferred regimen (3):  fluocinolone acetonide [[drug name|0.01% top.]] q12h-q24h for 14-28 days
**** Alternative regimen (1) tacrolimus 0.03%  top. q8h ('''Children (>2years)'''
**** Alternative regimen (2): pimecrolimus 1% top. q8h
**** Alternative regimen (3): crisaborole 2% top.
*  '''Moderate atopic dermatitis'''
** Topical corticosteroids and emollients are the mainstay of therapy
*** '''Adult'''
**** Preferred regimen (1): fluocinolone0.025%. q12h-q24h for 14-28 days
**** Preferred regimen (2): [[drug name|triamcinolone 0.1% top.]] q12h-q24h for 14-28 days
**** Preferred regimen (3): fluocinolone acetonide [[drug name|0.025% top.]] q12h-q24h for 14-28 days
**** Alternative regimen (1) tacrolimus 0.1% top. q8h ('''0.03% for adults who do not tolerate the higher dose)'''
**** Alternative regimen (2): pimecrolimus 1% top. q8h
**** Alternative regimen (3) crisaborole 2% top.
** '''Pediatric'''
*** Preferred regimen (1): fluocinolone0.025%. q12h-q24h for 14 days
*** Preferred regimen (2): [[drug name|triamcinolone 0.1% top.]] q12h-q24h for 14 days
*** Preferred regimen (3): fluocinolone acetonide [[drug name|0.025% top.]] q12h-q24h for 14-28 days
*** Alternative regimen (1) tacrolimus 0.03%  top. q8h ('''Children (>2years)'''
*** Alternative regimen (2): pimecrolimus 1% top. q8h
*** Alternative regimen (3) crisaborole 2% top.
* '''Severe atopic dermatitis'''
** Phototherapy or systemic immunosuppressant treatment is the mainstay of therapy
*** '''Adult'''
**** Preferred regimen (1): Phototherapy Ultraviolet light therapy (phototherapy) with PUVA (psoralens plus ultraviolet A radiation), 3 times a week
**** Preferred regimen (2): [[drug name|cyclosporine]] PO 3-5 mg/kg o.d. for 6 weeks ('''monitor BP and serum creatinine q2 weeks for three months, f/u q month)''' 
**** Alternative regimen (1) methotrexatePO
**** Alternative regimen (2): azathioprine PO
**** Alternative regimen (3) mycophenolate mofetil PO
**** Alternative regimen (3) dupilumab 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter
*** '''Pediatric'''
**** Preferred regimen (1):
**** Preferred regimen (2): [[drug name|cyclosporine]] PO 3 to 5 mg/kg per day o.d. for 6 weeks ('''monitor BP and serum creatinine q2 weeks for three months, f/b q month)''' 
**** Alternative regimen (1) Phototherapy Ultraviolet light therapy (phototherapy) with PUVA (psoralens plus ultraviolet A radiation), 3 times a week
**** Alternative regimen (2): azathioprine PO
**** Alternative regimen (3) mycophenolate mofetil PO
**** Alternative regimen (3) dupilumab 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter
* '''Severe refractory atopic dermatitis'''
** '''Adult'''
*** Preferred regimen (1): Intensive topical therapy
**** Soak and smear: Soak for 15 minutes in a tub of water. Apply desoximetasone 0.25% top. to the whole body, except the groin, axillae, and face
**** Wet wrap therapy: desoximetasone 0.25% top. then occluded with wet wraps q12h
*** Alternative regimen (1) Phototherapy: narrowband ultraviolet B or psoralen plus ultraviolet A  two to three times per week
*** Alternative regimen (2): cyclosporine PO 2.5 to 5 mg/kg o.d. ('''C/I -''' '''abnormal renal function, uncontrolled hypertension or infection, and malignancy''')
*** Alternative regimen (3): prednisone 40 to 60 mg o.d. for one week, then taper the dose over the following two to three week
*** Alternative regimen (4): methotrexate 7.5 to 25 mg single weekly dose with folic acid 1 mg o.d.
*** Alternative regimen (5): azathioprine 2 to 3 mg/kg
*** Alternative regimen (6):  mycophenolate mofetil 1 to 2 g/day
*** Alternative regimen (7):  mycophenolic acid 720 to 1440 mg/day
*** Alternative regimen (8)  dupilumab 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter
** '''Pediatric'''
*** Preferred regimen (1): Intensive topical therapy
**** Wet wrap therapy: desoximetasone 0.05% top. then occluded with wet wraps q12h-q24h for 2 to 14 days
*** Alternative regimen (1) Phototherapy: narrowband ultraviolet B (UVB)  3 times per week ('''older children > 6 years''')
*** Alternative regimen (2): cyclosporine PO 2.5 to 5 mg/kg o.d. for 2-4 months ('''monitor renal and hepatic function''')
*** Alternative regimen (3): methotrexate 0.5 mg/kg PO single weekly dose with folic acid 1 mg o.d.('''up to a maximum of 25 mg per week''')
*** Alternative regimen (4): methylprednisolone 0.5 mg/kg o.d. for 1-2 weeks tapered over one month
'''Management of Infection:'''
* '''Bacterial''' '''infections''': (most common bacteria - ''Staphylococcus. aureus'')
** Clinically infected skin:
*** Mupirocin 2% top. BID for one to two weeks
*** More extensive infection: oral antibiotic therapy with cephalosporins or penicillinase-resistant penicillins X two weeks
** Clinically uninfected skin:
*** liquid chlorine bleach-  0.5 cup or 120 ml of 6% bleach in a full bathtub [40 gallons or 150 L] of lukewarm water
* '''Viral infections:'''
** Herpes simplex:
*** Acyclovir 200 or 400 mg PO five times daily
*** Famciclovir 750 mg BID for one day or 1500 mg as a single dose
** molluscum contagiosum :
*** cryotherapy, curettage, cantharidin, and podophyllotoxin as first-line therapeutic options
* '''Fungal infections:'''
** Dermatophyte infections'''-''' topical or oral antifungals
'''Controlling pruritus:'''
* Preferred regimen''':'''
** Sedatives: diphenhydramine, hydroxyzine, and cyproheptadine
** Nonsedatives: fexofenadine, cetirizine or loratadine
* Alternative regimen:
** Topical doxepin
** Topical calcineurin inhibitors
***  Pimecrolimus 1% cream or tacrolimus 0.03% to 0.1%


==Gross Pathology==
'''Chronic inflammatory skin diseases'''
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
* Contact (allergic, irritant)
* Seborrhoeic dermatitis
** onset during the 1st days or weeks of life, absence of pruritus, and presence of greasy scaling on a yellow-red base
** Involvement of the top of the scalp (cradle cap), axilla, and diaper area makes it more likely the patient has '''seborrheic dermatitis''', vs excoriated dermatitis involving the extensor surfaces, face, and trunk favour '''AE.'''
* Psoriasis
* Lichen simplex chronicus
'''Infectious agents'''
* Candida
* Dermatophytes
* Herpes simplex
* Staphylococcus aureus
* Sarcoptes scabiei
** highly pruritic, erythematous papular lesions. In most cases, the typical burrows can be found on the flexor wrists, finger webs and genitalia. Similar symptoms in other family members
* HIV-associated dermatitis
'''Immunologic disorders'''
* Dermatitis herpetiformis
* Pemphigus foliaceus
* Graft-versus-host disease
* Dermatomyositis
'''Malignant Diseases'''
* Cutaneous T-cell lymphoma (mycosis fungoides, S´ezary syndrome)
* Histiocytosis X (Letterer-Siwe disease)
'''Congenital disorders'''
* Netherton’s syndrome
* Dubowitz syndrome
* Erythrokeratodermia variabilis
'''Immunodeficiencies'''
* Wiskott-Aldrich syndrome (immunodeficiency with thrombocytopenia and eczema)
* Thymic hypoplasia (DiGeorge syndrome)
* Hyper-IgE syndrome
* Severe combined immunodeficiency (SCID)
* Ataxia teleangiectasia
'''Metabolic Diseases'''
* Phenylketonuria
* Tyrosinemia
* Histidinemia
* Zinc deficiency
* Pyridoxine (vitamin B6) and niacin deficiency
* Multiple carboxylase deficiency


==Microscopic Pathology==
* '''Nonallergic reaction to medication'''
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
** Infliximab


==References==
==References==

Latest revision as of 16:56, 10 October 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

The mainstay of treatment for atopic dermatitis depends upon the severity of the disease and is treated with 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.

Conservative Therapy

Elimination of exacerbating factors Maintaining skin hydration Controlling pruritus
  • Avoid trigger factors such as low humidity, overheating of skin
  • Treating stress and anxiety
  • Avoid exposure to solvents and detergents
  • Treat skin infections such as Staphylococcus aureus and herpes simplex
  • Emollients and moisturizers
    • Thick creams, ointments (eg, petroleum jelly) with low/zero water content
    • Immediately after 5-minute, lukewarm baths BID
  • Bathing practices
    • Warm soaking baths or showers using mild or soap-free cleansers
  • Conservative
    • Tepid baths
    • Wet dressings (wet wraps)
    • Moisturizers containing anti-pruritic ingredients such as phenol, menthol, and camphor

Medical Therapy

  • Pharmacologic medical therapies for atopic dermatitis can be classified according to the several severity scales( (i.e SCORAD index, the eczema area and severity index [EASI], and the patient-oriented eczema measure [POEM]) which includes characteristics of the rash, questions about itch, sleep, impact on daily activities, and persistence of disease.

Atopic dermatitis

  • MIld atopic dermatitis:
    • Topical corticosteroids and emollients - mainstay therapy
      • Adult
        • Preferred regimen (1): desonide 0.05% top. q12h-q24h for 14-28 days
        • Preferred regimen (2): hydrocortisone 2.5% top. q12h-q24h for 14-28 days
        • Preferred regimen (3): fluocinolone acetonide 0.01% top. q12h-q24h for 14-28 days
        • Alternative regimen (1) tacrolimus 0.1% top. q8h (0.03% for adults who do not tolerate the higher dose)
        • Alternative regimen (2): pimecrolimus 1% top. q8h
        • Alternative regimen (3) crisaborole 2% top.
      • Pediatric
        • Preferred regimen (1): desonide 0.05% top. q12h-q24h for 14-28 days
        • Preferred regimen (2): hydrocortisone 2.5% top. q12h-q24h for 14-28 days
        • Preferred regimen (3): fluocinolone acetonide 0.01% top. q12h-q24h for 14-28 days
        • Alternative regimen (1) tacrolimus 0.03% top. q8h (Children (>2years)
        • Alternative regimen (2): pimecrolimus 1% top. q8h
        • Alternative regimen (3): crisaborole 2% top.
  • Moderate atopic dermatitis
    • Topical corticosteroids and emollients are the mainstay of therapy
      • Adult
        • Preferred regimen (1): fluocinolone0.025%. q12h-q24h for 14-28 days
        • Preferred regimen (2): triamcinolone 0.1% top. q12h-q24h for 14-28 days
        • Preferred regimen (3): fluocinolone acetonide 0.025% top. q12h-q24h for 14-28 days
        • Alternative regimen (1) tacrolimus 0.1% top. q8h (0.03% for adults who do not tolerate the higher dose)
        • Alternative regimen (2): pimecrolimus 1% top. q8h
        • Alternative regimen (3) crisaborole 2% top.
    • Pediatric
      • Preferred regimen (1): fluocinolone0.025%. q12h-q24h for 14 days
      • Preferred regimen (2): triamcinolone 0.1% top. q12h-q24h for 14 days
      • Preferred regimen (3): fluocinolone acetonide 0.025% top. q12h-q24h for 14-28 days
      • Alternative regimen (1) tacrolimus 0.03% top. q8h (Children (>2years)
      • Alternative regimen (2): pimecrolimus 1% top. q8h
      • Alternative regimen (3) crisaborole 2% top.
  • Severe atopic dermatitis
    • Phototherapy or systemic immunosuppressant treatment is the mainstay of therapy
      • Adult
        • Preferred regimen (1): Phototherapy Ultraviolet light therapy (phototherapy) with PUVA (psoralens plus ultraviolet A radiation), 3 times a week
        • Preferred regimen (2): cyclosporine PO 3-5 mg/kg o.d. for 6 weeks (monitor BP and serum creatinine q2 weeks for three months, f/u q month)
        • Alternative regimen (1) methotrexatePO
        • Alternative regimen (2): azathioprine PO
        • Alternative regimen (3) mycophenolate mofetil PO
        • Alternative regimen (3) dupilumab 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter
      • Pediatric
        • Preferred regimen (1):
        • Preferred regimen (2): cyclosporine PO 3 to 5 mg/kg per day o.d. for 6 weeks (monitor BP and serum creatinine q2 weeks for three months, f/b q month)
        • Alternative regimen (1) Phototherapy Ultraviolet light therapy (phototherapy) with PUVA (psoralens plus ultraviolet A radiation), 3 times a week
        • Alternative regimen (2): azathioprine PO
        • Alternative regimen (3) mycophenolate mofetil PO
        • Alternative regimen (3) dupilumab 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter
  • Severe refractory atopic dermatitis
    • Adult
      • Preferred regimen (1): Intensive topical therapy
        • Soak and smear: Soak for 15 minutes in a tub of water. Apply desoximetasone 0.25% top. to the whole body, except the groin, axillae, and face
        • Wet wrap therapy: desoximetasone 0.25% top. then occluded with wet wraps q12h
      • Alternative regimen (1) Phototherapy: narrowband ultraviolet B or psoralen plus ultraviolet A two to three times per week
      • Alternative regimen (2): cyclosporine PO 2.5 to 5 mg/kg o.d. (C/I - abnormal renal function, uncontrolled hypertension or infection, and malignancy)
      • Alternative regimen (3): prednisone 40 to 60 mg o.d. for one week, then taper the dose over the following two to three week
      • Alternative regimen (4): methotrexate 7.5 to 25 mg single weekly dose with folic acid 1 mg o.d.
      • Alternative regimen (5): azathioprine 2 to 3 mg/kg
      • Alternative regimen (6): mycophenolate mofetil 1 to 2 g/day
      • Alternative regimen (7): mycophenolic acid 720 to 1440 mg/day
      • Alternative regimen (8) dupilumab 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter
    • Pediatric
      • Preferred regimen (1): Intensive topical therapy
        • Wet wrap therapy: desoximetasone 0.05% top. then occluded with wet wraps q12h-q24h for 2 to 14 days
      • Alternative regimen (1) Phototherapy: narrowband ultraviolet B (UVB) 3 times per week (older children > 6 years)
      • Alternative regimen (2): cyclosporine PO 2.5 to 5 mg/kg o.d. for 2-4 months (monitor renal and hepatic function)
      • Alternative regimen (3): methotrexate 0.5 mg/kg PO single weekly dose with folic acid 1 mg o.d.(up to a maximum of 25 mg per week)
      • Alternative regimen (4): methylprednisolone 0.5 mg/kg o.d. for 1-2 weeks tapered over one month

Management of Infection:

  • Bacterial infections: (most common bacteria - Staphylococcus. aureus)
    • Clinically infected skin:
      • Mupirocin 2% top. BID for one to two weeks
      • More extensive infection: oral antibiotic therapy with cephalosporins or penicillinase-resistant penicillins X two weeks
    • Clinically uninfected skin:
      • liquid chlorine bleach-  0.5 cup or 120 ml of 6% bleach in a full bathtub [40 gallons or 150 L] of lukewarm water
  • Viral infections:
    • Herpes simplex:
      • Acyclovir 200 or 400 mg PO five times daily
      • Famciclovir 750 mg BID for one day or 1500 mg as a single dose
    • molluscum contagiosum :
      • cryotherapy, curettage, cantharidin, and podophyllotoxin as first-line therapeutic options
  • Fungal infections:
    • Dermatophyte infections- topical or oral antifungals

Controlling pruritus:

  • Preferred regimen:
    • Sedatives: diphenhydramine, hydroxyzine, and cyproheptadine
    • Nonsedatives: fexofenadine, cetirizine or loratadine
  • Alternative regimen:
    • Topical doxepin
    • Topical calcineurin inhibitors
      •  Pimecrolimus 1% cream or tacrolimus 0.03% to 0.1%

Chronic inflammatory skin diseases

  • Contact (allergic, irritant)
  • Seborrhoeic dermatitis
    • onset during the 1st days or weeks of life, absence of pruritus, and presence of greasy scaling on a yellow-red base
    • Involvement of the top of the scalp (cradle cap), axilla, and diaper area makes it more likely the patient has seborrheic dermatitis, vs excoriated dermatitis involving the extensor surfaces, face, and trunk favour AE.
  • Psoriasis
  • Lichen simplex chronicus

Infectious agents

  • Candida
  • Dermatophytes
  • Herpes simplex
  • Staphylococcus aureus
  • Sarcoptes scabiei
    • highly pruritic, erythematous papular lesions. In most cases, the typical burrows can be found on the flexor wrists, finger webs and genitalia. Similar symptoms in other family members
  • HIV-associated dermatitis

Immunologic disorders

  • Dermatitis herpetiformis
  • Pemphigus foliaceus
  • Graft-versus-host disease
  • Dermatomyositis

Malignant Diseases

  • Cutaneous T-cell lymphoma (mycosis fungoides, S´ezary syndrome)
  • Histiocytosis X (Letterer-Siwe disease)

Congenital disorders

  • Netherton’s syndrome
  • Dubowitz syndrome
  • Erythrokeratodermia variabilis

Immunodeficiencies

  • Wiskott-Aldrich syndrome (immunodeficiency with thrombocytopenia and eczema)
  • Thymic hypoplasia (DiGeorge syndrome)
  • Hyper-IgE syndrome
  • Severe combined immunodeficiency (SCID)
  • Ataxia teleangiectasia

Metabolic Diseases

  • Phenylketonuria
  • Tyrosinemia
  • Histidinemia
  • Zinc deficiency
  • Pyridoxine (vitamin B6) and niacin deficiency
  • Multiple carboxylase deficiency
  • Nonallergic reaction to medication
    • Infliximab

References

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