DIAGNOSIS dan PENATALAKSANAAN DERMATITIS ATOPIK

I. PENDAHULUAN

In 1925, Coca ~ntroducedt he concept of atopy, meaning"out of place" or "strange," to s~gniIyt he hereditary tendenw

to develon aller-e ~est o food and inhalant substances -~ -

Affected families may manifest eczema, asthma, and hayfever in any combination. In 1933, Wise and Sulzberger, .. introduced the concept of atopic dermatitis, emphasizingthe cutaneous manifestations of the atopic diathesis. Atopicdermatitis is also known as ntopic eczei?za, iizfantile eczelita,flerttrnl oczemn, dissenriilnted neurodenilntitis, and prurigodinthsique (Besilier). Dermatitis generally begins inchildhood, but varying manifestations often persist intoadulthood.Although the tendency to develop atopic dermatitis isinherited, inheritance patterns do not follow strict Mendeleinpatterns, and the overall prevalence of atopic disease isincreasi0g.A child is at increased risk of developing atopy ifeither parent is affected. More than one-quarter of offspringof atopic motheis develop atopic dermatitis in the first 3months of life. If one parent is atopic, more than half hisherchildren will develop allergic symptoms by age 2. This raterises to 79% if both parents are atopic.Atopic delmatitis can be divided into three stages: infantileatopic dermatitis, occurring from 2 months to 2 years of age;childhood atopic dermatitis, from 2 to 10 years; and adultatopic dermatitis. In all stages, pruritus is the hallmark ofatopic dermatitis. Itching often precedes the appearanceof lesions, hence the concept that atopic dermatitis is "theitch that ~ashes." Useful diagnostic criteria include those ofHanifin and Rajka, the UK Working Parly, and the AmericanAcademy of Dermatology's Consensus Conference onPediatricAtopic Dermatitis (Boxes 5-1 and 5-2) *andrew

Debate has added to the already wide variety of historical namesfor the condition. Currently, atopic dermatitis and atopic eczemaare the most widely used. The World Allergy Organization hassuggested that ‘eczema’ should be used as an umbrella term, andsubdivided it into atopic eczema and non-atopic eczema [8].Historical terms such as Besnier’s prurigo, disseminated neurodermatitis,

Spatexudativ Ekzem and prurigo diathesique are now little used. We continue to use the term atopic dermatitis until theclinical relevance of dividing the disease into subgroups is confi rmed. *Rook

II. DEFINISIDermatitis atopik adalah keadaan peradangan kulit kronis dan residif, disertai gatal, yang umumnya sering terjadi selama masa bayi dan anak-anak, sering berhubungan dengan kadar IgE dalam serum dan riwayat atopi pada keluarga atau penderita

III. GAMBARAN KLINIS

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IV. ETIOPATOGENESIS

1.2. Pathophysiology1.2.1. Inflammatory mechanismAtopic dermatitis is a disease included in the eczema_dermatitis group. The dominant mechanismsof atopic dermatitis in lesional skin are governed byTh2 cell-related cytokines such as IL-4 and IL-13, andchemokines such as TARC (thymus and activationregulatedchemokine) and eotaxin.2 Among suchchemokines, the so-called Th2 chemokines such asTARC_CCL17 and MDC_CCL22 deserve special attention.These chemokines are chemotactic for Th2cells expressing the chemokine receptor CCR4. Accordingly,Th2 cells are usually observed at an eczematoussite.3This is, however, a pathology in the acute stage,

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and Th1 cells producing IFN-and IL-12 are reportedlydominant in the chronic stage.4 Langerhans cellsand mast cells are involved in the inflammatory responseby expressing a high affinity IgE receptor(FcRI) that causes antigen presenting cells and mastcells to release histamine, cytokines, etc.The Th2 cytokines IL-4 and IL-13 stimulate fibroblaststo produce periostin, protein causing keratinocytesto produce TSLP,5 which induces TARC_CCL17production by dendritic cells.6 Serum TARC_CCL17levels are useful as a short-term disease marker foratopic dermatitis and the test is covered by health insurance.Research on Th17 as a new effector cell forallergic reactions7 and on Treg (regulatory T cell)8

that controls overreaction is also in progress.In an eczematous lesion of atopic dermatitis, antimicrobialpeptides (defensins, cathelicidins, etc.) are inhibitedfrom being expressed by keratinocytes.91.2.2. Skin dysfunctionsExpression of ceramide10 and filaggrin11 decreases in

skin with atopic dermatitis, particularly in lesions,and is considered as a primary cause of barrier dysfunctions.It is also considered as a secondary phenomenonassociated with inflammation and as acause of atopic dermatitis. Atopic dermatitis is accompaniedby an acute itch allegedly due to a loweredthreshold of itch. Involvement of IL-31 has been reportedas a cause of the above.12

It is often experienced that itch due to atopic dermatitiscannot be well controlled with antihistamines.Histamine, substance P, and their receptors havebeen shown to play an important role in itch at the peripherallevel. Recently, the role of endogenous

opioids such as beta-endorphin and their receptors initching at the central level has received attention. Ithas been reported that morphine induces itch viaGRP receptors.13

1.3. EtiologyAtopic dermatitis is caused by combination of geneticand environmental factors.1.3.1. Genetic factorsRegarding genetic factors, some etiological candidategenes associated with atopic dermatitis have been reported.Major candidate genes reported to date includeCTLA4, IL18, TLR9, CD14, CARD4, PHF11,TLR2, SCCE, MCC, IL4R, GM-CSF, TIM1, CARD15,GSTT1, SPINK5, eotaxin, TGF1, IL13, RANTES,IL4, and FcRI. In a recent GWAS of Japanese samples,“2q12 (IL1RL1_IL18R1_IL18RAP),” “3p21.33(GLB1),” “3q13.2 (CCDC80),” “6p21.3 (MHC region),”“7p22 (CARD11),” “10q21.2 (ZNF365),” “11p15.4 (OR10A3_NLRP10),” and “20q13 (CYP24A1_PFDN4) ” have been reported as candidate genes.14

1.3.2. Etiological and exacerbating factorsA wide variety of etiological and exacerbating factorshas been proposed, with the importance level of eachvarying among individual patients. In addition, inflammationassociated with this disease will be elucidatedby both allergic and non-allergic mechanisms. Etiologicaland exacerbating factors vary among agegroups. While the dominant factors in the first half ofchildhood include foods, sweating, physical irritation(including scratching), environmental factors, microbes

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_fungi, the dominant factors in the second halfof childhood to adulthood include environmental factors,sweating, physical irritation (including scratching),microbes_fungi, contact allergens, stress, andfoods (Fig. 1).It is commonly experienced that sweating inducesitch leading to the aggravation of atopic dermatitissymptoms. Clinically, psychological stress is wellknown to exacerbate atopic dermatitis symptoms. Althoughthe mechanism is mostly unknown, an increasein sensory nerve fibers containing substance Pand CGRP is observed at inflammatory skin sites ofpatients with this disease.15

VIII. PENATALAKSANAAN

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DAFTAR PUSTAKA

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