Chapter 14

ATOPIC DERMATITIS
(ATOPIC ECZEMA)
Donald Y. M. Leung, Lawrence F. Eichenfield, Mark Boguniewicz
Fitzpatricks Dermatology in General Medicine. 7th ed. New York:
McGraw-Hill Medical; 2008. P.146-58

Atopic dermatitis (AD)

Chronically relapsing skin disease
Most commonly during early infancy and
childhood
Frequently associated with abnonnalities in
skin barrier function & allergen sensitization

Epidemiology
AD major public health problem
worldwide
Prevalence in children of 10-20%
Prevalence of AD in adults is
approximately 1-3%
The prevalence much lower in agricultural
countries
There is also a female preponderance,
with an overall female/male ratio of
2
1.3:1.0

Jumlah anggota keluarga kecil

Etiologi dan
Patogenesis
Peningkatan
respon
imunologik

Gangguan
barier kulit
Gangguan
sistem imun
alamiah

Penurunan fungsi barier kulit akibat:

Penurunan regulasi gen yang berperan dlm
kornifikasi/keratinisasi (filaggrin dan loricrin)
Penurunan kadar ceramide
Peningkatan kadar enzim proteolitik endogen
Peningkatan penguapan kulit (trans-epidermal
water loss)
Sabun dan detergen, meningkatkan aktifitas protease
endogen, paparan thd protease eksogen dari debu tungau
rumah dan Staph.aureus juga merusak barier epidermis
5

Immunopathology of Atopic Dermatitis

Unaffected skin:
- mild epidermal
hyperplasia
- a sparse perivascular
Tcell infiltrate
- surface IgE.

Acute eczematous lesions:

- intercellular edema
(spongiosis) of
epidermis,
- dendritic APCs
- influx of T cells
- Eosinophils are rarely
present

Chronic skin:
- hyperplastic epidermis
with elongation of the rete
ridges
- prominent hyperkeratosis
- minimal spongiosis
- surface IgE increased

Cytokines and Chemokines

Orchestrated by the local expression of proinflammatory cytokines and chemokines.
Cytokines such as TNF- & IL-1, bind to
receptors on
the vascular endothelium, activating cellular
signaling pathways extravasation of
infIammatory cells.
Acute AD is associated with the production of
Th-2 type cytokines, notably IL-4 and IL-13.
Chronic AD involved IL-5, IL-12, IL-13, IL-11 and
TGF-1.
7

Genetics
Filaggrin gene is found on chromosome
lq21
Variants in the SPINK5 gene influence the
balance of protease versus protease
inhibitor activity
Functional mutations in promoter region of
the C-C chemokines, RANTES and eotaxin.

Patogenesis

Disfungsi
sawar kulit

Abnormalitas
imunologik

Disregulasi
apoptosis

Peran
superantigen
stafilokokus

Proksch dan Elias,

2001

Clinical Findings
Typically begins during infancy. 50% by the first
year of life and 30% between the ages of 1-5
years.
50 -80% of AD patients develop allergic rhinitis
or asthma
later in chiJdhood.
Pruritus may be intermittent, but is usually worse
in the early evening and night.
9

Acute lesions
Intensely pruritic, erythematous papules,
excoriation, vesicles over erythematous skin, and
serous exudate

Subacute
lesions
erythematous, excoriated and scaling papules.

Chronic lesions
thickened plaques of skin, accentuated skin
markings (lichenification), and fibrotic papules
(prurigo nodularis
10

In chronic AD, all three stages of skin

reactions frequently co-exist in the same
individual.
During infancy, generally more acute and
primarily involves the face, scalp, and
the extensor surfaces of the extremities.
In older children develops chronic lesions
with lichenification and localization of the
rash to the flexural folds of the
extremities
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12

13

14

15

16

Laboratory Tests
Not needed in the routine evaluation.
Serum IgE levels are elevated in approximately 7080% patients but 20-30% have normal result.
Some of these patients may sensitive to microbial
antigens, as well some of these patients show positive
reactions using the atopy patch test.
The majority of patients with AD also have peripheral
blood eosinophilia and increased spontaneous
histamine release from basophils.
17

Diagnosis & Differential Diagnosis

Diagnosis: based on
clinical findings by
Hanafin and Rajka
18

Lists of skin disorders that

share symptoms and
signs with AD.

Should be considered
and ruled out before a
diagnosis of AD is made.

19

Complications
Ocular Problems

21

Hand Dermatitis

22

Topical Therapy
CUTANEOUS HYDRATION

Berendam atau kompres (wet dressing)

Emolien mengatasi kulit kering krn kekurangan ceramide
dan steroid sparing, serta utk terapi pemeliharaan.

TOPICAL GLUCOCORTICOID THERAPY

Topical glucocorticoids are the cornerstone of treatment.
The ultrahigh-potency glucocorticoids should be used only
for very short periods of time and in areas that are
Iichenified but not on the face or intenriginous areas.
Mid potency glucocorticoids can be used for longer periods
to treat chronic AD involving the trunk and extremities.
23

TOPICAL CALCINEURIN
INHIBITORS
Tacrolimus ointment 0.03% has been approved for
intermittent treatment of moderate to severe AD in
children aged 2 years and older, with tacrolimus
ointment 0.1 percent approved for use in adults.
Pimecrolimus cream I percent is approved for
treatment of patients aged 2 years and older with mildmoderate AD.
Both drugs have proven to be effective with a good
safety profile for treaonent up to 4 years with
tacrolimus ointmencSl and up to 2 years with
pimecrolimus cream
24

Identification and elimination of

triggering factors
Important to identify and eliminate aggravating
factors that trigger the itch scratch cycle.
These include soaps or detergents, contact with
chemicals, smoke, abrasive dothing, exposure to
extremes of temperature and humidity, alcohol,
astringents, formaldehyde and other added
chemicals in new clothing.
Living conditions (temperature and humidity) control
to avoid problems related to heat, humidity and
perspiration.

25

Potential allergens can be identified by taking a careful

history and carrying out selective skin prick tests or
specific serum IgE levels.

Positive skin or in vitro tests should be confirmed with

controlled food challenges and elimination diets

lnfants and young children are more likely to have food

allergies, whereas older children and adults are more
likely to be sensitive to aeroallergens.
26

 Emotional stress does not cause AD, it often

exacerbates the illness.
Infectious treatment such as anti-staphylococcal
antibiotics (cephalosporins, dicloxacillin, oxacillin
or cloxacillin) or antiviral treatment for cutaneous
herpes simplex infections.
Treatment of pruritus (systemic antihistamines or
doxepin hydrochloride)

27

Preparat Tar
Memiliki efek anti-pruritus dan antiinflamasi
Berguna utk menurunkan potensi
glukokortikoid topikal, ttp tdk boleh
digunakan utk kulit yg inflamasi. skin
Sampo Tar dapat berguna utk dermatitis
skalp

28

Fototerapi
Broadband UVB,
broadband UVA,
narrowband UVB (311
nm), UVA-I (340 to 400
nm), and kombinasi UVA-B
dpt berguna utk
tambahan terapi DA.

Fotokemoterapi dgn
psoralen dan sinar UVA
diindikasikan utk pasienpasien DA dgn lesi luas
atau berat.

Hospitalisasi
Pasien-pasien DA yg mjd eritroderma atau DA berat dan
resisten thd terapi rawat jalan hrs dihospitalisasi sebelum
mempertimbangkan terapi-terapi sistemik alternatif.
29

Terapi Sistemik
GLUKOKORTIKOID SISTEMIK
Jarang diindikasikan untuk pengobatan DA
kronik.
Glukokortikoid oral jangka pendek dpt
berguna utk eksaserbasi akut DA sementara
modalitas terapi lainnya diberikan.
Penting utk menurunkan dosis dan memulai
perawatan kulit secara intensif.

30

SIKLOSFORIN
Bekerja terutama pd sel-sel T dgn menekan
transkripsi sitokin.
Pengobatan siklosporin jangka pendek
bermanfaat utk anak-anak dan dewasa dgn DA
berat atau refrakter thd terapi konvensional.
Umumnya digunakan dosis 5 mg/kg BB efektif
utk pengobatan jangka pendek atau jangka
panjang (1 thn), beberapa penulis
menggunakan dosis 150 mg (dosis rendah) atau
300 mg (dosis tinggi) per hari siklosporin
mikroemulsi.
31

ANTIMETABOLIT
Open-label studies melaporkan mikrofenolat
mofetil jangka pendek, 2 g per hari, sebagai
monoterapi memberikan remisi lesi-lesi kulit pd
dewasa dgn DA resisten thd pengobatan lain.
Tetapi, hrs dihentikan jika pasien tdk berespon
dalam 4-8 minggu.
Metotreksat telah digunakan untuk pasien-pasien
DA dengan penyakit yg rekalsitran, meskipun
studi-studi terkontrol msh kurang.
Azatioprin telah digunakan utk DA berat,
meskipun belum ada percobaan-percobaan
terkontrol yg pernah melaporkan hal ini.

32

Terapi-terapi yg belum
terbukti
INTERFERON-

Menekan respon IgE

dan penurunan
regulasi proliferasi
dan fungsi sel Th2.
Penurunan derajat
beratnya klinis DA
berkaitan dgn
penurunan jumlah
eosinofil dalam
sirkulasi.

OMALIZUMAB

Anti-lgE monoklonal
kurang efektif untuk
pasien DA dewasa,
tetapi memberikan
perbaikan yg
signifikan pada
pasien-pasien DA
remaja.
33

IMUNOTERAPI
ALERGEN

Studi-studi terkontrol
Studi-studi terkontrol
msh diperlukan utk
msh diperlukan utk
menentukan peran
menentukan peran
imunoterapi thd penyakit
imunoterapi thd penyakit
ini.
ini.
PROBIOTIK
Pemberian probiotik
Pemberian probiotik
perinatal berupa strain GG
perinatal berupa strain GG
Lactobacillus rhamnosus
Lactobacillus rhamnosus
menunjukkan penurunan
menunjukkan penurunan
insiden DA pd anak yg
insiden DA pd anak yg
beresiko tinggi selama 2
beresiko tinggi selama 2
tahun pertama kehidupan.
tahun pertama kehidupan.

FOTOFERESIS
EKSTRAKORPOREA
L

Penyaluran psoralenPenyaluran psoralentreated leukocytes

treated leukocytes
melalui sistem sinar
melalui sistem sinar
UVA ekstrakorporeal.
UVA ekstrakorporeal.
CHINESE
HERBAL

Respon biasanya
Respon biasanya
bersifat temporer, dan
bersifat temporer, dan
efektifitasnya bisa
efektifitasnya bisa
hilang meskipun terapi
hilang meskipun terapi
dilanjutkan.
dilanjutkan.
34

Prognosis dan perjalanan

penyakit
Periode remisi lebih sering terjadi dengan
pertambahan usia pasien.
Resolusi spontan DA telah dilaporkan tjd setelah
usia 5 thn (40%-60%) selama masa bayi, terutama
jika penyakitnya ringan.

35

TERIMA