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dr. Fajar Waskito, Sp.KK(K), M.Kes

dr. Agnes Sri Siswati, SpKK(K))

Department of Dermato Venereology

Faculty of Medicine
Gadjah Mada University
Inflammation of the skin
Not because of infections or malignancy
Itching, burning or stinging
Skin lesions are polymorphic

Dermatitis are divided into

Endogenous or

Prevalence :
•Exogenous dermatitis are the most prevalence
•Irritant contact dermatitis is the most prevalence in
most part of Asia, Africa and south America
•Allergic contact dermatitis is the most prevalence in
US and most European countries

Pathology :
•The histologic changes are often similar among
•Biopsy are usually done to rule out other conditions
•Histopathology can differentiate between acute and
chronic dermatitis, eventhough most are
Microscopic findings :

Acute dermatitis Chronic dermatitis

Epidermis Epidermis
Intercellular edema (Spongiosis) Spongiosis quietly absent
Intraepidermal vesicles Intraepidermal vesicles more
Mononuclear infiltrates dominant
Mononuclear infiltrates
Acanthosis more dominant
Parakeratosis are appear
Dermis Dermis
Vasodilatations Vasodilatations & perivascular
Perivascular infiltrates infiltrates are decrease
Thickening in sub-basal collagen
Allergic contact dermatitis
Repeated skin contact with substance
Elicit sensitisation via cell mediated immunity
Some factors that influence the occurrence :
Human : genetics (HLA), immune responses are in normal
Substance : antigenisity (potency), the degree of exposure

Potency : Mol. Weight 500 Da, antigenicity appears when bind to autolog skin

More frequent and longer contact of substance to the skin the

probability of the appearance of allergic reactions are more bigger
Skin : the degree of penetration
Sensitisation is easier on the damage or inflammed skin or in
occluded skin
Mechanisms of sensitization
Combining the substance (hapten) with skin
protein to form antigen
Processing antigen by Langerhans cell (APC)
Presenting antigen to lymphocytes in Lymph
Lymphocytes are altered and proliferate
Altered Lymphocytes are travelled throughout the
body to produce sensitivity of entire skin

It requires a minimum of 8 – 10 days for clinical allergy to be

demonstrated after the sensitization process has started.
Pathology :
The histologic are not diagnostic
Biopsies are just to rule out other conditions
Acute stages :
3 hours after application of allergen
Vasodilatation and perivascular infiltrates in the dermis
At 6 hours, changes in the dermis more pronounced.
Spongiosis of the lowermost epidermis and exocytosis.
12 – 24 hours, the changes in the epidermis more marked
(vesicles), acanthosis. Perivascular infiltrate in the dermis
more pronounced
After 2 days, spongiosis disappears; intraepidermal vesicles
and acanthosis are the main features with parakeratosis

Chronic stages :Acanthosis, hyperkeratosis, variable

inflammatory cell infiltrates.
Nickel allergy from metal accessory
SHOE ACD, linnen
collorant and rubber
Clinical manifestations :
Polymorphic, not well demarcated, lateralisation
Evaluate the locations & pattern of the lesions.

Confirmation test : Patch test or repetitive open

epicutaneous test
Example of substance that cause ACD in dentists :
Some substances have been used by dentists, may be have
same effects to dental assistants, dental laboratory
technicians and patients

The substances are : Glutaraldehyde, latex gloves, procaine,

Lidocaine, Eugenol, dental composite resin products
(Bisphenol A & Acrylate), the catalysts from the two
impression materials Impregum and Scutum. Mercury and
Metals in modern alloy (rare)
Treatment :
Non pharmacotherapy : Eliminations
Pharmacotherapy :
Systemic : antihistamin ?, short course steroid
Topical : Steroid
Irritant contact dermatitis (ICD)

ICD are divided into acute & chronic cumulative irritant

The mechanisms are non immunologic
Acute irritant can be sufferred on every individu (eg. strong acid
or strong alchali)
Chronic cumulative can elicit reactions if the substances are in
repeated contact and on skin damage (eg. The weak acid or
alchali, detergent)

Clinical manifestations :
The lesions usually are well demarcated on the skin contact.

Treatment are the same with ACD

Atopic dermatitis :
A multifactorial, chronic inflammatory skin disorder
in which genetic mutations and cutaneous
hyperreactivity to environmental stimuli play a
causative role
 Genetic background
 Disfunction of immune system (Tend to form IgE
in contact with common antigens)
 Tend to suffer Asthma bronchiale, Hay fever,
urticaria both in theirselves or their parents,
 Defects on neutrophiles chemotactics

Trigger factors : Climates, temperatures, humidity and

the conditions inwitch allergens are too much in their
Atopic dermatitis in clinical setting are divided
into :

Infantil (age 2 – 6 months)

The lesions are commonly occur on the face,
diaper area and on extensor surface. The lesions
tend to wet

Childhood (age 2 – 12 years)

The lesions are commonly flexural distributed,
and the lesions tend to dry

Lichenifications on the fold area, palmar and
areola mammae
A genetic predisposition
Increased levels of stratum corneum chymotryptic enzyme (protease enzyme)
premature breakdown of corneodesmosomes,

Skin barrier defects


Environmental exposure Immune response

• Washing with soap and detergents, or long- • During the first 6months of a baby’s
term application of topical corticosteroids life, the TH1 are switching to TH2 cells,
• Exogenous proteases from house dust mites • Increased production of IL-4, IL-5, IgE
and Staphylococcus aureus.
Defisiency of vital components of stratum
corneum & lack of keratinocyte differentiation

Decreasing Allergen
IL-4 • Involucrin penetration
IL-5 • Occludin Bacterial
IL-13 • Filaggrin colonization
IL-22 • Loricrin
• Claudins
Chronic skin • Keratin Skin barrier
inflammation • Desmogleins defects
• Desmocollin
• Lipid molecules
Diagnostic criterias of atopic dermatitis (Hanifin &
Minimally have been found 3 major criterias and 3
minor criterias
Major criterias :
 Pruritus
 Characteristic morphology and distribution of
the lesions
 Chronic recalcitrans dermatitis
 History of atopic in their parents or theirselves
Minor criterias :
Keratosis pilaris
Hiperlinearis palmaris
Reactivity to type I hypesensitivity testing
Serum IgE is increase
Tend to get bacterial infections (S. aureus, H. simplex
Hand & foot dermatitis
Dermatitis on areola mammae
Dennie Morgan folds
Keratoconus anterior/Subcapsulair cataract
Periorbital darkening
Facial pallor,
Pirtyriasis alba,
Anterior neck fold,
Itching when sweating,
Woolly toleransion,
Perifolicular papules,
Food intolerance,
Influenced by environment and emotion,
white dermographisme
Diepgen’s criteria
• Diatesis kulit atopic > 10
• Clinical performance: Sensitivity: 83-87,7%; spesivisity 83,9-87%
Atopic diathesis Point
Xerosis 3
Itching while sweating 3
White dermographisme 3
Wool intolerance 3
Pityriasis alba 2
Infraorbital fold 2
Heroghe’s sign 2
Hyperlinearis palmaris 2
Ear rhagade 2
Lips rhagade (perleche) 1
Cradle cap 1
Atopic history in the family 1
Facial pallor/erythema 1
Keratosis pilaris 1
Food intolerance 1
Allergy rhinitis 1
Allergy asthma 1
Metal sensitive 1
Photophobia 1
How to select moisturizers

• Carring adequately the skin barrier defect

• Improving filaggrin def & reduced natural skin lipids
• Restore the Intercellular lipid bilayer ability to absorb, retain &
redistribute water
• Penetrate & contribute to reorganization of the structure of skin layers

They’re facilitated by characteristic of such ingredients

• Occlusive (intercellular lipid bilayer such as ceramide, cholesterol & free
fatty acids) traps water because of hydrophobic film to retard TEWL of SC
• Humectans (NMF in corneocytes)
1. Absorbs, retain & redistribute water
2. Attract & bind water from deeper epidermis to SC
• Emollient (Natural lipid found on skin and sebum) that mimics epidermal
lipid are skin smoothening by filling the cracks between desquamating
Seborrheic dermatitis :
dermatitis that distributed on seborrheic area

Clinical manifestations :
White to yellow scales with erythema on well
demarcated area. Males are more prevalence

Seborrheic dermatitis is divided clinically into :

Infant type : appears on the first 2-3 months of their
lives, and the peak is on 6-8 weeks (may because of
hormonal effects from their mother)
Adult type : appears after puberty and the peak is on
18-40 years. Dandruff is one of the manifestations of
seborrheic dermatitis.
Nummular dermatitis
dermatitis in nummular (=coin, discoid)
configurations and very itchy

Predilections are especially on the extensor surface of

lower extremities

Predispositions are females on middle age. Trauma is

one of the initiating factors beside of emosional stress

Clinical manifestations are almost the same with tinea

corporis (ringworms), but the borders of the lesions
tend to vesiculous
Neurodermatitis = Lichen simplex chronicus

The chief of clinical manifestations are itching,

lichenifications without atopic predisposition that appears
especially on the nape of neck, lower extremities, vulva,
pubis, scrotum and ankle.

Lichenifications is as manifestation of repeated scrubbing

or scratching.

Emosional stress is known as aggravating factors

Napkin dermatitis is a general term to discribe
some dermatoses on the lower abdomen, genitalia,
buttock and upper thigh of the baby, children,
incontinentia and paralytic patients

Causatives :
As combinations of some factors eg. Wet, friction,
irritation, napkin and sometime the candida
Dermatitis intertrigo is dermatitis on the
fold areas

Predisposition factors are :

Friction between two surfaces of the skin

Clinical manifestations :
Circumscribed patch erythematous,
Sometimes this is superinfected with yeast
(Candida albicans)
Dermatitis venenata = cantharides dermatitis =
Primary irritant contact dermatitis

Dermatitis as manifestation of contact with strong

irritant (eg. Cantharidin)

Stasis dermatitis is dermatitis that appeared on the

distal site of varicous veins. It will appeared especially
on the medial part of lower extremities, inwitch the
vascularitations are not good if compare with
another regions.