Dermatitis & Urticaria

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

Department of Dermato Venereology

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

Dermatitis are divided into

Exogenous
Endogenous or

Acute
Chronic
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
dermatitis
Biopsy are usually done to rule out other conditions
Histopathology can differentiate between acute and
chronic dermatitis, eventhough most are
overlapping.
Microscopic findings :
Acute dermatitis
Epidermis
Intercellular edema (Spongiosis)
Intraepidermal vesicles
Mononuclear infiltrates
Dermis
Vasodilatations
Perivascular infiltrates
Chronic dermatitis
Epidermis
Spongiosis quietly absent
Intraepidermal vesicles are not
dominant
Mononuclear infiltrates
Acanthosis more dominant
Parakeratosis are appear
Dermis
Vasodilatations & perivascular
infiltrates are decrease
Thickening in sub-basal collagen
Allergic contact dermatitis
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 function
Substance : antigenisity (potency), the degree of exposure
Potency : Mol. Weight 5000 Da, antigenicity appears when bind to autolog skin
protein.
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
nodes
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.
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 :
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, and dry
skin.
Response to Delayed type hypersensitivity are
decrease
Defects on neutrophiles chemotactics

Trigger factors : Climates, temperatures, humidity and

the conditions inwitch allergens are too much in their
environments
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

Adulthood
Lichenifications on the fold area, palmar and
areola mammae
Diagnostic criterias of atopic dermatitis (Hanifin &
Rajka)
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 :
Xerosis
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
Conjunctivitis
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
Seborrheic dermatitis : is 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.
Dermatitis intertrigo is dermatitis on the fold areas

Predisposition factors are :

Sweating/humidity
Obesity
Friction between two surfaces of the skin
Occlusions

Clinical manifestations :
Circumscribed patch erythematous,
Sometimes this is superinfected with yeast
(Candida albicans)
Nummular dermatitis is 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
infections.
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.
 Management urticaria

Urticaria (1) :
• Urtica
• Transient edema in the upper dermis
• Transient leakage of plasma

Angioedema(1) :
• Edema in the upper/lower dermis and/or
subcutis
Four stages in the management of
urticaria

• Knowing the tipology of urticaria

• Knowing the causative factors
• Knowing the risk factors and some factors that
influence the uricaria
• Treatment and counceling stage
Tipology, causative factors and factors
that influence the urticaria (2)

Classifications Type

Physical urticaria

Ordinary urticaria Acute and chronic

episodic
Vasculitis urticaria

Angioedema without Def. C1 inh,

urtica Normal C1 inh
Contact urticaria
Frequency of the type ofurticaria (3)

Type % ase

Ordinary urticaria 60

Physical urticaria 35

Vasculitis Urticaria 5
 Pathogenesis of urticaria (4)
Idiopathic

Immunology
• Autoimmune (autoantibody FcɛRI or IgE)
• Ig E dependent (Type I hipersensitivitas)
• Immune complex (vasculitis urticaria)
• Complement dependent (def. C1-esterase inhibitor)

Non-immunology
• The substances that have direct effect on Mast cel (opiat,
codein, radiocontras, venoms, physical stimuli, estrogen, ACTH,
Thiamin)
• Aspirin, NSAID, pseudoalergen in the food (Salisilat, azo dyes,
food preservatives)
• ACE inhibitor
 Diagnosis of urticaria
are based on clinically
Laboratorium :
• Urticaria vaskulitis
• Deficiency of C1-esterase inhibitor
Simple clinical diagnosis of urtikaria
Onset Duration Urticaria
10 mnt. after < 1 hour Physical urticaria
stimulation
> 1 hour after > 1 day Delayed pressure
continously urticaria
pressure
10-30 mnt > 2 hours Contact urticaria k
exposed to
contactant
2 -24 Ordinary urticaria
hours
1–7 Vasculitis
days urticaria
Laboratory examinations
class Ax FBC SPT RAST WCD
Physical
Ord-acute
Ord-chron
Vasculitis
Angioedem
Contact

Klas ESR TA/TFT C4 ASST Biopsi Provok

Physical
Ord-acute
Ord-chronic
Vasculitis
Angioedema
Contact
Non farmacologic treatments

 Avoid the aggravating/precipatating factors (2)

 Inform how to prevent (2)

 Give symptomatic medicamentous (2)
 Consider for using NSAID (5)
 Consider for using codein, opiat (6)
 Consider for using ACE inhibitor (7)
Farmacologic treaments
First line
• Antihistamin H1
• Have sedative effects : Chlorpheniramin maleat,
Hidroksisin, diphenhidramin
• Have non sedative effects :Cetirizine, Loratadine,
Desloratadine, Fexofenadine
• Doxepin 10 mg
• Antihistamin H2
• Nifedipine
• Ketotifen fumarat
• Sodium chromoglycate
Second line
• cortikosteroid
• Stanozolol
• Sulfasalazine
• Methotrexate
Urticarial Vaskulitis
• Colchicine
• Dapsone + corticosteroid
• Indomethacine
• Hidroxychloroquine

All severe angioedem except of def. C1 ersterase inhibitor

can be given Adrenalin im/sc : 0,5 mL (pengenceran 1 :
1000) or inhalation
Third line
• Auto antibody hitamine-releasing :
• Plasmapharesis
• Cyclosporin A
• Immunoglobulin iv

Deficiency of C1-inh
Concentrate of C1 or fresh frozen plasma

Profilaksis
Steroid anabolic or plasmin inhibitor tranexamine acid
Development of treatment methode

• Imunomodulator that inhibit cytokine production

• Be careful on using of NSAID
• Downregulate production of autoimun antibodi
• Blocker of FcεRI mast cell
• Anti IgE substances