Eczema

Definition
Eczema/dermatitis is a type of
polymorphic inflammatory reaction pattern
involving the epidermis and dermis which
may be provoked by a number of external
or internal factors and can be defined
histologically by spongiosis and interstitial
vesicles.
 Eczema’s clinical stages
erythematous (dermatitis)
vesiculous (papulovesicular eczema)
exudative (oozing, weeping eczema)
crustification (crusted eczema)
descuamative (scaling eczema)
lichenification (lichenoid eczema)
 Clinical Features
Acute eczema: it is an erythema and
edema in plaques, usually with ill-defined
borders. Afterwards pruritic vesicles,
exudation, crusting and finally scaling. The
resolution is without scars.
Chronic eczema: it is less vesicular and
exudative, more scaly, pigmented and
thickened, more likely to develop painful
fissures and to be lichenified.
 Classification
Exogenous eczemas: irritant contact
dermatitis, allergic contact dermatitis;
Endogenous eczemas: atopic dermatitis;
Exo-endogenous eczemas: dyshidrotic
eczema, discoid (nummular) eczema,
seborrhoeic eczema (dermatitis), microbial
eczema, mycotic eczema, varicose
eczema, asteatotic eczema, etc.
Irritant contact eczema (dermatitis)
Irritant contact dermatitis: it is nonimmunologic local
inflammatory reaction following single or repeated
exposures to toxic chemicals.
 a. acute irritant contact dermatitis: strong irritants
produce it after a single application or a few applications.
Clinical aspect: erythema, edema, vesicles or bullae,
something necrosis. Reactions occur within minutes to
hours after exposure to the chemical agent, are localized
to the areas of maximal contact and have sharp borders.
In most cases, healing appears soon after exposure.
 b. chronic irritant dermatitis: it is due to repeated
insults by low grade irritants. The clinical appearance
ranges from dryness and cracking of the skin to
erythema, vesicles, scaling, fissuring and gradual
thickening. The lesions have a poor demarcation from
the surrounding skin. This dermatitis may takes weeks,
months or even years to develop.
Allergic contact eczema (dermatitis)
Allergic contact eczema (dermatitis): several or
many exposures are usually necessary before
sensitization
 acute allergic contact dermatitis is
characterized by erythema, edema, vesicles,
exudation, crusting and scaling. Pruritus is
present.
 chronic allergic contact dermatitis: the skin
becomes dry, scaly and thicker. Fissures and
lichenification may develop later. Secondary
dissemination to distant regions is frequent.
Special types:
 allergic phytodermatitis
 contact urticaria: nonimmunologic or allergic;
 phototoxic and photoallergic contact dermatitis;
 dermatitis for airborne agents et al.
Etiology of contact dermatitis
Contact irritants: alkalis, acids, phenolic
compounds, amines, organic solvents, sulfur,
retinoic acid, iodine, detergents, petroleum
products et al.
Contact allergens: nickel, chromium, cobalt,
formaldehyde resins, epoxy resins, acrylates,
topical drugs, cosmetics, plants, colorants,
perfumes, preservatives, et al.
Contact phyto-allergens: pentadecylcatechols
(phenolic compound), which are present in
poison ivy, poison oak, poison sumac, Brazilian
pepper, cashew nut tree, ginkgo tree, Indian
marker nut tree, lacquer tree, mango tree,
rengas tree.
 Pathogenesis of contact eczema
Irritant contact dermatitis: irritant substances are capable of
producing a direct toxic injury and an inflammatory reaction in
the skin in every person, after the contact. Immunological
processes are not involved. Factors affecting the cutaneous
response are: the substance’s chemical and physical
properties, concentration, vehicle, duration of exposure,
patient’s age, area of action, underlying dermatitis, genetic
make-up, environmental factors etc.
Allergic contact dermatitis is a type IV, delayed, cell-mediated
reaction. Initially, a hapten contacts the skin and forms a
hapten-carrier protein complex. This complex associated in
epidermal Langerhans cell, which presents this complete
antigen to a T-helper cell, causing the release of various
mediators. T-cell expansion in regional lymph nodes produces
specific memory and T-effectors lymphocytes which circulate
in the general bloodstream. The duration of process of
sensitization is 5 to 21 days. Upon re-exposure to the specific
antigen, a proliferation of activated T cell is produced, the
mediator release and the migrations of cytotoxic T-cells,
resulting in an inflammation, which appear in 48 to 72 hours
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 Atopic eczema: definition
Atopic eczema (dermatitis) is an acute,
subacute or chronic relapsing skin
disorder that usually begins in infancy
(after first 2 months) and is characterized
principally by marked pruritus, which with
rubbing and scratching leads to
lichenification (hyperplasia of the skin).
The serum IgE level is usually elevated.
A personal or family history of atopic
eczema, allergic rhinitis and asthma is
often associated.
Pathogenesis of atopic eczema
The pathogenesis of atopic eczema is complex, but
involves immunological abnormalities, environmental
factors and emotional influence
Immunological abnormalities in the atopic state include
increased serum total IgE and specific IgE antibodies to
ingested or inhaled antigens, and preferential activation of
the Th2 phenotype CD4 T-cells, which form IL-4 and IL-5.
The interleukins stimulate IgE synthesis by B-cells /
plasmocytes (type I hypersensitivity)
Staphylococci colonize the skin of patients with atopic
eczema, and staphylococcal exotoxins with superantigen
properties are also thought to play a pathogenic role in T-
an B-cell abnormal activity.
It has been shown that epidermal Langerhans cells
possess high affinity IgE receptors through which an
eczema-like reaction (type IV hypersensitivity) could be
mediated.
Both, type I and IV, hypersensitivities maintain and mutual
amplify vicious course of atopic eczema.
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Atopic eczema: genetic aspects
The inheritance pattern is probably autosomal-
dominant
60% of adults with atopic eczema have children
with atopic eczema
The prevalence in children is 80-85% when both
parents had atopic eczema
HLA haplotype associations:
 atopic eczema – HLA B9;
 hay fever (allergic rhinitis/conjunctivitis) – HLA B12;
 allergic asthma – HLA B2, B7 şi B40.
 Atopic eczema: eliciting factors
Foods: eggs, milk, peanuts, soybeans, fish, and wheat
Inhalants: specific aeroallergens, especially dust mites
Microbial agents: exotoxins of Staphylococcus aureus
may act as superantigens; group A streptococcus,
herpes simplex virus, fungus (candidiasis and
dermatophytosis)
Skin dehydration: frequent bathing and hand washing
Hormonal: pregnancy, menstruation, thyroid
Season: in temperate climates, usually improves in
summer, flares in winter
Clothing: pruritus flares after taking of clothing; wool
clothing or blankets directly in contact with skin
Emotional stress: primary or secondary resulting from the
disease
Atopic eczema: basic clinical features
(by Hanifin and Rajka)
Pruritus (if there is no scratching, there is
no eruption) - itch scratch rash itch;
Typical morphology and distribution of
lesions for age;
Chronic or chronically relapsing course;
Personal or family history of asthma,
allergic rhinitis, or atopic eczema.
Atopic eczema at different ages
Infantile phase (2 mo – 2 yrs): characterized by intense
itching, erythema, papules, vesicles, oozing and crusting;
typically location on cheeks, forehead, and scalp (acute
eczema).
Childhood phase (3-11 yrs): more chronic, lichenified
scaly patches and plaques that may have crusting and
oozing; classic areas include the wrists, ankles, backs of
the thighs, buttocks, and antecubital and popliteal fossae
(subacute eczema).
Adolescent/young adult phase (12-20 yrs): thick, dry,
lichenified plaques that involve the face, neck, upper
arms, back, and flexures (chronic or lichenified eczema).
Adult phase (>20 yrs): most commonly involves the
hands, sometimes the neck and face, and rarely diffuse
areas (lichenified eczema, nummular eczema,
neurodermitis). Only 10% of infantile or childhood cases
of atopic eczema persist into adulthood.
Atopic eczema: minor clinical features
Dry skin
Keratosis pilaris (follicular horny plugs)
Hyperlinear palms and soles
Periorbital bluish discoloration
Dennie-Morgan lines (double infraorbital fold)
Pityriasis alba (dry streptococcal skin infection)
Vascular abnormalities (skin pallor)
Cataracts
White dermatographism
 Dyshidrotic eczema
Supposed association with increased
sweat gland
Crops of clear, deep-seated vesicles on
the palms and sides of the fingers, rarely
present on soles as well
High prevalence of atopy
Sensibility to nickel, fungi, oral allergens,
etc.
 Nummular (discoid) eczema
Rapid onset of tiny papules and papulovesicles
that form erythematous, coin-shaped plaques,
ranged in size 1-10cm in diameter, resting on a
background of dry skin
Most commonly occur on the extensor surfaces
of the lower extremities, and often a bilaterally
symmetrical, may recur at the sites of previous
involvement, and are typically pruritic
It is related to dry skin, and aggravated by wool,
soaps, frequent bathing, and S. aureus
colonization – may be a clinical presentation of
atopic eczema in adults.
Seborrheic eczema (dermatitis)
Presents in infants from 2-10 weeks until 8-12
months, and then reappears at puberty
In adults, from the beginning – dandruff; then
dull or yellowish-red, sharply marginated, non-
pruritic lesions covered with greasy scales on
medial eyebrows, glabella, naso-labial crease,
eyelid margins, post-auricular and ear canal,
presternal or interscapular areas; intertriginous
areas, such the inframammary crease,
umbilicus, anogenital and genitocrural folds are
occasionally involved
Sensitizing to Pityrosporum or Malassezia
yeasts
 Eczema: treatment and prevention
1. Avoidance of as many irritants as possible;
2. Allergen avoidance;
3. Systemic therapy: antihistamines, glucocorticoids in severe cases;
4. Topical treatment:
 Drying agents (aluminum sulfate, calcium acetate), in acute, vesicular,
weeping eruptions;
 Corticosteroids: can be super, high, mid or low potent.
a. from superpotent corticosterids are: clobetasol dipropionate 0,05%
(Dermovate), bethamethasone dipripionate 0,5% (Locacorten) et al.
b. high potency corticosteroids are: fluocinonide 0,05% (Cyclocort),
methylprednisolone aceponate 0,1% (Advantan), mometasone furoate
0,1% (Elocom), hydrocortisone butirate 0,1% (Locoid) et al.
c. mid potency corticosteroids are: fluticasone propionate 0,05% (Cutivate)
et al.
d. low potency are: hydrocortisone acetate 0,25-2,5% et al.
 Solutions, lotions, gels or sprays are recommended for inflammatory,
exudativ lesions and for hairy areas.
 Creams and lotions are best intertriginous locations.
 Ointments have good action on chronic thickened lesions.
Atopic eczema: treatment / prevention
The avoidance of irritants and allergens.
Systemic therapy:
 antihistamines: sedating H1 antihistamines (promethayine, trimeprayine or
hidroxyyine, alternatively) and new H1 antihistamines (cetriyine, loratadine,
desloratodine, ebastine, levocetriyine, etc);
 Ketotifen – a mast cell degranulation inhibitor;
 Immunosupressive drugs: corticosteroids: are indicated in cases that do not
respond to antihistamines, topical steroids, lubricants etc. (0,5 – 1 mg/kg/day, 7-21
days); cyclosporine A (Sandimmun or Neoral – 2-5 mg/kg/day in short-term
therapy); azathioprine (Imuran, 50 mg twice daily); mycophenolate mofetil
(Cellcept, 2 g/day, orally); interferon gamma;
Topical treatment
Wet-to-dry comresses for acute, inflammatory and weeping phase;
Topical corticosteroids;
Topical antibiotics
Topical immunomodulators – Tacrolimus or Pimecrolimus
Physiotherapy
 PUVA
 Extracorporal photopheresis
 High-dose UVA therapy (340-400 nm)
 Combination of UVB irradiation with UVA irradiation
 Narrow-band UVB