Transcript Eczema (dermatitis) and Lichenification

Eczema (dermatitis) and
Lichenification
Ecema
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Definition
The word 'eczema' comes from the Greek for
'boiling' that are often seen in the early acute
stages of the disorder, but less often in its later
chronic stages.
Although the terms dermatitis and eczema are
nowadays generally regarded as synonymous , so
that all eczema is regarded as dermatitis but not
all dermatitis is eczema . The most common skin
conditions (20% of all new patients).
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Stages of eczema:There are three stages
1)Acute eczema: (primary lesions are
vesicles, blisters).
•HP: oedema in the epidermis
(spongiosis) progress to
intraepidermal vesicles, which may
form larger blisters.
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2)Subacute eczema: (less edema; few
vesicles) erythema and scale are present
in various patterns, usually with indistinct
borders.
HP: spongiosis diminished , thickening of
the prickle cell layer (acanthosis ), with
formation of a parakeratotic (retention of
nuclei in the horny layer)
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3)Chronic eczema: less vesicular and exudative;
more scaly and thickened; more likely to show
lichenification; and more likely fissure.
•HP:less spongiosis and vesication more
thickening of the prickle cell layer (acanthosis)
and horny layer (hyperkeratosis) and retention of
nuclei in the horny layer(parakeratosis).
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Pathogenesis
•It involves the interaction between three things :
a. Triggering factor ,
b. Keratinocytes ,
c. T-lymphocytes , which seems particularly important in most
eczema types
Allergic contact dermatitis is the consequence of an immune
reaction mediated by T cells against low molecular weight
chemicals known as haptens.
in allergic contact dermatitis arises as a result of two essential
stages: an induction phase, which primes and sensitizes the
immune system for an allergic response, and an elicitation phase,
in which this response is triggered. As it involves a cell-mediated
allergic response, ACD is termed a type 1V delayed type
hypersensitivity which is mediated by hapten-specific T cells.
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Pathogenesis
• Irritant contact dermatitis is a nonspecific response of
the skin to direct chemical damage that releases mediators
of inflammation predominantely from epidermal cells.
•In irritant contact dermatitis , the three predominant
processes are : *disturbed barrier function , *epidermal
cell damage and *release of inflammatory mediators
and cytokines , which induce morphological changes
apparent histologically and clinically as eczema
•It is not immune mediated
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Pathogenesis
Secondary dissemination :
A very characteristic feature of eczema is it's tendency to
spread far from it's point of origin . There are four main
mechanisms of dissemination :
1. Spread by contact with external allergen: e.g. a contact
dermatitis of the lower leg induced by lanolin ointment , may
spread to the hand and the face as a result of casual contact
during application of the ointment .
2. Spread by ingestion or injection of an allergen: an eruption
originally induced by sensitivity to topical allergen (e.g. allergic
contact dermatitis) may relapse after ingestion or injection of the
same chemical , e.g. medication that can be used topically or
systemically .
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Pathogenesis
Secondary dissemination :
3. Conditional hyperirritability ('angry back'
syndrome) : this term refers to the phenomenon
where by an area of inflamed skin on one part of the
body results in generalized hyperirritability of the skin
sites , that are distant from the primary site of
inflammation .
4. Bacterial hypersensitivity : heavily infected
eczema will some times disseminate in the absence of
demonstrable allergic sensitivity to topical medication ,
it is probably that allergy to bacteria or their products is
some times a factor in the dissemination .
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Classification:
Exogenous eczema
Irritant eczema
Allergic contact eczema
Photoallergic contact eczema
Eczematous polymorphic light eruption
Infective eczema
Dermatophytide
Post-traumatic eczema
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Endogenous eczema
Atopic eczema
Seborrhoeic eczema
Asteatotic eczema
Discoid eczema
Eyelid eczema
Exudative discoid and lichenoid chronic dermatosis
Chronic superficial scaly dermatitis
Pityriasis alba
Hand eczema
Venous eczema
Juvenile plantar dermatosis
Metabolic eczema or eczema associated with systemic disease
Eczematous drug eruptions
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Exogenous eczema
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Irritant and allergic contact eczema.
Irritant
everyone
Allergic
Only in the sensitized
Sensitization
No previous
sensitization
Two phases: sensitization phase
and elicitation phase
Mechanism
Nonimmunologic; a Delayed hypersensitivity
physical and
reaction.
chemical alteration
of epidermis.
Number of
exposure
Few to many
One or several to cause
sensitization.
Nature of
substance
Organic solvent,
soap
Low-molecular-weight hapten
(metals, formalin)
Incidence
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Concentration Usually high
of substance
required
Mode of onset Usually gradual as
epidermal barrier
becomes
compromised
Distribution
Borders usually
indistinct
Investigative Trial avoidance
procedure
Management Protection and
reduced incidence
of exposure
dermatitis
Napkin dermatitis;
May be very low
Once sensitized, usually rapid; 1248h after exposure.
May correspond exactly to
contactant (watchband)
Trial avoidance, patch testing, or
both
Complete avoidance
Lip-stick dermatitis; nylon; dyes14
Napkin (diaper) dermatitis:
the most common type is irritant in origin, and is
aggravated by the use of waterproof plastic pants.
The mixture of faecal enzymes and ammonia
produced by urea-splitting bacteria, if allowed to
remain in prolonged contact with the skin, leads to a
severe reaction. The fold remain unaffected in
contrast to intertrigo, inverse psoriasis, and
candidiasis.
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Infective dermatitis (microbial eczema):
•eczema that is caused by microorganisms or their
products , which clears when the organisms are
eradicated . This should be distinguished from
infected eczema , in which eczema is complicated
by secondary infection (bacterial or viral) .
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Dermatophytid:
•A reaction, at a remote site, to a dermatophyte
infection. This diagnosis should be suspected
when the presence of a dermatophyte infection
has been established and no fungus can be
demonstrated in the dermatophytid lesions.
•The diagnosis is supported further by clearing of
the dermatophytid after the dermatophyte has
been eradicated.
•Eczematous vesicles on the hands or feet are the
commonest pattern
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Endogenous eczema:
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Atopic dermatitis
• The word ‘atopy’ comes from the Greek
‘without a place’. It was introduced years ago
to designate a group of patients who had a
personal or family history of one or more of
the following diseases: high fever, asthma,
very dry skin, and eczema.
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Stages of AD:
three stages:
1-Infantile AD: Occurring from 2 months to 2
years of age.
2-childhood AD: From 2-10 years.
3-Adults AD.
In all stages, pruritus is present. Itching often
precede the appearance of lesions, hence the
concept that AD is “the itch that rashes”.
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Infantile Atopic Dermatitis
• 60% of case AD present in the first year of life, after 2
months of age
• Begin as itchy erythema and scaling of the cheeks
• Distribution include scalp, neck, forehead, wrist, and
extensors
• May become desquamate leading to erythroderma.
• Most cases the symptoms will disappear toward the
end of the second year.
• Egg, peanut, milk, wheat, fish, soy, and chicken may
exacerbate infantile AD
Involvement of the cheeks is characteristic of the infantile pattern of AD.
Childhood Atopic Dermatitis
• Characterized by less exudative lesions.
• Distribution: antecubital and popliteal fossae,
flexor wrist, eyelids, and face.
• A vicious cycle may be established (the itchscratch cycle), as pruritus leads to scratching,
and scratching causes secondary changes that
themselves cause itching.
• Severe atopic dermatitis involving more than
50% of body surface area is associated with
growth retardation.
Childhood Atopic Dermatitis
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Adult Atopic Dermatitis
• Distribution: antecubital and popliteal fossae,
the front side of the neck, the forehead, and
area around the eyes.
• Atopic individuals are at greater risk of
developing hand dermatitis than are the rest
of the population
• Lichenification and prurigo-like papules are
common.
• 70% develop hand dermatitis some times in
their lives
Adult Atopic Dermatitis
Associated features and complications:
Cutaneous stigmata:
• Dennie-Morgan fold: a linear transverse fold just
below the edge of the lower eyelids.
• Pityriasis alba: poorly marginated hypopigmented,
slightly scaly patches on the cheeks, upper arms,
trunk, in young children.
• Keratosis pilaris: horny follicular lesionsof arms, legs,
cheeks, and buttocks.
• Hertoghe’s sign – thinning of the lateral eyebrows
• Hyperkeratosis and hyperpigmentation of the neck
“dirty neck”
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Vascular Stigmata
• Headlight sign – perioral, perinasal and
periorbital pallor
• White dermographism – blanching of the skin
at the site of stroking .
• Low finger temperature.
• Pronounced vasoconstriction on exposure to
cold.
Ophthalmologic abnormalities:
cataracts.
Infection
• More than 90% of chronic lesions contain
Staph aureus.
• Eczema herpeticum – generalized herpes
simplex infection.
• Vaccination against smallpox is
contraindicated in person with atopic
dermatitis. Even when condition is in
remission, widespread and even fatal vaccinia
can occur. Complicated varicella.
• Warts; molluscum contagiosum.
Triggering factors
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Temperature change and sweating
Decreased humidity
Excessive washing
Contact with irritant substances
Contact allergy
Aeroallergens
Microbic agents
Food (eggs, milk, fish)
Emotional stress
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Pathogenesis and immunology
The pathogenesis of atopic dermatitis is unknown,
but the disease seems to be the result of genetic
susceptibility, immune dysfunction and epidermal
barrier dysfunction
Genetic:
• The concordance rate for AD is higher among
monozygotic twins (77%) than among dizygotic twins
(15%).
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Pathogenesis and immunology
Elevated IgE and the inflammatory response:
•The IgE level is increased in the serum of many
patients with AD, but 20% of AD have normal serum
IgE.
•The level of IgE do not correlate with the activity of
the disease; therefore elevated serum IgE levels can
only be considered supporting evidence for the
disease.
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Blood eosinophilia:
•Blood eosinophil counts correlate with disease
severity; especially with severe AD and concomitant
respiratory allergies.
•Degranulation of eosinophils in the dermis may
induce histamine release from basophils and mast
cells and stimulate itching, irritaion.
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Pathogenesis and immunology
Immunology
• Activation T helper cell type 2 (Th2).
• Th2 produces IL-4, 5, 10, and IL-13, and
inhibition of the Th1 response.
• IL-4 and IL-5 produce elevated IgE and
eosinophilia in tissue and peripheral blood.
• IL-10 inhibits delayed type hypersensitivity
• Th2 maybe sensitive to house mites or grass
pollen.
Immunology
• Monocytes produces elevated amount of
prostaglandin E2 (PGE2)
• PGE2 reduces gamma-interferon production
• PGE2 also directly enhances IgE production
from B cells
Immunology
• Langerhans cells of AD patient stimulate
helper T cells into Th2 phenotype without the
presence of antigen
• Langerhans cells have IgE bound to their
surface receptors. These IgE are associated
with atopic antigens, such as house dust mites
Criteria for diagnosis of AD
Major criteria: (must have three of the following)
1) Pruritus
2) Typical morphology and distribution:
• flexural lichenification in adults;
• facial and extensor involvement in infancy.
3) Chronic or chronically relapsing dermatitis
4) Personal or family history of atopic disease (asthma,
allergic rhinitis, AD)
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Minor criteria:(must also have three of the following)
1) Xerosis (dry skin)
2) Ichthyosis\hyperlinear palms\keratosis pilaris
3) IgE reactivity (immediate skin test reactivity,
radioallergosorbent test positive)
4) Elevated serum IgE
5) Early age of onset
6) Tendency for cutaneous infections ( S. aureus and herpes
simplex virus)
7) Tendency to nonspecific hand\foot dermatitis
8) Nipple eczema
9) Cheilitis(inflammation of the lips)
10) Recurrent conjunctivitis
11) Dennie-Morgan infraorbital fold
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Minor criteria:(must also have three of the following)
12) Keratoconus (bilateral protrusion of the cornea)
13) Anterior subcapsular cataracts
14) Orbital darkening
15) Facial pallor\facial erythema
16) Pityriasis alba
17) Itch when sweating
18) Intolerance to wool and lipid solvents
19) Perifollicular accentuation
20) Food hypersensitivity
21) Course influenced by environmental and\or emotional
factors
22) White dermographism or delayed blanch to cholinergic
agents
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Treatment:
1-explanation, reassurance and encouragement.
2-the avoidance of exacerbating factors.
3-topical steroids. Principles are use weaker steroid that
controls the eczema effectively; review their use regularly
(check for local and systemic side-effects); avoid using potent
and very potent steroids for children.
4-the regular use of bland emollients, either directly to the
skin or in the form of oils to be used in the bath.
5-those with Ichthyosis should use ointments rather than
creams.
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Treatment:
6-the scratch-itch cycle can often be interrupted by
occlusive bandaging, and nails should be kept short.
7-sedative antihistamines, e.g. trimeprazine or
hydroxyzine.
8-systemic antibiotics, e.g. erythromycin.
9-systemic steroids for generalized and severe cases.
10- UVB, UVA or even PUVA therapy may be useful for
severe cases.
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Note the Dennie–Morgan
lines and central facial
pallor.
Keratosis pilaris
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Seborrhoeic dermatitis
• It is chronic, characterized by redness, and
scaling in the area with a rich supply of
sebaceous glands, namely the scalp, face,
upper trunk, and in the body folds.
• Affects infancy (within the first months), and
adults, most between 20-50 years old.
• It is common occurring in 2-5% of the
population.
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Etiology
• May be related to increased sebum secretion,
abnormal sebum composition, certain drugs (arsenic,
gold methyl-dopa, cimetidine, neuroleptics)
• May be related to the presence of the lipophilic yeast
Malassezia furfur ( also known as Pityrosporum
ovale).
• The density of yeast has been correlated with the
severity of the disease. P. ovale may also be
abundant on the scalp of patients who have no
clinical signs of the disease, and the yeast may only
be pathogenic in predisposed individuals.
• May be cutaneous marker of HIV infection and AIDS,
especially when severe, atypical, and therapy
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resistant
Clinical features
1) Infants (cradle cap): infants commonly
develop a greasy adherent scale on the
vertex of the scalp.
2) Young children (tinea amiantacea and
blepharitis): one patch or several patches,
range from 2-10 cm of dense scale appear
anywhere on the scalp. The scale suggests
fungal scalp disease, which explains the
designation tinea. Amiantacea, meaning
asbestos, refers to the platelike quality of the
scale, which resembles genuine asbestos.
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Clinical features
3) Adolescents and adults (classic seborrheic
dermatitis):
• Dandruff (Pityriasis sicca): represents a mild form of
seborrhoeic dermatitis: fine, dry, white scalp scaling
with minor itching. The distribution of scaling and
inflammation may become more diffuse and occur in
the seborrheic area.
• Scaling of the ears may be misjudged as eczema or
fungus infection.
• Older patients especially with neurologic problems
tend to have more chronic and extensive disease.
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Treatment
• Topical steroids tend to produce a rapid effect,
but on the face can produce steroid rosacea.
• Antiyeast medications: ketoconazole.
• Oral antifungals. Oral itraconazole;
200mg\day.
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Discoid eczema(nummular eczema)
•It is a chronic, pruritic, inflammatory dermatitis
occurring in the form of coin-shaped plaques composed
of grouped small papules and vesicles on an
erythematous base. It is especially common on the
extremities during winter months; often seen in atopic
individuals.
•Usually begins on the lower legs, dorsa of the hands, or
extensor surfaces of the arms.
•Treatment: topical steroids; intralesional steroids
Systemis: AB if secondary infection present;
antihistamines; corticosteroids.
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Asteatotic eczema
Also known as xerotic eczema; winter itch; eczema
craquelé; and asteatotic eczema. These terms are all
applied to dehydrated skin showing redness, dry scaling,
and fine crackling that may resemble crackled porcelain or
the fissures in the bed of a dried lake or pond.
•favored sites are the anterior shins, extensor arms,
and flank. Elderly persons are particularly
predisposed, and xerosis appears to be the most
common cause of pruritus.
•seen most frequent during the winter, when there is
low humidity. Bathing with hot water and harsh soaps
contribute.
•limitation of the use of soap, and prompt application
of an emollient are usually effective.
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Pityriasis alba
• It is a form of subclinical dermatitis, frequently
atopic in origin. It presents as poorly
marginated, hypopigmented, slightly scaly
patches on the cheeks, upper arms, and trunk,
typically in young children. Exposure to the
sun makes the patches more obvious. It
usually responds to emollients and mild
topical steroids.
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Acute vesiculobullous hand eczema
(pompholyx, dyshidrosis)
• Idiopathic acute vesicular hand dermatitis is
not related to blockage of sweat duct.
• Primary lesions are macroscopic, deep-seated
multilocular vesicles resembling tapioca on
the sides of the fingers, palms, and soles.
• The eruption is symmetrical and pruritic, with
pruritus often preceding the eruption.
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Venous eczema
•Also known as gravitational eczema (stasis eczema).
•It is a cutaneous marker for venous insufficiency.
•Presents as erythema and a yellowish or light-brown
pigmentation of the lower third of the lower legs.
• Varicose veins are usually present .
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Juvenile plantar dermatosis
• It is eczematous disorder of children.
• The disease is caused by the repeated
maceration of the feet by occlusive shoes,
especially athletic shoes.
• It usually begins as a patchy, symmetrical,
smooth, red glazed macules on the base or
medial surface of the great toes, sometimes
with fissuring and desquamation.
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Lichenification: lichen simplex (localized neurodermatitis)
• As a result of long continued rubbing and
scratching, the skin becomes thickened and
leathery. The normal markings of the skin
become exaggerated. This change, known as
lichenification. Ex. lichen simplex .
• lichen simplex: it is an eczematous eruption
that is created by habitual scratching of a
single localized area.
• The disease has a predilection for the back
and sides of the neck, and the extremitiesespecially the wrists and ankles.
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