Download Atopic Dermatitis

Atopic Dermatitis
by
Leow Atomic Chuan Tse (Group1)
B.Agri.Sc(Hons); Dip.Ed., PhD (Toxicology);
Grad.Dip.CS (1st Class Hons); MDiv (1st Class Hons)
Eczema/Atopic Dermatitis
Eczema is a nonspecific term for many
types of skin inflammation (dermatitis).
Atopic Dermatitis is a type of eczema,
and it is a long term skin disease.
“Atopic” refers to a tendency to develop
allergy conditions. “Dermatitis” means
swelling of the skin or inflammation of
the skin.
The most common
inflammatory skin condition
Most confusing skin ailment for
both patients and their
nondermatologic health care
providers
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Atopic dermatitis is the most common type of eczema. It is a chronic,
inflammatory, itchy skin condition with unpredictable course of flares and
remissions. It affects 5% to 10% of the United States population.
Most cases begin in childhood (often in infancy); however may start any age.
The disease frequently
remits spontaneouslyreportedly in 40% to 50%
of children- but it may
return in adolescence or
adulthood and possibly
persist for a lifetime.
Typically families are advised that children “will grow out of eczema”
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(About 2 in 3 children with atopic eczema grow out of it by their mid
teens)
Atopic dermatitis is an
inherited Type I
hypersensitivity
disorder of the skin.
It is usually
associated with
personal or family
history of hay fever,
asthma, allergic
rhinitis or sinusitis.
M
M.
P.
Grandfather Grandmother
MOM
Grandfather
P.
Grandmother
DAD
BABY
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Type 1 Hypersensitivity
• In type 1 hypersensitivity, an antigen is presented to CD4+ Th2
cells specific to the antigen that stimulate B-cell production of
IgE antibodies also specific to the antigen. The difference
between a normal infectious immune response and a type 1
hypersensitivity response is that in type 1 hypersensitivity the
antibody is IgE instead of IgA, IgG, or IgM. During
sensitisation, the IgE antibodies bind to Fcε receptors on the
surface of tissue mast cells and blood basophils.Mast cells and
basophils coated by IgE antibodies are "sensitised." Later
exposure to the same allergen cross-links the bound IgE on
sensitised cells, resulting in degranulation and the secretion of
pharmacologically active mediators such as histamine,
leukotriene (LTC4 and LTD4), and prostaglandin that act on the
surrounding tissues. The principal effects of these products are
vasodilation and smooth-muscle contraction.
• Type 1 hypersensitivity can be further classified into an
immediate and late-phase reaction. The immediate
hypersensitivity reaction occurs minutes after exposure and
includes release of vasoactive amines and lipid mediators,
whereas the late-phase reaction occurs 2–4 hours after exposure5
and includes the release of cytokines.
Normal Skin
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Skin of Acute
Eczema
Eczematous epidermis
contains
intercellular and
intracellular fluid
that appears in a
sponge-like
formation
(spongiosis);
Vasodilatation of the
dermis occurs,
resulting in the
clinical
manifestation of
ACUTE eczema.
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Classification of atopic dermatitis(AD)/eczema
Non-allergic AD
(Intrinsic） AD
Coexiatence
Transition
IgE mediated AD
（Classical AD）
●Impaired barrier function
●Abnormal sweating
●Altered innate immunity
(Defensin, Toll like receptor, NALP
proteins (linked to autoimmune
disease))
●Emotional stress
Allergic AD
(Extrinsic） AD
Non IgE AD
T cells
Eczema
Itch
Xerosis
Eosinophils
IgG（Autoantibody）
Etc.
Allergy 2001:56:813-824
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Pathphysiology of atopic dermatitis
Chemicals
Bacteria
Allergens
Barrier dysfunction
Horny layer
IgE
Epidermis
FceR1
Cytokine
Dendritic cell
Chemokines
Dermis
Inflammatory cells
Th2
Lymphocytes
Th2 Allergic Inflammation
IgE
FceR1
Mast cells
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Damage of barrier function
and keratinocytes
SCRATCH
Stratum corneum
Dendritic cell
epidermis
FceR1
Elongation of peripheral nerve
release of substance P
dermis
chemical mediators
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Immunology of Atopic Dermatitis
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Mechanism of Pruritus
N ENGL J MED 2008; 358:1483-1494April 3, 2008
The most important symptom in atopic dermatitis is
persistent pruritus, which impairs the patient's
quality of life. The lack of effect of antihistamines
argues against a role of histamine in causing atopic
dermatitis–related pruritus. Neuropeptides,
proteases, kinins, and cytokines induce itching.
Interleukin-31 is a cytokine produced by T cells that
increases the survival of hematopoietic cells and
stimulates the production of inflammatory cytokines
by epithelial cells. It is strongly pruritogenic, and
both interleukin-31 and its receptor are
overexpressed in lesional skin. Moreover, interleukin31 is up-regulated by exposure to staphylococcal
exotoxins in vitro. These findings implicate
interleukin-31 as a major factor in the genesis of
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pruritus in atopic dermatitis.
Intense Itching and Unceasing
Scratching
Clincal features of atopic dermatitis
Itch is an unpleasant sensation to
evoke scratching
Rothman S1941(Samuel Hafenreffer 1660)
Scratching aggravates atopic dermatitis
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Acute Eczema
Appears as “itchy” erythematous patches, plaques, or
papules that may develop into vesicular lesions, or may
continue as a less nonvesicular, erythematous eruption.
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Chronic Eczema
Later, the epidermis will
thicken (acanthosis) and
retain parakeratosis
(abnormal
keratinization of the
squamous epithelium),
resulting in an
overabundance of
cellular infiltrate in the
dermis.
These changes account for
the scale and
lichenification of
CHRONIC eczema.
The epidermis shows hyperkeratosis,
acanthosis, and a prominent granular layer.
There is liquefaction degeneration16at the
dermal-epidermal interface.
Lichens on a tree
• The word “Lichen” has a Greek origin and
denotes the superficial growth of an algae
and fungus on the bark of a tree
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Chronic Eczema
(aka: Chronic eczematous dermatitis)
• Has a hallmark lichenification (plaque with an exaggeration or
hypertrophy of the normal skin markings).
• Scale and hemorrhagic crusts can result from scratched or drying
vesicles.
• Older lesions exhibit hypo or hyper pigmentation.
Hypo-pigmentation
Lichenification
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Severity
Atopic dermatitis can present
with a wide spectrum of
severity.
 mild, recurrent, localized
itchy rash on “dry” skin or
 more severe, extensive
eruption that can be
accompanied by unremitting
pruritus, sleepless nights,
secondary cutaneous
bacterial infections, and/or
embarrassing lichenification.
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Psychosocial Effects
Psychosocial problems, such as poor self-image,
anger, and frustration may lead to depression and
social isolation.
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Different Phases of Atopic
Dermatitis
The character and distribution of the skin rash tends
to vary according to the patient’s age.
Any or all manifestations of atopic dermatitis may
exist in a single patient.
The different phases of atopic dermatitis are not
always clearly distinct.
Infantile Phase
Childhood Phase
Adolescent and Adult Phase
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Infantile Phase
Eruption may become generalized, in most cases it first
manifests with severe “cradle cap” or severe intertriginous
(inflammatory) rashes (groin, neck, axillae).
As the patient approaches age 2 years, the flexor creases become
involved.
Lesions consist of scaly, red, and occasionally oozing plaques
that tend to be symmetric.
Occurs on the
 scalp
 face, particularly
cheeks
 neck
 chest
 extensor extremities
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Childhood Phase
(patients aged 2 years to 12 years of age)
These patients tend to be less acute and lesions less exudative than
those seen in infancy.
Inflamed lesions become lichenified (especially in Asian and
African-American patients)
secondary to chronic rubbing symmetrically, with characteristic
distribution in the flexural folds and scratching.
Lesions tend to occur.
Occurs on the:
Antecubital and popliteal fossae
Neck, wrists, and ankles
May occur on the eyelids, lips, scalp,
and postauricular areas
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Adolescent and Adult Phase
(patients 12 years and older)
Post inflammatory hyper or hypo pigmented
changes tend to be seen.
The appearance of atopic dermatitis may change to
a more poorly defined, itchy, erythematous rash,
possibly with papules and/or plaques.
Lichenified plaques of
atopic dermatitis are
typically less well
demarcated than are the
plaques seen in psoriasis.
These plaques tend to
blend into surrounding
normal skin.
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Possible Complications
Pruritus (itching) may interfere with sleep. Pruritis is
increased by repeated scratching and rubbing, which
leads to lichenification, oozing, and secondary bacterial
infection.
Secondary infection with Staphylococcus aureus
may trigger relapse of atopic dermatitis.
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Clinical Aspects
Clues to diagnosing Atopic Dermatitis:
• Persistent Xerosis (abnormal dry, “sensitive” skin)
• “Allergic Shiners” (darkened or tanned coloring
in the periorbital areas)
• Hyperlinear palmar creases (exaggerated skin
creases or lines in the palms of the hand.
• Follicular eczema (Lesions accentuated around
hair follicles )
• Ichthyosis vulgaris (an inherited skin disorder in
which dead skin cells accumulate in thick, dry
scales)
• Keratosis Pilaris (skin condition that looks like
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small goose bumps)
Differential Diagnosis
Diagnosis of atopic dermatitis is generally not difficult,
especially in patients with atopic history. The following
should be considered or excluded:
Contact Dermatitis
Determine whether the patient was exposed to a substance that could cause
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contact dermatitis. The location of the lesions may suggest an external cause.
Differential Diagnosis
Psoriasis
 Lesions are generally in extensor locations (elbows,
knees, and other large joints) rather than the flexor
creases. May be palmar or plantar as seen in this image.
 Patients typically have a positive family history of
psoriasis.
Psoriasis is less pruritic than eczema,
lesions tend to be clearly demarcated
from normal surrounding skin, and
the scale of psoriasis tends to be
thicker in appearance.
However, psoriasis may at times be
clinically indistinguishable from
atopic dermatitis 28
Differential Diagnosis
Tinea
A positive KOH test or
fungal culture result will
confirm
(remember, an unresolved
eczematous-like rash,
worsening with topical
corticosteroids could be
tinea)
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Japanese guide line for atopic dermatitis
Diagnosis
Katayama et al.(JSA)
Allergology International 2011
Assessment of dermatitis
Evaluation of
Aggravation factors
Skin care
Rectification of aberrant
Drug
therapy
skin barrier functions
Appropriate guidance
for
patients in daily life
Clean of the skin
Bathing・Showering・
Emolient
Emolients
Tacrolims(Face)
Steroid ointment
Anti-hisitamine
Imunosuppresants
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Narrow Band UVB Phototherapy
• Eczema light therapy refers to the use of ultraviolet
(UV) light to treat the skin rash and itching of eczema.
Exposing the skin to UV light suppresses overactive
skin immune system cells that cause inflammation
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Management
In children, NICE ( National Institute for Health and Clinical
Excellence) suggest a treatment schema based on severity:
• mild atopic eczema
– emollients
– mild potency topical corticosteroids
• moderate atopic eczema
– emollients
– moderate potency topical corticosteroids
– topical calcineurin inhibitors e.g. pimecrolimus
– bandages
• severe atopic eczema
– emollients
– potent topical corticosteroids
– topical calcineurin inhibitors
– bandages
– phototherapy
– systemic immunosuppressive therapy (cyclosporine,
azathioprine, interferon-gamma)
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Aggravating factors in atopic dermatitis
Katayama et al.(JSA)
Allergology International 2011
Infants～2 y
2 y～13 y
13 y～Adult
1.Foods (Egg,milk,wheat,etc)
1.Sweat,dryness,scratching
2.Sweat,dryness,scratching
2.Slaver,soap,shampoo, cloth
3.Slaver,soap,shampoo, cloth
3.Bacteria, fungus,etc.
4.Environmental factors
4.Environmental factors
5.Bacteria, fungus etc.
5.Stress
6.Foods
*Aggravation factors are different in each patient.
Start to eliminate responsible factors after sufficient evaluation.
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Avoidance
Irritants:
– Recommend non-irritant
fabric, such as cotton. Wool
may induce itching
– Overheating and sweating:
Excess dryness or
humidity should be
avoided.
An air conditioner or
humidifier in a child’s
bedroom may help to
avoid the dramatic
changes in climate
that may trigger
outbreaks.
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Avoidance
Allergens:
Environmental
elimination of
airborne substances
may bring lasting
relief.
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Thank You
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