Atopic Dermatitis 2 nd seminar prepared during my post graduation days..This seminar prepared under guidance of Dr Srinivas

2. ATOPIC DERMATITIS
Presenter: Dr. Ravindra G O
Moderator: Dr. Srinivasa.K
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3. OVERVIEW;ATOPIC DERMATITIS
• Definition
• Description of rash
• Epidemiology
• Atopic march
• Etiopathogenesis
• Clinical features
• Phases of atopic dermatitis
• Diagnosis and Treatment
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4. ATOPIC DERMATITIS
DEFINITION:-
•It is an itchy, chronic, or
chronically relapsing,
inflammatory skin condition.
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5. DESCRIPTION OF RASH IN AD
• The rash is characterised by itchy papules
(occasionally vesicles in infants) which
become excoriated and lichenified, and
typically have a flexural distribution .
• The eruptions is frequently associated with
other atopic conditions in the individuals or
other family members.
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8. EPIDEMIOLOGY
• AD is the most common chronic relapsing
skin disease seen in infancy and
childhood.
• Prevalence rate of atopic dermatitis is 10-
12% in children and 0.9% in adults(US).
• Race
- The male to female ratio for AD is 1:1.4
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9. • Age
- In 85% of cases ,AD occurs in the first year of
life
- In 95% of cases , it occurs before age 5 years.
• Frequently occurs in families with other atopic
diseases, such as Asthma, allergic rhinitis, and
food allergy.
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10. “Atopic March”
• Infants with AD are predisposed to
development of allergic rhinitis and/or
asthma, food allergies in childhood c/d “THE
ATOPIC MARCH”.
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12. ETIOPATHOGENESIS
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Disruption of the
skin barrier
function
+
Abnormalities in
the immune
response
Genetics Environment
• Multifactorial condition whose etiology is not
entirely understood

13. Disruption of skin Barrier function
Defective renewal of the stratum corneum
• Water can easily get out of the skin-dry skin.
• Allergen and infectious agents can easily get
in
i. Prone for infection
ii. IgE reactivity.
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14. Disruption of Skin Barrier function
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15. Molecular basis of skin barrier
dysfunction
Multiple molecular abnormalities have been
identified
• Most important being reduced levels of the
protein FILAGGRIN.
An important structural component of the
stratum corneum.
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16. Others are
Reduced level of the source of natural
moisturizing factor(NMF)
• Mixture of small molecules that bind water
and help maintain skin hydration.
Reduced levels of CERAMIDES—waxy lipids that
are also important for preventing water loss.
Tight junction formation also appears to be
defective .
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18. GENETICS
Susceptible loci on
1q21,3p24-22,3q21
and 17q25 associated
with atopic dermatitis.
Other associated with
concurrent
asthma3p26-
24,3q14,4p15-20p
Genome screening for asthma and AD-
overlapping loci; 13q and 20p.
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19. GENETICS ..cont..
Polymorphism in gene
encoding the Beta-chain
of high affinity IgE (JOB
)receptor FCER1b
Genes on chr.5q CK
genes cluster
Associated with
polymorphisms in IL-4
gene with AD.
. Variants of RANTES
gene promoter region
associated in AD.
Other genes:
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20. GENETICS cont..
• There are several genetic syndromes with known
single-gene defects that have atopic eczema as a
feature.
• Examples include ichthyosis vulgaris (filaggrin; FLG),
• Netherton syndrome (SPINK-5),
• SAM severe dermatitis, allergies,
• metabolic wasting (Desmoglein 1),
• Wiskott–Aldrich syndrome (WASp),
• Omenn syndrome (SCID RAG1/2),
• hyper IgE (Jobs syndrome - STAT3, DOCK8), and IPEX
(Foxp3).
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22. CLINICAL FEATURES
Boys>>Girls
Age of onset is between 2 to 6 months in
majority of cases, but it may start at any age ,
even before the age of 2 months in some cases.
The distribution of eruption –varies with age.
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24. PHASES OF AD
• INFANTILE PHASE
• CHILDHOOD PHASE
• ADULT PHASE
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25. INFANTILE PHASE
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• AD is usually noticed soon after
birth
• Usually sparing the diaper area and
the nose
Key features
• The earliest lesions affect the creases(ante cubital and
popliteal fossae)
• Later localize to cheeks , forehead ,scalp and extensor
surface of legs
• However ,they may occur in any location on the body.
Areas of
distribution
• Ill-defined ,erythematous ,scaly, and
crusted patches and plaques
• lichenification is seldom seen in
infancy.
Characteristic
skin lesion

26. INFANTILE PHASE
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27. CHILDHOOD PHASE
• Xerosis is often generalized
• Erythema and scaling around the eyes can
be seen
• Dennie-morgan folds(ie.,increased folds
below the eyes)-often seen
Key features
• Flexural creases
• The antecubital and popliteal fossae
• Buttocks-thigh creases are often
affected
Areas of
distribution
• Lichenification is the characteristic of
childhood AD
• It signifies chronic scratching and is
seen mostly over the folds, bony
protuberans.
Characteristic
skin lesion
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31. ADULT PHASE
• XEROSIS IS PROMINENT
KEY FEATURES
• Lesions become more diffuse
• Cubital fossa and popliteal fossa and
sometimes neck,face and hand
AREA OF
DISTRIBUTION
• Lichenification may be present
• A brown macular ring around the neck is
typical but not always present
Characteristic
skin lesion
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33. ATOPHIC HAND ECZEMA
A patchy ,somewhat vesicular and lichenified eczema
is common manifestation of Ad in childhood..
Nails often involved coarse pitting and
ridging.
Chronic hand eczema may persists to adult life and is
frequently a contributing factor in what is called to be
CONSTITUTIONAL HAND ECZEMA.
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35. AAD 2014 GUIDELINES
(MODIFICATIONS TO HANIFIN-RAJKA CRITERIA)
ESSENTIAL FEATURES(MUST BE PRESENT)
• Pruritus
• Eczema
• Typical morphology/age-specific pattern
• Chronic/relapsing history
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36. Important features(present in most cases,adds
diagnostic support)
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– Early age onset
– Atopy
• Personal /family history
• IgE reactivity
• iii. Xerosis.

37. Exclusionary conditions(conditions that should be
excluded)
i. Scabies
ii. Seborrheic dermatitis
iii. Contact dermatitis
iv. Ichthyoses
v. Cutaneous T-cell lymphoma
vi. Psoriasis
vii. Photosensitivity dermatoses
viii.Immune deficiency diseases
ix. Erythroderma of other causes
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38. Additional considerations in diagnosis of AD
• No reliable biomarker exists for diagnosis of AD
• Laboratory testing is seldom necessary
 CBC can be useful to exclude immune deficiency
 IgE level can be helpful to confirm an atopic pattern
 Skin swab can be helpful to identify S.aureus
superinfection
• Allergy and RAST is of little value.
• Biopsy can be helpful to rule out other conditions(eg,
cutaneous T-cell lymphoma)
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39. PEARLS OF AD TREATMENT
• The current therapeutic options for AD is not
curative.
• Approach should be
o Individualized because of varied clinical
presentations and disease burdens.
o Dynamic to respond to changes over time.
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40. OBJECTIVES OF TREATMENT
• To manage flares
• Exacerbations
SHORT
TERM
• To control symptoms
between flares
• Active lesion absent
• But skin is dry and itchy
LONG
TERM
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41. TREATMENT DURING EXACERBATION
1. Topical corticosteroids
2. Topical calcineurin inhibitors
3. Supportive measures
• Antihistaminics
• Antibiotics
4.Others
• Oral steroids
• Immunosuppressions--
• Crisaborole
• Dupilumab
• Phototherapy
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42. • Immunosuppression;
Tacrolimus(0.1 and 0.03% ointment) and
• Pimercrolimus (0.1% cream)
• Use when the continued use of topical
steroids is ineffective or inadvisable.
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44. TREATMENT DURING REMISSION
• Daily bathing
• Emolients (moisturisers)
• Trigger avoidance
• Topical steroids (intermittent basis)
– Form cornerstone of therapy
– Applied over non inflammatory areas immidietely
after hydration of the skin
– Alliviate itching
– May suffice in mild cases without any additional
therapy.
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45. PREVENTION OF AD
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46. TAKE HOME MESSAGE
• AD is a chronic pruritic inflammatory skin
disease with a wide range of severity.
• Pathogenesis is multifactorial.
– Genetics‘
– Skin barrier dysfunction
– Impaired immune response
– Environmental factors
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47. TAKE HOME MESSAGE
• Diagnosis is mainly clinical
– Itching
– Early age of onset
– Age wise distribution
– Comes and goes
• Treatment of the AD includes long term use of
emollients and gentle skin care as well as
short term treatment of acute flares.
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48. REFERENCES
• Color textbook of pediatric dermatology,4th
edition.
• Nelson textbook of Pediatrics,20th edition
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