2. introduction
• Atopic dermatitis is a chronic inflammatory skin disease associated
with cutaneous hyperactivity to environmental triggers that are
otherwise innocuous to non atopic individuals and is often the first
step in the atopic march that results in asthma and allergic rhinitis.
• The clinical phenotype that characterizes atopic dermatitis is the
product of interactions between susceptibility genes, the
environment, defective skin barrier function, and immunologic
responses.
• An understanding of the relative role of these factors in the
pathogenesis of AD is important and has implications for therapy
5. GENETIC FACTORS
• Twin concordance rate for monozygotic twins is 0.72 and only 0.23
for dizygotic twins. This means environmental factors are implicated
in about a third of the cases.
• Numerous susceptibility loci have been implicated and include 1q21
(locus for gene encoding fillagrin protein)
• Other genes affected apart from FLG gene include IL4, SPINK5,
RANTES,IL18, NOD1, DEFB1 e.t.c
• Similar to genes associated with other diseases like asthma, COPD,
HIV, sepsis, Crohns and sarcoidosis
6. ENVIRONMENTAL FACTORS
• UV exposure from sunlight and vitamin D production in the skin
• Tobacco smoking and environmental pollutants
• Urban and rural dwelling and history of recent travel.
• Breast feeding and delayed weaning
• Obesity and physical exercise
• Family size ,exposure to infective agents ,…..the hygeine hypothesis
7. CLINICAL FEATURES
• Varied and depend on the age of patients, and phase of the disease.
• Presentation include:
Itching
Erythema
Papules and vessicle
Eczematous areas with crusting
Hyper and hypopigmentation
Excoriation and lichenification
Xerosis
Secondary Infections
15. ADULTHOOD
• Similar to that in late childhood.
• Lichenification of the flexure areas may be seen
• Hand Eczema occurs in up to 50% of adult cases and might be
persistent from childhood eczema
• Nipple eczema, perioral dermatitis and prurigo nodule are all
features.
16.
17.
18. INVESTIGATIONS
• Initial Diagnosis is rarely aided by investigations. Relevant
investigation however include:
• Total serum IgE
• Skin prick tests
• Patch test for concomittant ACD
• Bacteriological and Viral skin swabs and culture and sensitivity testing
19. • Histology usually not indicated but show spongiosis, disruption of
desmosomes and formation of microvessicles and(exocytosis) in the
acute phase.
• Chronic form, spongiosis is difficult to appreciate, there is marked
acanthosis, hyperkeratosis,hypergranulosis and minimal
parakeratosis.
20. DIAGNOSIS
• Based on history and examination findings .
• The Hanifin and Rajka major and minor diagnostic criteria is a
comprehensive tool for diagnosis of atopic dermatitis.
• The UK working party diagnostic criteria is a revision of Hanifin Rajka
which is simpler to use and suitable for both epidemilogical studies
and in the clinic setting.
21. Hanifin and Rajkal diagnostic criteria
Major Criteria: Must have three or more of:
• Pruritus
• Typical morphology and distribution
• Flexural lichenification or linearity in adults
• Facial and extensor involvement in infants and children
• Chronic or chronically-relapsing dermatitis
• Personal or family history of atopy (asthma, allergic rhinitis, atopic
dermatitis)
22. Hanifin and Rajkal diagnostic criteria Contd.
• Minor criteria: Should have three or more of the following:
• Xerosis
• Ichthyosis,palmar hyperlinearity or keratosis pilaris
• Immediate type skin test reactivity
• Raised Serum IgE
• Early age of onset
• Tendency towards cutaneous infections (especially S.Aureus and
herpes simplex)
23. Minor criteria contd.
• Tendency toward non specific hand and foot dermatitis
• Nipple eczema
• Cheilitis
• Recurrent conjuctivitis
• Dennie – Morgan infraorbital folds
• Keratoconus
• Anterior subscapular cataracts
• Orbital darkening
24. HANIFIN AND RAJKA DIAGNOSTIC CRITERIA
FOR ATOPIC DERMATITIS CONTD.
Facial pallor or facial erythema
Pityriasis alba
Anterior neck folds
Itch when sweating
Intolerance to wool and lipid solvents
Perifollicular accentuation
Food intolerance
Course influenced by environmental factors
White demographism or delayed blanch
25. U.K. working party’s diagnostic criteria
History of pruritus plus 3 or more of the following:
• Onset under the age of 2 years (not used if child is less than 4yrs)
• History of involvement of skin creases
• History of a generally dry skin in the past year
• Personal history of asthma or hay fever or positive family history in
patients <4yrs.
• Visible flexural dermatitis
26. ASSesing Severity
•Assesing severity of lesion is part of initial
assesment.
•The best scores being used currently are the
EASI and SCORAD scales as they are the most
validated scales. They also show good
validity, reliability and sensitivity.
29. TREATMENT
• Counselling is a very important and initial treatment strategy
• Explaining in simple language the aetiology and clinical
course of the disease
• Basic skin care practices.
• Decrease frequency and duration of baths. The wrinkle
sign signals that bath time is already prolonged
• Identification and avoidance of triggers
30. TREATMENT CONTD.
• First line Treatment:
• Emollients
• Topical corticosteroids (TCS)
• Anti histamines
• Antibiotics, antifungal and antiviral agents when necessary
• Topical calcineurin inhibitors (TCI) for “steroid phobia” or lesions on the face
• Maintenance :TCS and TCI twice weekly and daily emolients
31. Poor response?
• Second line treatment:
• Reassess patient
• Short course topical potent steroids
• Review diet in children and intensify search for triggers and re emphasize
need for avoidance
• Consider admission
• Physical methods like wet wraps and phototherapy (for adults only)
39. Concluding remarks
•A good understanding of the pathogenesis
and disease course of AD by the physician
translates to better education of the patient
and this results in better outcomes.
•Basic skin care practices and TCS will often
suffice
40. •However there are resistant cases, and some
factors may necessitate use of systemic
therapy in some patients.
•New treatments in development hold
tremendous promise in the treatment of AD.
42. Major resources
• Rooks Textbook of dermatology (8th edition)
• Medscape
• Journal of Allergy and Immunology
Notes de l'éditeur
. Many bacteria and viruses elicit a TH1-mediated immune response, which down-regulates TH2 responses. The first proposed mechanism of action of the hygiene hypothesis stated that insufficient stimulation of the TH1 arm and stimulating the cell defense of the immune system, leads to an overactive TH2 arm. This in turn stimulates the antibody-mediated arm of the immune system, which lead to allergic diseases63, 64
