a topi c dermatitis l.
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a topi c dermatitis

Atopic Dermatitis

Doctor Anne ISVY

UVSQ

general information
General information
  • Atopic Dermatitis = atopic eczema
  • Chronic inflammatory pruritic skin disorder
  • Periods of remission marked by acute inflammatory relapses: “flares”
  • Role of allergic reactions still a matter of debate
general information3
General information
  • Most common skin disease in infants and children
  • Can appear at any age:
    • Typically before the age of 5 years
    • Clears by adolescence
    • Can persist into adulthood
  • Associated with asthma and allergic rhinitis
epidemiology
Epidemiology
  • Prevalence in industrialised countries has increased in recent decades,
  • 10-20% in childhood according to various studies, country dependent:
    • lifetime occurrence: 20% in boys and 19% in girls in 1 104 children aged 3-11 years in Birmingham, UK

Kay J et al, J Am Acad Dermatol, 1994

    • lifetime occurrence: 17% in 6 755 Turkish children aged 10-11 years

Civelek E et al, J Investig Clin Immunol, 2011

  • Increasing prevalence with improving lifestyle, nutrition, environmental factors, standard of living
pathophysiology congenital skin barrier defects
PathophysiologyCongenital skin barrierdefects

ALLERGENPENETRATION

Cutaneous hyper-reactivity to environmental stimuli

Xerosis of the skin

Reduction of hydrolipidic film

Abnormal cohesion of stratum corneum cells

slide6

PathophysiologyAllergenpenetration

  • Langerhans cells: antigen-presenting cells
    • Process antigenic material in the stratum spinosum of the epidermis and present it on their surface
    • Migrate to lymphoid tissue and interact with naïve-T cells
  • Induction of activation by specific IgE on the surface
  • Production of inflammatory cytokines (IL-1, IL-6, IL-8 et TNF-a)
  • Recruitment of inflammatory cells
slide8

PathophysiologySensitisation

ECZEMA DAMAGE

  • New contact with allergen:
    • Specific T-cell activation
    • Production of inflammatory cytokines IL-4 and

IL-5

    • Specific IgE production
    • Recruitment of eosinophils
slide9

ClinicalpresentationAtopic background

Allergic rhinoconjunctivitis

Allergic conjunctivitis

Asthma

Family history of atopy in 60% of cases

slide10

ClinicalpresentationElementarylesions

Eczematiform patches: poorly definederythematous or squamous papules or vesicles (fluid-filled bumps)

Weeping, crusted lesions, fissures

Xerosis and pruriginous

Scratches and excoriations

Lichenification: thickened, scaly, red or grey skin

slide11

Scratches and excoriations

Erythematous papules or vesicles

slide12

Lichenification

Diffuse thickening of the epidermis, with resulting accentuation of skin lines

Represents chronic disease

slide13

ClinicalpresentationSites

  • Infant: exudative lesions
    • Face: eyes, infra-orbital folds, cheilitis, cheeks, forehead
    • Scalp
    • Limbs: extensor surfaces
    • Bottom
  • Children from 2 years to puberty: lichenified lesions
    • Limbs: flexor surfaces: elbow flexure, popliteal spaces
    • Neck
    • Back of hands and feet, wrists, ankles
slide18

ClinicalpresentationSites

  • Adult phase
    • Begins at puberty and frequently continues into adulthood
    • Dry, scaling, erythematous papules and plaques
    • Large lichenified plaques from chronic lesions
  • Sites
    • Flexural folds
    • Face
    • Neck
    • Upper arms and back
    • Dorsa of the hands, feet, fingers and toes
    • Nails
slide21

Cheilitis

Nail lesions

slide22

Diagnosis

  • Based on the findings of:
    • The history
    • The physical examination
slide23

DiagnosisHanfin and Rajka diagnostic criteria

  • Main features:
    • Pruritus
    • Eczema (acute, sub-acute, chronic)
    • Chronic or relapsing history
  • Frequently associated features:
    • Onset at a young age
    • Atopy (personal or family history, IgE reactivity)
    • Xerosis
  • Other features:
    • Atypical vascular responses (facial pallor, white dermographism or delayed blanch)
    • Keratosis pilaris, palmar hyperlinearity and ichthyoses
    • Ocular or periorbital changes
    • Perioral changes or periauricular lesions
    • Perifollicular accentuation, lichenification, prurigo
slide24

Keratosis pilaris

White dermographism

diagnosis
Diagnosis
  • No specific laboratory findings
    • Elevated IgE levels found in > 80% of affected patients
    • IgE levels are also elevated in patients with other atopic diseases
diagnosis26
Diagnosis
  • In case of ineffective treatment
    • Allergy skin tests (patch-test): if suspicion of contact dermatitis
    • Skin biopsy: to eliminate differential diagnosis
      • Acute phase: spongiosis (intercellular oedema between the epidermal keratinocytes leading to micro-or macrovesicles), infiltration of leukocytes, mostly lymphocytes, into the epidermis and upper dermis
      • Chronic phase: inflammation and spongiosis mild or completely absent, thickening of the epidermis, acanthosis (thickening of the stratum spinosum), hyperkeratosis (thickening of the stratumcorneum) and parakeratosis (dysfunction of the keratinisation)
slide27

DiagnosisHistopathology

Spongiosis

Lymphocytes in the epidermis

Lymphocytes surrounding dermal vessels

differential diagnosis
Differentialdiagnosis
  • Scabies
  • Seborrhoeic dermatitis
  • Psoriasis
  • Neurodermatitis
  • Systemic illnesses (malignancy, thyroid disorders and hepatic or renal failure) can cause pruritus and excoriations
  • Adults with new-onset pruritus: thorough history and complete physical examination to exclude systemic disease
  • Contact dermatitis:
    • history reveals exacerbation of the rash after contact with a particular substance
    • standard therapy unsuccessful

patch testing to identify cause of allergic contact dermatitis

complications
Complications
  • Infection
    • Lesions at any stage can develop secondary infections
    • Cause of exacerbation of eczema
      • Impetigo (staphylococcal and streptococcal infections) with crusting and weeping lesions
      • Risk of widespread herpes simplex virus infection (Kaposi's varicelliform eruption):
        • painful vesicles on an erythematous base in areas of dermatitis or on normal-appearing skin
        • constitutional symptoms can also develop
slide31

Impetigo

Highly contagious gram-positive bacterial infection of the superficial layers of the epidermis

complications33
Complications
  • When the lesions resolve, areas of hyperpigmentation or

hypopigmentation can

persist

impact
Impact

School absenteeism

Emotional stress

Sleep disturbance

Relationship problems children-parent

Irritability

Social stigma of a visible skin disorder

Mental depression in adults

treatment
Treatment
  • Education of patients and parents
    • Chronic disorder
    • Course of disease by flares
    • No risk of underdevelopment
    • Repeated treatment
    • Reassure apprehension over topical corticosteroid use
    • Fight against
      • Infection
      • Inflammation
      • Dryness
slide36

TreatmentNon-medicated management

Maintenance of an effective skin barrier

  • Avoid hot (> 33°C) and long (> 5 minutes) baths
  • Use soft and superfatted soaps
  • Avoid wool clothes, prefer cotton long sleeved underwear
  • Avoid close contact with herpes infected individuals (Kaposi's varicelliform eruption)
  • Respect normal immunisation schedule
  • No systematic food avoidance +++
slide37

Treatment Emollients

  • Mainstay of general management
  • Should by applied continuously, even if no inflammatory skin lesions
  • Once or twice daily
    • Vaseline
    • Other ointments and creams
    • Polidocanol reduces pruritic symptoms
    • Preparation with urea: intensive hydration
slide38

TreatmentTopicalglucocorticosteroids

  • First-line therapy in acute flare-ups
  • Control of moderate to very severe disease
  • Potency determined by a vasoconstriction assay utilising a numerical scale ranging from class 4 (weakest), to class 1 (superpotent)
  • Potential local side-effects:
    • Striae, petechiae, telangiectasia, atrophy, acne or rosacea (incidence correlates with length of use and potency of product)
  • Systemic side-effects remain debatable:
    • Possible suppression of the hypothalamic-pituitary-adrenal (HPA) axis
    • In rare and extreme instances, growth retardation in children
    • Systemic absorption is determined by the extent and severity of disease, drug formulation and drug potency

Callen J et al. Br J Dermatol, 2007

slide40

TreatmentTopicalglucocorticosteroids

  • Higher strength for brief periods (1 to 2 weeks) to gain quick control of disease flares
  • Choice of topical corticosteroid depends on:
    • Age of patient
    • Severity of disease
    • Area of body
  • Class 3 recommended for infants with mild disease
  • Class 2 possible for moderate-to-severe flares (except on the face and bottom of infant)
  • Class 1 should not be used in children under 12 years of age and are limited to a 1- to 2-week course in patients with severe flares
slide41

TreatmentTopicalglucocorticosteroids

  • Acute flare-ups:
    • Apply once a day (better in the evening)
    • In combination with emollient skin care
    • Count the number of tubes used between 2 consultations
    • Initial therapy: high potent steroid
    • Secondary: time-dependant dose reduction or change to lower potency
  • Applied on unaffected skin twice weekly prevents future flare-ups
slide42

TreatmentTopicalcalcineurininhibitor

  • Topical anti-inflammatory therapy as second-line
  • Tacrolimus ointment (0.03%) and pimecrolimus cream (1%) approved in children > 2 years
  • Tacrolimus (0.1%) ointment: only for use in adults
  • Useful alternative for sensitive skin areas (face,

intertriginous areas)

  • Side-effects :
    • Transient burning sensation of the skin
    • Viral infections (eczema herpeticum, eczema molluscatum)
    • No evidence of a causal link with cancer
slide43

TreatmentNew nonsteroidalbarriercreams

  • Approved as “medical devices” by the FDA
  • For mild-to-moderate atopic dermatitis in both paediatric and adult patients
  • Example: Atopiclair®
    • Hyaluronic acid which acts as a moisturising agent
    • Glycyrrhetinic acid, which is believed to have anti-inflammatory effects
    • Other factors thought to have anti-oxidant properties and to restore the barrier function of the skin
slide44

TreatmentPhototherapy

Standard second-line treatment for adults

PUVA, broad-band UVB, narrow-band UVB, UVA

Combination with corticosteroids in acute flare phases

UV therapy is restricted to adolescent > 12 years

slide45

TreatmentSystemic

  • No systemic steroid

(risk of relapse after discontinuation, side effects)

  • Antihistamines
    • Sedative properties
    • Useful as a short-term adjuvant to topical treatment

during relapses with severe pruritus

  • Hyposensitisation (immunotherapy):
    • Not established for the treatment of AD
    • Well-controlled studies needed
slide46

TreatmentSystemic

  • Cyclosporin A:
    • Reduces levels of proininflammatory cytokines
    • Severe refractory disease
    • Side effects: renal toxicity, blood pressure
    • 3-5mg/kg/d 2 months and dose reduction during 6 months to avoid relapse after stopping
    • Monitoring of blood pressure and renal function
slide47

TreatmentSystemic

  • Azathioprine
    • Non licensed indication
    • Evidence of efficacy in severe recalcitrant disease
    • Side effects: myelosuppression, hepatotoxicity, gastrointestinal disturbances, increased susceptibility for infections, skin cancer?
slide48

TreatmentFuture Perspectives

  • Increasing knowledge of the cellular and molecular aspects of atopy
  • Inhibiting components of the allergic inflammatory response
    • Cytokine modulation (TNF inhibitor)
complications of treatment
Complications of treatment
  • Kaposi's varicelliform eruption
    • Emergency admittance
    • Treatment with acyclovir (Zovirax, 500 mg/m2 x3 per day; slow perfusion: 20 mg/kg/8 hours)
  • Impetigo (< 5 lesions)
    • Daily bath
    • Topical antiseptic (chlorhexidine)
    • Topical antibiotic: fusidic acid or mupirocin (x2/day, 5 days)
  • Widespread impetigo (> 5 lesions, fever):
    • +/- avoid school, family circle examination
    • systemic antibiotic 7-10 days:
      • Macrolides: erythromycin, josamycin
      • Penicillins: cloxacillin, amoxicillin + clavulanic acid
      • Synergistin: pristinamycin
      • Oral fusidic acid
conclusion
Conclusion
  • Most common skin disease in children
  • Prevalence still increasing
  • Complex disease, many features still not understood
  • Treatment :
    • Partner with doctor
    • Education++
    • Emollients and topical corticosteroids
conclusion51
Conclusion
  • Need new appropriate studies:
    • On prevention of atopic dermatitis
    • Systematic reviews concerning treatment
    • Knowledge of cellular and molecular aspects of atopic disease
slide54

Correct answer

AD is the most common skin disease in infants and children (10-20% prevalence in childhood)

Next question

slide55

Wrong answer

AD is the most common skin disease in infants and children (10-20% prevalence in childhood)

Next question

slide57

Correct answer

There are congenital defects of the skin barrier that allow allergen penetration to stimulate the atopic response

Next question

slide58

Wrong answer

There are congenital defects of the skin barrier that allow allergen penetration to stimulate the atopic response

Next question

slide59

Diagnosis of atopic dermatitis is easy because IgE levels are always elevated

CORRECT

WRONG

slide60

Correct answer

There is no specific laboratory test to diagnose AD; although >80% of patients have elevated levels of IgE this is also true in other atopic diseases e.g. allergic rhinitis, asthma etc.

Next question

slide61

Wrong answer

There is no specific laboratory test to diagnose AD; although >80% of patients have elevated levels of IgE this is also true in other atopic diseases e.g. allergic rhinitis, asthma etc.

Next question

slide62

Atopic dermatitis can have a great impact on both the child’s and the parents’ lives

CORRECT

WRONG

slide63

Correct answer

AD can have a profound impact on both the patient and their family: problems include absenteeism from school, depression, irritability and sleep disturbance

Next question

slide64

Wrong answer

AD can have a profound impact on both the patient and their family: problems include absenteeism from school, depression, irritability and sleep disturbance

Next question

slide66

Correct answer

Emollients are the mainstay of the general management of AD and should be used continuously, applied once or twice every day even in the absence of inflammatory skin lesions

Return to start

slide67

Wrong answer

Emollients are the mainstay of the general management of AD and should be used continuously, applied once or twice every day even in the absence of inflammatory skin lesions

Return to start