atopic dermatitis1
TRANSCRIPT
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-DefinitionEpidemiology PathogenesisPathogenesis Clinical ManifestationsClinical Manifestations DiagnosisDiagnosis Differential DiagnosisDifferential Diagnosis ComplicationsComplicationsTreatmentPrognosisPrevention
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ATOPIC DERMATITIS Introduction:
The word "dermat itis"
skin inflammation
Atopic" refers to diseases that are hereditary, tend to run in families, and often occur together. Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in early infancy (an adult-onset variant is recognized)
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ATOPIC DERMATITIS Introduction:
characterized by:pruritus eczematous lesions xerosis (dry skin) lichenification (thickening of the skin and an increase in skin markings).
Atopic dermatitis (AD), or eczema is the most common chronic relapsing skin disease seen in infancy and childhood.
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EPIDEMIOLOGY It affects 10-30% of children worldwide
frequently occurs in families with other atopic diseases, such as asthma, allergic rhinitis, and food allergyAD may be more common among Caucasian and Chinese persons, but it affects all races.
Sex: The male-to-female ratio is 1:1.4.
Begins in infancy with 50% occurring in 1st year of life & 30% diagnosed between 1 to 5 yr of age.
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PATHOGENESISPATHOGENESIS
1. Genetic predisposition 2. Defective skin barrier 3. Abn immune response
Host Environment Environment Allergens Irritants Infections Pollutants Stress Weather change
AD
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PATHOGENESISPATHOGENESIS
Family history of atopy Child risk of atopy
Biparental (same allergy)Biparental or uniparental + sibling (different allergy)Uniparental or siblingNone
50-80%40-50
20-405-15
Genetic Predisposition
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PATHOGENESISPATHOGENESIS Defective skin barrier defective barrier function in the stratum
corneum of Atopic dermatitis patients, leading to excess transepidermal water loss the entry of antigens that result in the
production of inflammatory cytokines to impairment of innate immunity
Mutations in the filaggrin gene, which encodes a protein necessary for terminal differentiation of epidermis, have been shown in up to 50% of severe patients with AD.
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PATHOGENESISPATHOGENESISAbnormal immune responseAbnormal immune response The immune hypothesis invokes an
imbalance in the T lymphocytesAcute AD: TH 2 cells predominating cytokine
production of interleukins 4, 5, 12, and 13 and granulocyte macrophage colony-stimulating factor, causing:
an increase in IgE and lowered interferon gamma levels.
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PATHOGENESISPATHOGENESISAbnormal immune responseAbnormal immune response chronic AD: the TH 1-type cells predominate. Other cell types
are also involved in the process, including eosinophils, Langerhans cells, keratinocytes, and B cells.
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EXACERBATING FACTORS(TRIGGERS)
Environmental FactorsFood
Cow’s milk, egg, peanuts, soy, wheat, fishAeroallergens
House dust mitesIrritants
wool, acrylic, soaps, detergentsMicrobes
S. aureus toxins (superAg specific IgE)Extreme of temperature & humidity, sweating, stress
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FLARE FACTORS IN ATOPIC DERMATITIS
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CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONSIntense pruritus, especially at
night, and cutaneous reactivity are the cardinal features of ADScratching and excoriation cause increased skin inflammation that contributes to the development of more pronounced eczematous skin lesionsEczematous eruption leads to lichenified dermatitis
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CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS Acute AD: intensely pruritic erythematous
papules and plaques with secondary excoriations; Vesicles and serous crusting also seen
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CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
Erythematous, scaling papules & plaques with excoriation
Sub-acute
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CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS Chronic AD: characterized by thickened,
hyperkeratotic plaques with lichenification as well as prurigo nodularis (“picker’s nodules
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CLINICAL PHASES
Three Stages of Atopic DermatitisInfantile Atopic DermatitisChildhood Atopic DermatitisAdolescent and Adult Stage
Atopic Dermatitis
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CLINICAL PHASESInfantile Phase ( 0-2 years) 60% of case AD present in the first
year of life, after 2 months of age Xerosis occurs early and often involves
the whole body Begin as itchy erythema of the cheeks
Most cases the symptoms will disappear toward the end of the second year
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CLINICAL PHASES
Oozing, crusted, erythematous, scaly plaques on the scalp and face, sparing the diaper areaWhen baby begins to crawl, the extensor extremities become more involved
Infantile Phase
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CLINICAL PHASESInfantile Phase May become desquamate leading to
erythroderma. The role of food allergy in infantile and
childhood atopic dermatitis has been clarified
Egg, peanut, milk, wheat, fish, soy, and chicken may exacerbate infantile AD
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The skin is often dry, scaly and red with small scratch marks made by sharp baby nails.
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Involvement of the cheeks is characteristic of the infantile pattern of AD.
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CLINICAL PHASES
Childhood Phase ( 2-12 years ) Characterized by less acute lesions Distribution: antecubital and popliteal fossae, flexor wrist, eyelids, and face. Persistent rubbing and scratching leads to lichenified plaques and excoriations Severe atopic dermatitis involving more than 50% of body surface area is associated with growth retardation
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Childhood Phase
erythematous crusted patches located in the antecubital fossae
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CHILDHOOD ATOPIC DERMATITIS
marked lichenification and postinflammatory hyperpigmentation
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ADOLESCENCE/ ADULT ATOPIC DERMATITIS
Age > 12 years old
Flexural lichenified eczema with facial involvement in periorbital regions , Upper trunk, shoulders, scalp affected
chronic remissions and exacerbations
70% develop hand dermatitis some times in their lives
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ADOLESCENCE/ ADULT ATOPIC DERMATITIS
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ADOLESCENCE/ ADULT ATOPIC DERMATITIS
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DIAGNOSISDIAGNOSIS
Hannifin & Rajka diagnosis of AD in 1980 MAJOR FEATURES
1.pruritus2.typical morhology and distribution
Facial and extensor eczema in infants and childrenFlexural eczema in adolescent
3.chronicity4. Personal or family family history of atopy
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DIAGNOSISDIAGNOSIS ASSOCIATED FEATURES
Keratosis Pilaris – perifollicular hyperkeratosis on extensor arms, thighs and cheeks
Ichthyosis Vulgaris – This common genetic d/o is seen in 50% of AD patients
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Dennie-Morgan Lines - symmetric, prominent fold (single or double) just beneath the margin of the lower eyelid Periorbital darkening or “allergic shiners” - asymptomatic, symmetric, blue-gray discolorations of the periorbital skin with accentuation of the lower orbit (seen in up to 60% of atopic patients)
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DIAGNOSISDIAGNOSIS Associated features
Ant. Subcap. CataractXerosis
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• Pityriasis Alba - patches of hypopigmentation with fine scale, most common on the face, most noticeable in darkly pigmented children.
•Chelitis - dry, crusty, chapped lips or fissuring of the commissures aggravated by licking.
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ASSOCIATED FEATURES
Keratoconus
Hertophe’s sign:thinning or loss of the outer third of the eyebrows
Conical deformity of the cornea
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Periorbital milia Discrete, 1- to 2-mm
dome-shaped white or yellowish papulonodules
Occur individually or in clusters
Due to rubbing
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• Lichen Simplex Chronicus - due to chronic rubbing
• Prurigo Nodularis – “picker’s nodules” Intensely and paroxysmally pruritic. Mostly on extremities.
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ASSOCIATED FEATURES
Palmar hyperlinearity
Dermographism
Nipple eczema
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ASSOCIATED FEATURES Immediate skin test reactivityElevated serum IgEEarly age of onsetTendency toward cutaneous infectionsNonspecific hands & feet dermatitisFacial pallor/ erythemaCourse influenced by environmental factors
DIAGNOSISDIAGNOSIS
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DIFFERENTIAL DIAGNOSESDIFFERENTIAL DIAGNOSESAtopic dermatitis Eczematous D/O of Infancy Systemic D/O with
eczematous dermatitisScabies Atopic dermatitis Wiskott-Aldrich syndrome
Seborrheic dermatitis Seborrheic dermatitis Selective IgA deficiency
Allergic contact dermatitis
Scabies X-linked agammaglobulinemia
Mycosis Fungoides Psoriasis Ataxia-telangiectasia
Nummular eczema Allergic contact dermatitis Chronic granulomatous disease
Dermatophytosis Irritant contact dermatitis Biotin deficiency
HIV-associated disease Ichthyosis vulgaris Cystic Fibrosis
Familial keratosis pilaris Tinea corporis Netherton syndrome
Dermatitis herpetiformis Nummular eczema Langerhans cell histiocytosis
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DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSIS
Seborrheic dermatitis
Scabies Contact dermatitis
Localized to areas of exposure & not associated w/ xerosis
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COMPLICATIONSCOMPLICATIONS
Infections (BacterialInfections (BacterialStaphylococcus aureusStaphylococcus aureus
Seen in >90% of AD Seen in >90% of AD skin lesionsskin lesions
Moist oozing red scaly plaques & pustules with honey colored crust formation, folliculitis, impetigo & pyoderma.
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COMPLICATIONSCOMPLICATIONSInfections (Viral)
Herpes simplex (Eczema herpeticum
Painful cluster of vesicles on erythematous base that ulcerate & then form crust
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COMPLICATIONSCOMPLICATIONS
Molluscum contagiosum
Smooth dome shape papule (2-6 mm) with central umbilication
Infections (Viral)
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Eczema Vaccinatum• Serious complication that occurs in atopics receiving the smallpox vaccine.
• Vaccinia lesions spread to skin that is currently or recently affected by AD.
• Tx: Vaccine Immune Globulin (VIG)
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COMPLICATIONSCOMPLICATIONS
Infections (Fungal)Malassezia furfur
Usually in head and neck dermatitis
Trichophyton rubrum
Exfoliative dermatitis: may develop in patients with extensive skin involvement
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COMPLICATIONSCOMPLICATIONSExfoliative dermatitisassociated with
,
caused by: superinfection (e.g., with toxin-producing S. aureus or
HSV infectioninappropriate therapy
In some cases, the withdrawal of systemic glucocorticoids used to control severe AD precipitates exfoliative erythroderma
generalized redness, scaling, crusting, systemic toxicity, lymphadenopathy, and fever
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COMPLICATIONSCOMPLICATIONS Ocular
Cataracts may be a primary manifestation of AD or from extensive use of systemic and topical glucocorticoids, particularly around the eyes
Atopic keratoconjunctivitis usually bilateral
itching, burning, tearing, and copious mucoid discharge
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COMPLICATIONSCOMPLICATIONS Ocular
Vernal conjunctivitis typically occurs in younger patients is associated with papillary hypertrophy of the upper eyelid conjunctiva
Keratoconus i
conical deformity of the cornea
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TREATMENT The treatment of AD requires a
systematic, multifaceted approach that incorporates:
healing the skin and keeping it healthy
identification and elimination of flare factors
treating symptoms when they do occur
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TREATMENTCutaneous Hydration Lukewarm soaking baths for 15-20 min followed by the application of an occlusive
emollient Hydrophilic ointments of varying degrees of
viscosity can be used according to the patient's preference
Occlusive ointments are sometimes not well tolerated
Dressings may also serve as effective barriers against persistent scratching
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TREATMENTTopical Corticosteroids There are 7 classes of topical glucocorticoids Potency classified from group I (most potent)
to VII (least potent) First introduced in the 1950s and are
currently the mainstay of prescription therapy for atopic dermatitis
Safe and effective when used as recommended
Weakest steroid that will keep the eczema under control should be used
Potent steroids should be used in short pulses, generally 2-3 weeks
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TREATMENTFACTORS TO CONSIDER WHEN CHOOSING A
TOPICAL STEROID Age of patient Site to be treated Total area of body to be treated Severity of disease Duration of treatment
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TOPICAL STEROIDS• Group I• Temovate Cream/Ointment• Ultravate Cream/Ointment• Psorcon Cream/Ointment• Diprolene Ointment•• Group II• Diprolene Cream• Halog Cream/Ointment• Lidex Cream/Ointment• Topicort Cream/Ointment•• Group III• Aristocort Cream/Ointment• Cutivate Ointment• Elocon Ointment• Kenalog Cream/Ointment• Topicort Cream• Valisone Ointment
• Group IV• Elocon Cream• Synalar Cream/Ointment• Westcort Ointment•• Group V• Aristocort Cream• Cutivate Cream• Dermatop Cream• Kenalog Cream• Locoid Cream/Ointment•• Group VI• Aclovate Cream/Ointment• DesOwen Cream/Ointment• Synalar Cream• Hytone Cream
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TREATMENT• Local side effects of TCS
hyperpigmentation Telangiectasia Acne
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TREATMENT
Skin atrophyStriae
Local side effects of TCS
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TREATMENTAdverse effects of TCS Suppression of hypothalamic-pituitary-
adrenal axis Iatrogenic Cushing’s syndrome Growth retardation in infants and childrenThese effects are usually associated with the
large body surface area use of potent TCS.
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TREATMENT Topical Calcineurin Inhibitors Pimecrolimus cream 1% (Elidel) is indicated for mild to moderate AD. Tacrolimus ointment 0.1% and 0.03%
(Protopic) is indicated for moderate to severe AD. Both are approved for short-term or
intermittent long-term treatment of AD in patients ≥2 yr whose disease is unresponsive to or who are intolerant of other conventional therapies .
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TREATMENT Topical Calcineurin Inhibitors may be better than topical corticosteroids in
the treatment of patients whose AD is poorly responsive to topical steroids patients with steroid phobia, and of patients with face and neck
dermatitis, in which ineffective, low-potency topical corticosteroids are usually used because of fears of steroid-induced skin atrophy.
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TREATMENTTar Preparations are useful in reducing the potency of topical
glucocorticoids required in long-term maintenance therapy of AD.
Tar shampoos can be particularly beneficial for scalp dermatitis.
Adverse effects associated with tar preparations include skin irritation, folliculitis, and photosensitivity.
Antihistamines
Systemic Corticosteroids
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TREATMENTCyclosporine is a potent immunosuppressive drug
that acts primarily on T cells by suppressing cytokine gene transcription.
(5 mg/kg/day) for short-term and long-term (1 yr) use has been beneficial for children with severe, refractory AD.
Possible adverse effects include renal impairment and hypertension.
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TREATMENTPhototherapy Natural sunlight is often beneficial to patients with
AD as long as sunburn and excessive sweating are
avoided. Many phototherapy modalities are effective for AD,
including ultraviolet A-1, ultraviolet B …) Phototherapy is generally reserved for patients in
whom standard treatments fail. Short-term adverse effects with phototherapy include
erythema, skin pain, pruritus, and pigmentation. Long-term adverse effects include predisposition to
cutaneous malignancies.
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TREATMENTUnproven Therapies
Other therapies that may be considered in patients with refractory AD are as follows.
Interferon-γ Omalizumab Allergen Immunotherapy Probiotics Chinese Herbal Medications Antimetabolites
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PROGNOSIS Spontaneous resolution of AD has been reported
to occur after age 5 yr in 40-60% of patients affected during infancy.
Earlier studies suggested that approximately 84% of children outgrow their AD by adolescence;
later studies reported that AD resolves in approximately 20% of children monitored from infancy until adolescence and becomes less severe in 65%.
Of those adolescents treated for mild dermatitis, >50% may experience a relapse of disease as adults, which frequently manifests as hand dermatitis, especially if daily activities require repeated hand wetting.
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PROGNOSISPredictive factors of a poor
prognosis: widespread AD in childhood concomitant AR & asthma family history of AD in parents/sibling early age of onset being an only child very high serum IgE levels filaggrin gene null mutations
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PREVENTION Breast-feeding or a feeding with a
hypoallergenic hydrolyzed formula may be beneficial.
If an infant with AD is diagnosed with food allergy, the breast = feeding mother will need to eliminate the implicated food allergen from her diet.
Identification and elimination of triggering factors is the mainstay for prevention of flares as well as for the long-term treatment of AD.
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Flawless Skin
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