-DefinitionEpidemiology PathogenesisPathogenesis Clinical ManifestationsClinical Manifestations DiagnosisDiagnosis Differential DiagnosisDifferential Diagnosis ComplicationsComplicationsTreatmentPrognosisPrevention

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)

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.

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.

PATHOGENESISPATHOGENESIS

1. Genetic predisposition 2. Defective skin barrier 3. Abn immune response

Host Environment Environment Allergens Irritants Infections Pollutants Stress Weather change

AD

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

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.

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.

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.

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

FLARE FACTORS IN ATOPIC DERMATITIS

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

CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS Acute AD: intensely pruritic erythematous

papules and plaques with secondary excoriations; Vesicles and serous crusting also seen

CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

Erythematous, scaling papules & plaques with excoriation

Sub-acute

CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS Chronic AD: characterized by thickened,

hyperkeratotic plaques with lichenification as well as prurigo nodularis (“picker’s nodules

CLINICAL PHASES

Three Stages of Atopic DermatitisInfantile Atopic DermatitisChildhood Atopic DermatitisAdolescent and Adult Stage

Atopic Dermatitis

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

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

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

The skin is often dry, scaly and red with small scratch marks made by sharp baby nails.

Involvement of the cheeks is characteristic of the infantile pattern of AD.

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

Childhood Phase

erythematous crusted patches located in the antecubital fossae

CHILDHOOD ATOPIC DERMATITIS

marked lichenification and postinflammatory hyperpigmentation

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

ADOLESCENCE/ ADULT ATOPIC DERMATITIS

ADOLESCENCE/ ADULT ATOPIC DERMATITIS

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

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

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)

DIAGNOSISDIAGNOSIS Associated features

Ant. Subcap. CataractXerosis

• 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.

ASSOCIATED FEATURES

Keratoconus

Hertophe’s sign:thinning or loss of the outer third of the eyebrows

Conical deformity of the cornea

Periorbital milia Discrete, 1- to 2-mm

dome-shaped white or yellowish papulonodules

Occur individually or in clusters

Due to rubbing

• Lichen Simplex Chronicus - due to chronic rubbing

• Prurigo Nodularis – “picker’s nodules” Intensely and paroxysmally pruritic. Mostly on extremities.

ASSOCIATED FEATURES

Palmar hyperlinearity

Dermographism

Nipple eczema

ASSOCIATED FEATURES Immediate skin test reactivityElevated serum IgEEarly age of onsetTendency toward cutaneous infectionsNonspecific hands & feet dermatitisFacial pallor/ erythemaCourse influenced by environmental factors

DIAGNOSISDIAGNOSIS

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

DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSIS

Seborrheic dermatitis

Scabies Contact dermatitis

Localized to areas of exposure & not associated w/ xerosis

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.

COMPLICATIONSCOMPLICATIONSInfections (Viral)

Herpes simplex (Eczema herpeticum

Painful cluster of vesicles on erythematous base that ulcerate & then form crust

COMPLICATIONSCOMPLICATIONS

Molluscum contagiosum

Smooth dome shape papule (2-6 mm) with central umbilication

Infections (Viral)

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)

COMPLICATIONSCOMPLICATIONS

Infections (Fungal)Malassezia furfur

Usually in head and neck dermatitis

Trichophyton rubrum

Exfoliative dermatitis: may develop in patients with extensive skin involvement

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

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

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

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

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

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

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

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

TREATMENT• Local side effects of TCS

hyperpigmentation Telangiectasia Acne

TREATMENT

Skin atrophyStriae

Local side effects of TCS

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.

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 .

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.

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

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.

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.

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

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.

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

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.

Flawless Skin