Atopic dermatitic презентация

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Atopic dermatiticDefinition 
 Atopic dermatitis is a chronic, pruritic inflammatory skin diseaseEpidemiology
 affects up to 25% of children and 2–3% of adults
Pathogenesis
 complex 
 genetic, immunologic, and environmental factors
 dysfunctional skin barrierrisk factors 
 family history of atopy - 70%; develops 2-clinical findings 
 Erythema
 Edema 
 Xerosis 
 erosions/excoriations 
 oozingEssential features— must be present
  Pruritus 
 Eczema (acute, subacute, chronic) 
 TypicalImportant features
  seen in most cases, adding support to the diagnosis:Associated features
  help to suggest the diagnosis of atopic dermatitis butExclusionary conditions
  • Scabies • Seborrheic dermatitis • Contact dermatitis (irritantPatients with presumed atopic dermatitis should have their diagnosis based onCommon associations/comorbidities
  food allergies, asthma, and allergic rhinitis/rhinoconjunctivitis.
 AD canSCORAD (Scoring Atopic Dermatitis) 
 Extent of the areas affected (%)
 IntensityBiomarkers
 May be IgE elevated (including allergen-specific)
 new T-lymphocyte subsets, asTopical corticosteroids for patients who failed to respond to good skinclinical situations in which topical calcineurin inhibitors (TCI) may be preferablePhototherapy
  second line treatment, after failure of first-line treatment (emollients,Cyclosporine is effective and recommended as a treatment option for patients



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Atopic dermatitic


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Definition Atopic dermatitis is a chronic, pruritic inflammatory skin disease that occurs most frequently in children, but can also affect adults. It follows a relapsing course. often associated with elevated serum immunoglobulin (IgE) levels and a personal or family history of type I allergies, allergic rhinitis, and asthma. Atopic eczema is synonymous with AD.

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Epidemiology affects up to 25% of children and 2–3% of adults onset is most common between 3 and 6 months of age approximately 60% of patients develop the eruption in the first year of life and 90% by 5 years of age Majority have resolution by adulthood, 10 to 30% develop symptoms as adults

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Pathogenesis complex genetic, immunologic, and environmental factors dysfunctional skin barrier and dysregulation of the immune system

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risk factors family history of atopy - 70%; develops 2- 3-fold higher in one atopic parent, 3-5-fold if both parents are atopic; maternal history - more predictive loss of function mutations in the filaggrin (FLG) gene encoding profilaggrin (degradation products - filaggrin monomers - key roles in the terminal differentiation of the epidermis and formation of the skin barrier including the stratum corneum)  Filaggrin breakdown products are part of natural moisturizing factor, which contributes to epidermal hydration and barrier function.  FLG null mutations confer a risk for earlier-onset AD, and for more severe, persistent disease most studies of dietary modification of the maternal or infant diet do not show a protective effect, except breastfeeding for the first 6 months

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clinical findings Erythema Edema Xerosis erosions/excoriations oozing and crusting, and lichenification vary by patient age and chronicity of lesions Pruritus is a hallmark of the condition that is responsible for much of the disease burden borne by patients and their families.

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Essential features— must be present  Pruritus  Eczema (acute, subacute, chronic) Typical morphology and age specific patterns: 1. Facial, neck, and extensor involvement in infants and children 2. Current or previous flexural lesions in any age group 3. Sparing of the groin and axillary regions Chronic or relapsing history

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Important features  seen in most cases, adding support to the diagnosis: • Early age of onset • Atopy • Personal and/or family history • Immunoglobulin E reactivity • Xerosis

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Associated features  help to suggest the diagnosis of atopic dermatitis but are too nonspecific to be used for defining or detecting atopic dermatitis for research and epidemiologic studies: • Atypical vascular responses (facial pallor, white dermographism, delayed blanch response) • Keratosis pilaris/ pityriasis alba/ hyperlinear palms/ icthyosis • Ocular/periorbital changes • Perifollicular accentuation/ lichenification/ prurigo lesions

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Exclusionary conditions  • Scabies • Seborrheic dermatitis • Contact dermatitis (irritant or allergic) • Icthyoses • Cutaneous T-cell lymphoma • Psoriasis  • Photosensitivity dermatoses • Immune deficiency diseases • Erythroderma of other causes

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Patients with presumed atopic dermatitis should have their diagnosis based on the criteria summarized above Patients with presumed atopic dermatitis should have their diagnosis based on the criteria summarized above skin biopsy or other tests (such as serum IgE, potassium hydroxide (KOH) preparation, patch testing, and/or genetic testing) may be helpful to rule out other or associated skin conditions.

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Common associations/comorbidities food allergies, asthma, and allergic rhinitis/rhinoconjunctivitis. AD can be the start of the “atopic march,” given the frequent subsequent development of one or more of the other atopic conditions. Sleep disturbance - common due to significant itch Depression, attention deficit hyperactivity disorder (ADHD) in children

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SCORAD (Scoring Atopic Dermatitis)  Extent of the areas affected (%) Intensity of a typical lesion (absent = 0; mild = 1; moderate = 2; severe = 3) with respect to: Erythema Edema-papules Crust formation Excoriation Lichenification Dryness of unaffected areas 3. Subjective symptoms: Itching (0-10 on visual analog scale)Sleep disturbance (0-10 on visual analogue scale) SCORAD = A/5 + 7 x B/2 + CA = % Extent/100B = Intensity/18C = Subjective symptoms/20VALUES = Mild: 1-14 Moderate 15-39 Severe 40-103 

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Biomarkers May be IgE elevated (including allergen-specific) new T-lymphocyte subsets, as well as novel cytokines and chemokines: serum levels of CD30, Macrophage-Derived Chemoattractant (MDC), interleukins (IL)-12, -16,-18,-31, and Thymus and Activation-Regulated Chemokine (TARC) none of these markers shown sensitivity or specificity to support general clinical use for diagnosis or monitoring. Markers for prognosis: high total serum IgE levels and filaggrin gene null mutations trend to predict a more severe course

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Topical corticosteroids for patients who failed to respond to good skin care and regular use of emollients alone. Topical corticosteroids for patients who failed to respond to good skin care and regular use of emollients alone. twice-daily application of corticosteroids, evidence suggests that once-daily application of some corticosteroids may be sufficient

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clinical situations in which topical calcineurin inhibitors (TCI) may be preferable to topical steroids Side effects to steriods Sensitive areas (e.g., face, anogenital, skin folds) Steriod-induced atrophy Long-term uninterrupted topical steriod use TCI are recommended for use on actively affected areas as a steroid-sparing agent For patients with AD <2 years of age with mild to severe disease, off-label use of 0.03% tacrolimus or 1% pimecrolimus ointment can be recommended. Pimecrolimus cream and tacrolimus ointment may cause skin burning and pruritus, especially when applied to acutely inflamed skin. Initial treatment of patients with AD using topical corticosteroids should be considered to minimize TCI application site reactions. Patients with AD should be counseled about the possibility of these reactions. Proactive, intermittent use of TCI as maintenance therapy (2-3 times per week) on areas that commonly flare is recommended to help prevent relapses while reducing the need for topical corticosteroids, and is more effective than the use of emollients alone.

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Phototherapy second line treatment, after failure of first-line treatment (emollients, topical steroids, and topical calcineurin inhibitors). Phototherapy can be used as maintenance therapy in patients with chronic disease. Phototherapy treatment of all forms should be under the guidance and ongoing supervision of a physician knowledgeable in phototherapy techniques. The light modality chosen should be guided by factors such as availability, cost, patient skin type, skin cancer history, patient use of photosensitizing medications, etc. The dosing and scheduling of light should be based upon minimal erythema dose (MED) and/or Fitzpatrick skin type

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Cyclosporine is effective and recommended as a treatment option for patients with AD refractory to conventional topical treatment. Cyclosporine is effective and recommended as a treatment option for patients with AD refractory to conventional topical treatment. Azathioprine is recommended as a systemic agent for the treatment of refractory atopic dermatitis Methotrexate Mycophenolate mofetil Systemic steroids should be avoided if possible for the treatment of AD. Their use should be exclusively reserved for acute, severe exacerbations and as a short-term bridge therapy to other systemic, steroid-sparing therapy.

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