A T O P I C  D E R M A T I T I S
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A T O P I C  D E R M A T I T I S A T O P I C D E R M A T I T I S Document Transcript

  • Please purchase PDFcamp Printer on http://www.verypdf.com/ to remove this watermark. ATOPIC DERMATITIS:CLINICAL IMPLICATIONS &MANGEMENT By Dr M.YOUSRY ABDEL-MAWLA Atopic dermatitis (AD) : chronically relapsing& genetically determined skin disorder with an immunologic basis. Major clinical characteristics Pruritus u Typical morphology and distribution (ie, flexural lichenification and linearity inu adults, facial and extensor involvement in infants and young children) Chronic or chronically relapsing dermatitis u Personal or family history of atopy (eg, asthma, allergic rhinoconjunctivitis, u Minor characteristics Xerosis (dry skin) u Ichthyosis/palmar hyperlinearity/keratosis pilaris u Hand and/or foot , cheilitis & nipple eczema u Susceptibility to cutaneous infection u Erythroderma u Pityriasis alba u Pruritus with sweatingu White dermographism.u Intolerance of woolu Impaired cell-mediated immunityu Immediate type I skin test response u Recurrent conjunctivitisu Keratoconusu Anterior subcapsular cataractsu Orbital darkening u Infraorbital fold (eg, Dennie pleat, Morgan fold) u Sensitivity to emotional factors u Peripheral blood abnormalities in AD Increased IgE levels,u Eosinophilia, u Chronic macrophage activation u Increases in IL-4- and IL-5-secreting TH 2-type cells. u Decreases in interferon gamma (IFN-gamma)-secreting TH 1 cells. u Increased spontaneous histamine release from basophilsu Increased serum levels of eosinophil cationic protein and soluble E-selectin (sE-u selectin) Immunologic pathways involved in the progression of AD The acute skin lesions : associated with marked infiltration of TH 2 cells.u
  • Please purchase PDFcamp Printer on http://www.verypdf.com/ to remove this watermark. Chronic AD : infiltration of eosinophils and macrophages. A switch to T helper typeu 1 (TH 1) cellular responses. This biphasic switch TH 2/TH 1 switch in immune responses : paralleled clinicallyu and histologically by acute papulation and spongiosis followed by development of lichenification, epidermal hyperplasia, and dermal fibrosis. Mechanisms of Chronic Skin Inflammation in AD -Epidermal keratinocytes produce increased levels of chemokines enhancing theu chemotaxis of eosinophils. -Mechanical trauma: induces the release proinflammatory cytokines fromu epidermal kera-tinocytes. The prolonged survival of eosinophils:due to Increased IL-5 expression u Colonization by superantigen-producing Staphylococcus aureus: Superantigensu stimulate epidermal macrophages & Langerhans cells to produce cytokines The environmental triggers: Xerosis , Contact with aeroallergens, Infectiousu agents Foods,Climate and Psych The xerotic epidermis due to ceramides reduction, provokes and sustainsu inflammation by activation of an epidermis-initiated cytokine cascade. Bacterial skin flora in both lesional and nonlesional skin in AD secreteu ceramidase, metabolizing ceramide and adding to the deficiency of ceramide in the stratum corneum MANGEMENTS Rehydration of the stratum corneum. Adequate rehydration preserves the stratum corneum barrier.u Hydrophobic lotions and creams, such as Cetaphil u Baths : followed by the immediate application of an occlusive emollientu Emollients : hydrophobic and ointment-based; eg vaseline petrolatumu jelly,urea(10%), alpha-hydroxy acid, and lactic acid preparations. MEDICATIONS Topical corticosteroids : applied only to areas of acute exacerbations. emollientsu should be used over the remainder of the skin. Formulations of steroids in ascending order of occlusiveness are lotions,u creams, gels, and ointments. Systemic corticosteroids :in severe chronic AD. Prednisone:(1-2 mg/kg/d PO for 7-u to 14-d pulse therapy; followed by slow taper) .Decreases inflammation by reversing increased capillary permeability andu suppressing PMN activity. Antihistamines(diphenhydramine, hydroxyzine, or doxepin):systemicu antipruritics, sedatives, and mild anxiolytics.. .. Antimicrobials u Gamma linolenic acidu Evening primose oil(Epogram500 mg/day x1-3 months) Immunomodulators in Atopic dermatitis
  • Please purchase PDFcamp Printer on http://www.verypdf.com/ to remove this watermark. Topical immunomodulators:u Topical tacrolimus (FK506, Protopic) Topical pimecrolimus (ASM981, Elidel). Systemic immunomodulators:u Cyclosporine (Sandimmune) Mycophenolate mofetil . Interferon-gamma (IFN-?) Intravenous immunoglobulin. Mechanisms of macrolides immunosuppressive action Bind to their respective immunophilins ± Inhibit the phosphatase action of calcineurin ± Block nuclear translocation of the cytoplasmic subunit of the nuclear factor of± activated T cells transcription factor. Reduce itching and inflammation by suppressing the release of cytokines from T± cells. OTHER IMMUNOMODULATORS Interferonsu IFN-? therapy(50ug/m2 subcutaneous injection dailyx 3 months) correlates with decreased total circulating eosinophil counts. Intravenous ?-globulin (IVIG)( 2 g/kg,): immunomodulatory and anti-u inflammatory actions. Improves glucocorticoid receptor binding affinity Leukotriene antagonists u Zafirlukast (AccolateTab.: 20 mg). Phosphodiesterase inhibitorsu PDE inhibitors ( Ro 20-1724) reduce IL-10 and PGE2 by atopic monocytes. A Therapeutic Modality Ultraviolet light UVB including Narrow band UVB(311nm ) settings u A closing remark in AD Corticosteroids, UV therapy, and the immunosuppressant macrolides are allu therapeutic agents that are likely to be effective in controlling the complex inflammatory cascades of chronic AD.