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					Atopic Dermatitis



  Alyson W. Smith, MD
   Director of Pediatric Allergy
      St. Barnabas Hospital
   Atopic dermatitis (AD) is a chronic, highly
    pruritic, eczematous skin disease that follows
    patients from early childhood into puberty and
    sometimes adulthood.




   Also referred to as eczematous dermatitis,
    the disease often has a remitting/flaring
    course, which may be exacerbated by social,
    environmental, and biological triggers.
                   Prevalence
   Approximately 15% in the US and Europe
   This represents a profound increase in recent
    years (from as low as 3% in 1960)
        Natural History of Atopic
               Dermatitis
   60% of pts develop AD by 1 year of age.
   85% of pts develop AD by age 5.
   Earlier onset often indicates a more severe course.
   Many cases resolve by age 2, improvement by puberty
    is common.
   50%-60% of pts develop respiratory allergies or asthma.
   80% of occupational skin disease occur in atopics.
   It is rare to see AD after age 50.
                    The Atopic March
   Bergmann (1998, Clin Exp Allergy)
           Prospective birth cohort study, N 1314, 5yo
           If AD at 3 mos and one parent/sibling atopic >50% chance of asthma
           at age 5-6
   Castro-Rodriquez (1999, AJRCCM)
           Longitudinal, retrospective study, N 986
           If AD and parental asthma; >75% chance of asthma during school
    years.
                         Filaggrin
   Filaggrins are filament-associated proteins which bind to
    keratin fibers in epithelial cells
   Individuals with truncation mutations in the gene coding for
    filaggrin are strongly predisposed to a severe form of dry skin,
    ichthyosis vulgaris, and/or eczema
   It has been shown that almost 50% of all severe cases of eczema
    may have at least one mutated filaggrin gene.
Ichythosis vulgaris
         Infantile atopic dermatitis




   Infants less than one year old often have widely distributed eczema.
    The skin is often dry, scaly and red with small scratch marks made by
    sharp baby nails.
   The cheeks of infants are often the first place to be affected by
    eczema.
   The diaper area is frequently spared due to the moisture retention of
    diapers. Just like other babies, they can develop irritant diaper
    dermatitis, if wet or soiled diapers are left on too long.
                    Toddlers and pre-schoolers




   As children begin to move around, the eczema becomes more localized
    and thickened. Toddlers scratch vigorously and the eczema may look
    very raw and uncomfortable.
   Eczema in this age group often affects the extensor (outer) aspects of
    joints, particularly the wrists, elbows, ankles and knees. It may also affect
    the genitals.
   As the child becomes older the pattern frequently changes to involve the
    flexor surfaces of the same joints (the creases) with less extensor
    involvement. The affected skin often becomes lichenified i.e. dry and
    thickened from constant scratching and rubbing,
   In some children the extensor pattern of eczema persists into later
    childhood.
     Atopic dermatitis in school-age children




   Older children tend to have the flexural pattern of eczema and it most
    often affects the elbow and knee creases. Other susceptible areas
    include the eyelids, earlobes, neck and scalp.
   Many children develop a 'nummular' pattern of atopic dermatitis. This
    refers to small coin-like areas of eczema scattered over the body. These
    round patches of eczema are dry, red and itchy and may be mistaken
    for ringworm (a fungal infection).
   Mostly the eczema improves during school years and it may completely
    clear up by the teens, although the barrier function of the skin is never
    entirely normal.
Xerosis (dry skin)
Lichenification
Nummular Eczema
Keratosis pilaris
Palmar hyperlinearity
             AD
(Juvenile Plantar Dermatosis)
      Food Allergy and Atopic Dermatitis
   Children:
      Moderate-Severe AD ( up to 33%) have (transient)
        clinically significant food allergy
      Increasing severity of AD ~ increasing risk
        of food allergy
   Adults:
      Low incidence (<2%)

   Foods responsible (~85% of cases):
      Outgrown: Milk, egg, soy, wheat

      Persistent: Peanut, nuts, fish, shellfish
    Evaluation of Food Allergy in AD
 Laboratory studies
      Specific IgE (Immunocap)-ONLY if clinically
      indicated!
      Skin prick testing
Clinical evaluation:
      Elimination diets
      Oral food challenges
             Physician supervised
             Open, single blind, double-blind,
                   placebo controlled
                    Triggers
   Irritants
                            •Heat/Sweating
         Wool
                            •Contactants
         Soaps/detergents
                                  incl. Dust mites
         Disinfectants
                            •Psychological
         “Occupational”
                            •Foods (IgE-induced)
         Tobacco smoke      vaso-dilatory items
   Microbial agents        •Aeroallergens
         Staph aureus       •Hormones
         Viral infection    •Climate
         ?Dermatophytes
                   Managing AD
                   (Preventative)
   Prevent “scratching” or rubbing
       a) apply cold compresses to itchy skin
   Carefully eliminate all the triggers of itch
       a) environmental, occupational, and
              temperature control
       b) bathing – soapless cleansers, Dove
       c) LUBRICATION –
              LUBRICATION
                    LUBRICATION
               Managing AD
                (Palliation)
   Topical anti-inflammatory agents
      a) corticosteroids (ointments>creams)
        more potent - when “acute”
        least potent needed for “chronic”
      b) Tacrolimus 0.1% ointment,
          Pimecrolimus 1% Cream
                   Corticosteroids

   These are the cornerstones of therapy of atopic
    dermatitis. The following principles should be
    adhered to while instituting topical steroid therapy:
   High potency steroids are used for a short period to
    rapidly reduce inflammation.
   Maintenance therapy, if needed is best done with
    mild steroids like hydrocortisone.
   On face and intertriginous areas, mild steroids
    should be used, mid-potency formulations are used
    for trunk and limbs.
                    Corticosteroids
   Topical steroids are applied initially twice or three times a day.
    After the symptoms are lessened, frequency of application
    should be reduced. Intermittent use if topical steroid may be
    alternated with application of emollients.
   Ointments are superior to creams or lotions.
   The potential side-effects of topical steroids should always be
    kept in mind.
      Systemic steroids: a short course of systemic steroids
    (prednisolone, triamcinolone) may occasionally be needed to
    suppress acute flare-ups.
      Intralesional steroids (triamcinolone acetonide) may help
    resolve thickened plaques of eczema not responding to topical
    agents
              Calcineuron Inhibitors
                   Indications
   Protopic (tacrolimus) Ointment, both 0.03% and 0.1% for adults; 0.03% for
    children aged 2-15 years
      For short-term and intermittent long-term therapy in the treatment of
        moderate to severe atopic dermatitis in patients
           For whom the use of alternative, conventional therapies are deemed
             inadvisable because of potential risks
                                      or
           Who are not adequately responsive to, or are intolerant of alternative,
             conventional therapies.
   Elidel (Pimecrolimus Cream 1%) for patients 2 years of age and older
      For short-term and intermittent long-term therapy in the treatment of
        mild to moderate atopic dermatitis in non-immunocompromised patients
           For whom the use of alternative, conventional therapies are deemed
             inadvisable because of potential risks
                                      or
           Who are not adequately responsive to, or are intolerant of alternative,
             conventional therapies.
           Calcineuron Inhibitors

           Advantages                Limitations
   A Rx option to CS        •Off-label for children
   No steroid atrophy              <2 yrs.
   For adults and child-    •Burning, stinging,
         ren >2yrs.                 itching, after
   Sx improvement within           application – often
         1-3 weeks.                 minimal and
                                    transient.
   Long-term intermittent
         use                 •Black box warning
             Basis for FDA concern
   Because of a perception by physicians and patients that topical pimecrolimus
    and tacrolimus are safer than steroid preparations, they had been increasingly
    been used as first-line therapy and off label. There were almost 2 million
    prescriptions written of these topical medications for children between June
    2003 and May 2004 and approximately half a million were for those under 2
    years of age.
   Known toxicity of immunosuppressant doses of systemically administered
    tacrolimus: lymphoproliferative disease, photocarcinogenicity, and increased risk
    of nonmelanoma skin cancers
   Animal studies in mice, rats, and monkeys have found an increased risk of
    lymphoma and skin cancers with topical and oral exposure to calcineurin
    inhibitors (dose used 30x maximum human dose in monkey study)
   March 2010-46 cancer cases and 71 infection cases have been reported in
    patients aged 16 and younger from 2004 to 2008 with Novartis' Elidel and
    Astellas' Protopic.
   More controlled studies are needed on the use
       of TCI, especially in patients less than two
       years.
   Long term effects not known.
   Should only be used as a second line agent.
                    Emollients

Atopic dermatitis patients frequently have dry skin
  which is aggravated during winter months.
Xerosis (dryness) breaks the barrier function of the
  skin and promotes infection and inflammation.
Ointments are preferred over lotions or creams.
Emollients should be applied immediately after a
  soaking bath to retain the moisture.
Emollients containing urea or alpha-hydroxy acids
  often cause stinging or burning sensations.
                     Antihistamines

   Antihistamines give variable results in controlling
    pruritus of atopic dermatitis since histamine is not the
    only mediator of itching in atopic patients.
   Any of the non-sedating antihistamines like cetirizine,
    loratadine or fexofenadine may be used.
   The conventional antihistamines like diphenhydramine
    or hydroxyzine may give better results for their
    additional actions as a sedative or anxiolytic.
   Topical antihistamines should be avoided for their
    sensitizing potential.
                       Antimicrobials

Infections and colonization with Staphylococcus aureus may aggravate
   or complicate AD.
Antibiotics like erythromycin, cephalosporins, or cloxacillin are
   usually prescribed.
Dermatophytosis or Pityrosporum infections are treated with
   antifungals.
Acyclovir or other appropriate antiviral agents should be promptly
   advised for treatment of herpes simplex infections.
        Oral immunomodulators

   Cyclosporine:
    By virtue of its immunomodulating action, cyclosporine has
    a limited role in controlling atopic dermatitis in recalcitrant
    adult cases. The potential side effects should always be kept
    in mind.
   Azathioprine:
    This immunosuppressive agent has also been used in severe
    adult cases. Again, potential side effects limit its role in
    selected cases.
                     Other Therapies
Tar
   may be useful, particularly for the scalp, over the counter, smelly, stained
   clothes
Phototherapy
    Ultraviolet B (UVB) alone, or in combinations with UVA may be beneficial
       in selected patients.
Probiotics
    The rationale for their use is that bacterial products may induce an immune
       response of the TH 1 series instead of TH 2 and could therefore inhibit the
       development of allergic IgE antibody production.
Chinese herbal medicine
    Some Chinese herbal preparations contain prescription medications,
       including prednisone, and have been associated with cardiac and liver
       problems.
    Bleach baths-A randomized, investigator-blinded, placebo-controlled trial
       including 31 patients showed that intranasal mupirocin ointment and
       diluted bleach (sodium hypochlorite) baths improved atopic dermatitis
       symptoms in patients with clinical signs of secondary bacterial infection.
             Complications of AD
   Secondary Infection
       a) bacterial
                impetiginization
                “super-antigenicity”
       b) viral
                localized – verruca, molluscum, herpes
                systemic – Kaposi’s herpetiform eruption
       c) mycotic
                Dermatophyte
                Candidal
            Staphylococcus aureus & Skin
   S. aureus –a saprophytic bacteria detected in 5% to 30% of
    healthy persons skin and in 20% of their nares.
   S. aureus – carriage rate in AD is 76% for uninvolved skin, 93%
    for lesional skin and 79% for the anterior nares.
   S. aureus colonization has potential to modify dermatologic
    diseases, in particular, S. aureus enterotoxins A-E – can act as
    “superantigens”.
   Superantigens bind as intact proteins to T-cell receptors and
    MHC class II molecules.
S. aureus & Skin
             HSV- ezcema herpeticum
   Clusters of multiple, uniform, 2-3mm crusted papules and
    vesicles develop in untreated or poorly controlled atopic
    dermatitis. The initial infection may be accompanied by
    fever, malaise, and lymphadenopathy.
   Complications: keratoconjunctivitis and viremia (multiple
    organ involvement with meningitis and encephalitis)
   Tx: acyclovir (PO for mild, localized symptoms),
    hospitalization for febrile, ill-appearing or young infants, No
    steroids or calcineurin inhibitors
      Differential Diagnosis of Atopic
                 Dermatitis
   Dermatitis
         -Contact
         -Seborrheic
   Immunodeficiencies
   Metabolic Diseases
   Neoplastic Diseases
   Infection and Infestation
         -Candida
         -Herpes simplex
         -Scabies
   Psoriasis
              Seborrheic dermatitis




   Flaky, white to yellowish scales form on oily areas
   Involvement of the top of the scalp (cradle cap), axilla, and
    diaper area
         Allergic Contact Dermatitis
Inflammation of the skin caused by direct contact with an irritating substance
Skin lesion or rash at the site of exposure
     Lesions of any type: redness, rash, papules (pimple-like), vesicles, and bullae (blisters)
     May involve oozing, draining, or crusting
     May become scaly, raw, or thickened
     Dx: patch testing
     Tx: avoidance, topical steroids




         Uroshiol                                                Textile dye
          Uroshiol                     Nickel
Patch testing
             Irritant Contact Dermatitis
Irritant contact dermatitis occurs when chemicals or physical agents damage the surface
of the skin faster than the skin is able to repair the damage.

Irritants include such everyday things as water, detergents, solvents, acids, alkalis,
adhesives, metalworking fluids and friction.




                                                                          47-year-old housekeeper was
                                                                          the result of chronic hand
                                                                          washing combined with
                                                                          surfactant and other solvent
                                                                          exposures
           Immunodeficiencies
   Wiskott-Aldrich syndrome
    -X-linked recessive disease
    -Eczema, thrombocytopenia, and
    immunodeficiency
   DiGeorge syndrome
   Hyper-IgE syndrome
   Severe combined immune deficiency
    Hyper IgE (Job Syndrome)




Characterized by recurrent skin abscesses, pneumonia with
pneumatocele development, and high serum levels of IgE.
Facial, dental, and skeletal features are also associated with
this syndrome.
Job Syndrome
             Metabolic disease
   Phenylketonuria
   Tyrosinemia
   Histinemia
   Multiple carboxylase deficiency
   Essential fatty acid deficiency
           Neoplastic Diseases
   Cutaneous T-cell lymphoma
   Histiocytosis X
   Sezary syndrome

**Skin lesions that do not heal with normal
  medications!
                         Histiocytosis
   Langerhans cell histiocytosis often produces a seborrheic dermatitis-like
    eruption that involves the axilla or diaper area. Lesions are erythematous or
    red-brown papules that may become eroded. Petechiae often are present.
                              Scabies
Sites of predilection include the interdigital folds on the hands and feet, the
    anterior axillary folds, the areolae of the breasts and the peri-umbilical
    region.
The pathognomonic lesions of scabies are comma-shaped or irregularly
    convoluted burrows.
At the end of each burrow, the mite is just discernible with the naked eye as
    a dark point.
                           Psoriasis
Psoriasis is a chronic autoimmune disease that appears on the skin. It commonly
causes red, scaly patches to appear on the skin, although some patients have no
dermatological symptoms. The scaly patches commonly caused by psoriasis, called
psoriatic plaques, are areas of inflammation and excessive skin production.
              When to Refer….
   When the diagnosis is uncertain
   When patients have failed to respond to
    appropriate therapy
   If treatment of atopic dermatitis of the face or
    skin folds with high potency topical
    corticosteroids is being contemplated
   If treatment with systemic immunosuppressive
    agents is being considered
                                  Prevention?
   There is evidence that for infants at high risk of
    developing atopy, breastfeeding for at least 4 months or
    breastfeeding with supplements of hydrolyzed infant
    formula decreases the risk of atopic dermatitis and cow
    milk allergy in the first 2 years of life.
   There is modest evidence that the onset of atopic
    disease may be delayed or prevented by the use of
    hydrolyzed formulas compared with formula made with
    intact cow milk protein, particularly for atopic
    dermatitis.
Effects of Early Nutritional Interventions on the Development of Atopic Disease in Infants and Children:
    The Role of Maternal Dietary Restriction, Breastfeeding, Timing of Introduction of Complementary
    Foods, and Hydrolyzed Formulas PEDIATRICS Volume 121, Number 1, January 2008

				
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