20% of children in developed countries. often occurs before the age 5. typically clears by adolescence. only 1-3% of adults affected. patients will often have a personal or family hisotry of atopy (edema, asthma or allergic rhinitis)
pathogenesis: Genetics- skin barrier dysfunction from a filaggrin mutation. impaired immune response- activation of TH2 immune response, frequency staph infections (impetigo), environmental factors - decreed infectious agents and antigenic pollutants may play are role in development, high altitude, low temperatures, low humidity.
in infants: acute/weeping/crusting dermatitis. distribution is usally on face, cheeks, forehead, scalp, extensor extremities, and tends to spare the diaper area
in childhood: less oozing, more lichenificaiton, distribution is more localized in the flexure areas: neck wrists ankles, anticupital and popliteal fossa, hands and feet, if facial involvement it is more periocular/perioral
in teens/adults: lechenification predominates, prurigo nodular may be a manifestation. distribution is flexural . severity decreases with age and may become more localized with isolated insolvent of hands, eyelids, nipples.
associated conditions: xerosis, hyper linear palms, keratosis pillars, pityriasis alba, intolerance to wools