1 / 21

ATOPIC DISEASE

ATOPIC DISEASE. D. pteronyssinus. ATOPIC DISEASE. Atopic dermatitis. Aller g ic IgE mediated asthma. IgE mediated rhinitis. Food allergy IgE mediated. Cause & hypothesis of ATOPIC DISEASE. hygiene. Genetic hypothesis Hygiene hypothesis Shift from Th1 to Th2

jess
Télécharger la présentation

ATOPIC DISEASE

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. ATOPIC DISEASE

  2. D. pteronyssinus ATOPIC DISEASE Atopicdermatitis AllergicIgEmediated asthma IgEmediated rhinitis FoodallergyIgEmediated

  3. Cause & hypothesis of ATOPIC DISEASE hygiene • Genetichypothesis • Hygiene hypothesis • Shift from Th1 to Th2 • Decreased number/activity of regulatory T cells • Changes in indoor air quality • Changes in life style

  4. Changes in life style

  5. Systemic Model for AtopyDisease • Systemicallergicinflammationconveysthe concept that allergy is a systemicimmunologicdysfunctionwithlocalmanifestations

  6. TheHygieneHypothesis • Improvedhygieneinindustrializedsocieties - Improved public health - Use of vaccines and antibiotics • Decreased infections that normally stimulate the immune system to work against asthma. • The following have a decreased risk ofasthma: - biggerfamilies - earlyplacementinday-care - exposure to farm animals and products- exposure to bacterialendotoxins - limited use of antibiotics

  7. ATOPIC TRIAD

  8. TheAtopicMarch • “Atopicmarch” 1.Atopic dermatitis (±foodallergy) – 2/3.inhalant allergy - allergicrhinitis -3/2. asthma •Food Allergy (0 – 1 year old) • Eczema (3 months – 2-3 years old) • Allergic Rhinitis (2 years – adulthood) • Asthma (3 years – adulthood)

  9. “AtopicMarch” Incidence 0 5 10 15 Age (years)

  10. AtopicEczema & AllergyDermatitis • Distribution of the rash typically varies with age: 1) In infancy (3 months to 2 years) the cheeks, wrists and extensoraspects of the arms and legs are usually involved.The entire body may be affected but the nappy area is usually spared. 2) In young children (2 years to 12 years) flexor surfaces, the neck, wristsand ankles are generally involved. 3) In teenagers and young adults flexural surfaces, the face(especially periorbital region), hands and feet are frequentlyaffected.

  11. Association Between AD and Asthma Bergmann (1998, clinexpallergy) - prospective birth cohort study, n= 1314, 5 y - if AD at months 3 and one parent/sibling atopic: -> 50%chance of asthma at age of 5-6 Castro-Rodriguez (1999, AJRCCM) - longitudinal, retrospective study, n = 986 - if AD and parental asthma: -> 75% chance of asthmaduringschoolyears Leung (JACI 2000) - if AD before age of 5: -> 80% chance to develop asthmaorallergicrhinitis.

  12. AllergicRhinitis and Asthma: • TwoRelatedConditions • Linked by One Common Airway

  13. Risk • Asthmain 40% of AR patients • Rhinitis in 75%- 80% of asthmatics • Rhinitis increases risk of asthma 3-fold “One airway” hypothesis • Nasal and lung pathology is similar • Nasal allergen challenge lower airwayinflammation

  14. Asthma HISTORY • Past / Family History of atopy (allergy) esp. rhinitis(hay fever), conjunctivitis, eczema or urticaria may point to asthma • History of childhood asthma important (but not all asthma begins in childhood - some present for the first time in adult life and these patients tend not to be allergic)

  15. Pathogenesis of asthma Type I hypersensitivity Type IV hypersensitivity “remodeling” H. HogenEsch, 2009

  16. Allergy and Asthma are manifestations of complex and dynamic networks Environmental component Genetic component Allergen exposures Lifestyle Medications etc… SNPs, etc. Genes and pathways Cell, immune, and inflammatory phenotypes, etc. Bronchoconstriction, Mucus Secretion, Hyperreactivity, IgE levels, Airway Structure

  17. Risk factors and phenotypes vary over time H E A L T H O U T C O M E S M A C R O S O C I A L E N V T E N V I R O N M E N T M I C R O S O C I A L S U B C L I N I C A L LIFE COURSE PERSPECTIVE C L I N I C A L Psycho-neuro-endocrine cascades Psycho-neuro-immune cascades (Physiological Reactions)

  18. Pathogenesis of ChildhoodAsthma • Sensitization • Foodallergy • Eczema • AllergicRhinitis • RecurrentWheezing +Genetics+Environment +Age+ Allergens →Asthma

  19. Food Allergies: 90% accounted for by 5 foods • 5 most common allergens in infants•Cow Milk•Soy•Wheat•Peanuts/Tree nuts•Egg Cowmilk protein: • •the most common food antigen in infants

  20. But …. • > 50% of children who develop allergy do not have a family history

  21. On thebegininig….. AD TheEnd...

More Related