Transcript asthma

氣喘: 風雲再起
Asthma: an old disease, a new
challenge of future
王圳華 醫師
Chun-Hua Wang, MD
Schematic representation of a) pro-asthmatic epithelium with a close relationship between altered epithelial
cell transcription factors, goblet cell metaplasia and T-helper cell (Th) type 2 inflammation. b) The altered
epithelium also interacts with the underlying mesenchyme in a chronic wound response to contribute
towards airway wall remodelling and ongoing inflammation
Clinical phenotypes of asthma
Haldar P et al, AJRCCM 2008
Adult Asthma
Low dose or high dose
GINA Guideline
Well controlled
Not Well controlled
Step down
Compliance
Succeed
Self
Management
With minimal
medications
Identify triggering
factors
NO
Yes
Severe Asthma
Fail
Avoid / Treat
Not Well Controll
Asthma
Bad
compliance
Compliance monitor
Good compliance
GERD
Rhinitis
Sinusitis
Emotional
Occupational
Drug induced
Exercise
Menstruation
History
Therapeutic trial
No identified causes
Induced Sputum
Blood
Breath condensate
FeNO
Bronchial biopsy
Airway
remodeling
Allergic (IgE)
Neutrophilic
Eosinophilic
Severe Asthma
Severe Asthma
Inflammation
(steroid insensitive)
High airway hyperresponsiveness
Structural Changes
High collapsibility of airways
Lung hyperinflation
Genomics
Environmental Factors
Host Factors
Epigenetics
Allergen, virus, or
oxidant stress
induced injury
Acute inflammation
Epithelial shedding
Submucosal inflammation
Chronic stimulation
Anti-IgE
Higher level of IL-13,antibodies
TGF-b1
(Omalizumab)
CCL19
CXCL12
Recruit bone-marrowderived fibrocytes
CCR7
CXCR4
EGFR
EGF, TGF-b
CTGF
Fibroblast
Myofibroblast
Recruit fibrocytes to
submucosa, ASM
Tissue repairing
Fibroblast
proliferation
Myofibroblast
Airway remodeling
?
ASM
Neutrophil
PDE4
inhibitors
Eosinophils
Anti-IL5
antibodies
Progressive remodeling
Poorly control
Airway
remodeling
Allergy
Enviromental
?
Anti-elastase
Thermoplasty
?
Anti-IgE Ab
Fibrocytes
Oxidative stress
Mast cells