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ASTHMA AND COPD: MECHANISM OF ACTION OF GLUCOCORTICOIDS, β2-AGONISTS AND THEIR COMBINATION
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Introduction
 
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Key Learning Points and Assessment Test
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Key Learning Points
Key Learning Points
  • Combining an ICS with a LABA is supported by a good scientific rationale more in asthma than in COPD.

  • Biological effects of glucocorticosteroids are variously mediated in cells:

    • Direct genomic pathway/trans-activation process;
    • Indirect genomic pathway/trans-repression;
    • Non-genomic pathway.

  • Corticosteroids are the mainstay of therapy in asthma, since they interfere with the pathophysiological activity of all the cells and mediators involved in the chronic inflammation underlying asthma disease. On the contrary, in COPD they minimally affect the inflammatory component of the pathology and they are currently used only in association to a bronchodilator in late stages of the disease.

  • The pharmacological activity of β2-agonists is due to their interaction with specific receptors (β2-adrenergic receptors), widely distributed in the lungs. Their activation determines airway smooth muscle relaxation (bronchodilation) and important additional non-bronchodilator effects.

  • Whereas bronchodilators, including β2-agonists, represent the cornerstone in COPD therapy, in asthma they are used only in association with corticosteroids in moderate-to-severe persistent asthma.

  • The combined administration of a LABA and an ICS has been proved to be clearly efficacious sometimes in asthma and COPD: the final improved clinical effect is due to the mutual interaction of the two classes at pathophysiological (particularly in asthma) and molecular levels (asthma and COPD).

  • Several studies have widely demonstrated the clinical benefits of combining a LABA and an ICS, more in asthma than in COPD.
   
   
Assessment
 
   
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