Both asthma and COPD are airway obstructive diseases caused by chronic inflammation. However,
airway obstruction in asthma is mostly episodic and reversible, while in COPD,
it is persistent and progressive. More importantly, the inflammatory pattern
is markedly different in the 2 conditions: inflammation is driven mainly by macrophages
and neutrophils in COPD, whereas, in asthmatic airways, activated mast cells and eosinophils
are more prominent. In fact, asthma is a type 1 hypersensitivity disease in which
IgE-sensitized mast cells, upon re-exposure to certain triggers, release a number of
inflammatory chemicals that are responsible for bronchospasms during an asthmatic attack.
Notably among these are leukotrienes, which not only cause bronchoconstriction but
also attract eosinophils to the lungs, amplifying the impact of inflammation.
Despite the differences, many of the drugs used to treat asthma and COPD overlap. These include
inhaled bronchodilators, to widen the airways; and inhaled corticosteroids, to control inflammation.
Bronchodilators can be short-acting or long-acting. Short-acting medications
are used as emergency treatment for acute bronchospasm attacks,
while long-acting agents are used to control the disease in the long-term.
Inhaled corticosteroids are first-line therapy for long-term management of asthma,
while long-acting bronchodilators are first-line treatment for moderate COPD.
Patient with severe COPD are typically prescribed both bronchodilators and corticosteroids.
Inhaled bronchodilators act to modulate the effect of autonomic regulation in the lungs. They either
stimulate the sympathetic arm - the “fight or flight” state – which increases respiratory
volume; or, suppress the parasympathetic response, which has the opposing effect. Accordingly,
there are 2 classes of inhaled bronchodilators: - β2-agonists activate β2- adrenergic receptors
of the sympathetic pathway. Sympathetic activation leads to production of cAMP which,
in turn, causes relaxation of airway smooth muscles in several ways. These drugs are
highly selective for β2- adrenergic receptors, which are present predominantly in the lungs.
β2-agonists can be short-acting (SABA), long-acting (LABA) or ultra-long-acting (U-LABA).
- Muscarinic antagonists bind to and prevent activation of muscarinic receptors that
mediate the parasympathetic response in airway smooth muscles and mucous glands.
Some drugs are non-selective – they bind to all subtypes of muscarinic receptor,
while others are more selective for the M3 subtype expressed in smooth muscles.
Most muscarinic antagonists are long-acting (LAMA).
For moderate to severe COPD, combinations of a long-acting muscarinic antagonist
and a long-acting beta-agonist are typically preferred over a higher dose of either drug alone.
This is because these 2 classes of drugs appear to amplify the effect of each other.
Another class of medications that is usually used as a second-line treatment are inhibitors
of the enzyme phosphodiesterase-4, PDE-4, which degrades cAMP. Inhibition of PDE-4 leads to
increased levels of cAMP, producing smooth muscle relaxation, as well as anti-inflammatory effect.
Finally, there are some drugs that are more specific for asthma. These include
mast cell stabilizers and anti-IgE antibody, which reduce mast cell-induced inflammation;
and leukotriene modifiers which exhibit both bronchodilator and anti-inflammatory effects.