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. 2013 Apr 25:7:17-34.
doi: 10.4137/CCRPM.S7211. Print 2013.

Pharmacotherapies for COPD

Stan Ejiofor  1 , Alice M Turner
Affiliations

Pharmacotherapies for COPD

Stan Ejiofor et al. Clin Med Insights Circ Respir Pulm Med. .

Abstract

This review article summarizes the main treatments for chronic obstructive pulmonary disease, their mechanisms, and the key evidence from trials supporting their use. Drug classes covered were short acting beta agonists (SABA), short acting muscarinic antagonists (SAMA), long acting beta agonists (LABA), long acting antimuscarinics (LAMA), inhaled corticosteroids (ICS), LABA/ICS combinations, specific phosphodiesterase (PDE4) inhibitors, non-specific PDE inhibitors, mucolytics, and oxygen. Non-specific therapies, such as opiates for relief of dyspnoea and therapies for smoking cessation, are also covered briefly. For each class of drug, mechanisms of action are described, key clinical trial results are reported, and available agents compared. Finally, the place of each drug in therapy is compared between current worldwide guidelines.

Keywords: chronic obstructive pulmonary disease; disease management; pharmacotherapies.

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Figures

Figure 1
Figure 1
Mechanism of action of Beta agonists. Notes: Binding of the agonist to the receptor results in a change in protein structure, which enables interaction with intracellular G proteins, production of cAMP and then protein kinase A, which mediates the bronchodilating effects via its actions on smooth muscle.
Figure 2
Figure 2
Location of anti-muscarinic receptors. Notes: M1 receptors are expressed in peribronchial ganglia, whilst M3 are present on bronchial smooth muscle cells; both mediate bronchomotor tone and reflex bronchoconstriction. M2 receptors are located in the post ganglionic para-sympathetic nerve and act as auto receptors. The figure shows their relationship to one another. Adapted from Lipson DA (2006).
Figure 3
Figure 3
Mechanism of action of ICS. Notes: When a glucocorticoid (GCS) binds to the GCR the heat shock proteins are detached resulting in a conformational change and formation of a GCR dimer. This dimerization is necessary for the binding of the GCR to the glucocorticoid response element (GRE) which is an area of DNA responsible for up or down regulating gene expression.
Figure 4
Figure 4
Classifying disease severity by GOLD. Notes: Patients are categorised by the combination of severity of spirometric impairment (GOLD airflow) or exacerbations and mMRC or CAT. Whilst it is recognised that spirometry or exacerbations and mMRC or CAT may result in different groups for some patients, GOLD recommends that treatment should be according to whichever method chosen results in the higher risk.
See this image and copyright information in PMC

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