Abstract
Chronic obstructive pulmonary disease (COPD) is a major incurable global health burden and is currently the 4th largest cause of death in the world. Importantly, much of the disease burden and health care utilisation in COPD is associated with the management of its comorbidities (e.g. skeletal muscle wasting, ischemic heart disease, cognitive dysfunction) and infective viral and bacterial acute exacerbations (AECOPD). Current pharmacological treatments for COPD are relatively ineffective and the development of effective therapies has been severely hampered by the lack of understanding of the mechanisms and mediators underlying COPD. Since comorbidities have a tremendous impact on the prognosis and severity of COPD, the 2015 American Thoracic Society/European Respiratory Society (ATS/ERS) Research Statement on COPD urgently called for studies to elucidate the pathobiological mechanisms linking COPD to its comorbidities. It is now emerging that up to 50% of COPD patients have metabolic syndrome (MetS) as a comorbidity. It is currently not clear whether metabolic syndrome is an independent co-existing condition or a direct consequence of the progressive lung pathology in COPD patients. As MetS has important clinical implications on COPD outcomes, identification of disease mechanisms linking COPD to MetS is the key to effective therapy. In this comprehensive review, we discuss the potential mechanisms linking MetS to COPD and hence plausible therapeutic strategies to treat this debilitating comorbidity of COPD.
Highlights
Chronic obstructive pulmonary disease (COPD) is a major incurable global health burden and is currently the 4th largest cause of death in the world (Vogelmeier et al, 2017)
The causal relationship and the underlying mechanisms for the development of these two chronic diseases are intertwined in nature, it is apparent that the major risk factor for the onset of COPD is cigarette smoking, while that for metabolic syndrome (MetS) is obesity
In COPD, systemic inflammation may result from the spill over of lung-derived pro-inflammatory mediators including white blood cells, CRP, IL-6 and fibrinogen
Summary
Chronic obstructive pulmonary disease (COPD) is a major incurable global health burden and is currently the 4th largest cause of death in the world (Vogelmeier et al, 2017). Much of the disease burden and health care utilisation in COPD is associated with the management of its comorbidities (e.g. skeletal muscle wasting, ischemic heart disease, cognitive dysfunction) and infectious viral and bacterial acute exacerbations (AECOPD) (Vogelmeier et al, 2017). Many patients with COPD present with metabolic syndrome (MetS) a cluster of conditions including diabetes and prediabetes (insulin resistance), abdominal obesity, high cholesterol and high blood pressure. The morbidity and motility rate are amplified when MetS is coupled with COPD (Alberti et al, 2005; Sin & Man, 2003b). We discuss the mechanisms of cross-talk, clinical significance and therapeutic strategies for COPD and MetS
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