Chronic obstructive pulmonary disease (COPD) is a complex condition involving more than airflow obstruction, with systemic effects on cardiac function, gas exchange, and comorbidities such as ischaemic heart disease, heart failure, osteoporosis, anaemia, lung cancer, depression, and diabetes. Systemic inflammation from COPD can lead to skeletal muscle wasting, cachexia, and worsen comorbidities. Comorbidities increase hospitalisations, mortality, and healthcare costs, and require careful evaluation. Current therapies for comorbidities, such as statins and peroxisome proliferator-activated receptor agonists, may benefit COPD patients. New anti-inflammatory treatments, like phosphodiesterase 4 inhibitors, may have significant side effects, so future inhaled drugs are needed. Reversing corticosteroid resistance, such as with antioxidants, is another approach. More research is needed on COPD comorbidities and their treatment. Systemic inflammation in COPD is marked by increased cytokines, chemokines, and acute phase proteins, and is associated with skeletal muscle atrophy, cachexia, and comorbidities. Cytokines like IL-6, TNF-α, and IL-1β contribute to systemic inflammation and comorbidities. Chemokines and adipokines also play roles in COPD. Acute phase proteins like CRP are elevated in COPD and are linked to cardiovascular risk. Fibrinogen and serum amyloid A are also increased in COPD. Surfactant protein D is a marker of lung inflammation. Circulating cells show abnormalities, including monocytes and neutrophils, which may contribute to inflammation. Lymphocytes and natural killer cells are also affected in COPD. COPD leads to impaired functional capacity, reduced exercise capacity, and increased mortality. Functional capacity is measured by exercise tests and is important for assessing COPD severity. Pulmonary and systemic factors contribute to functional limitation. Patients with COPD are often inactive, leading to muscle wasting and malnutrition. Muscle dysfunction in COPD is associated with loss of muscle mass and strength, and is linked to poor outcomes. Mechanisms include systemic inflammation, oxidative stress, and impaired protein metabolism. Treatments like pulmonary rehabilitation can improve exercise capacity and muscle function. Cardiovascular disease is common in COPD, with increased risk of myocardial infarction and heart failure. COPD and atherosclerosis share risk factors, and systemic inflammation may contribute to both. Pulmonary arterial hypertension is also common in COPD, with increased pulmonary artery pressure and right ventricular dysfunction. Arterial stiffness and endothelial dysfunction are associated with COPD. Normocytic anaemia is common in COPD, with resistance to erythropoietin. Osteoporosis is prevalent in COPD, with risk factors including age, smoking, and systemic inflammation. Depression is common in COPDChronic obstructive pulmonary disease (COPD) is a complex condition involving more than airflow obstruction, with systemic effects on cardiac function, gas exchange, and comorbidities such as ischaemic heart disease, heart failure, osteoporosis, anaemia, lung cancer, depression, and diabetes. Systemic inflammation from COPD can lead to skeletal muscle wasting, cachexia, and worsen comorbidities. Comorbidities increase hospitalisations, mortality, and healthcare costs, and require careful evaluation. Current therapies for comorbidities, such as statins and peroxisome proliferator-activated receptor agonists, may benefit COPD patients. New anti-inflammatory treatments, like phosphodiesterase 4 inhibitors, may have significant side effects, so future inhaled drugs are needed. Reversing corticosteroid resistance, such as with antioxidants, is another approach. More research is needed on COPD comorbidities and their treatment. Systemic inflammation in COPD is marked by increased cytokines, chemokines, and acute phase proteins, and is associated with skeletal muscle atrophy, cachexia, and comorbidities. Cytokines like IL-6, TNF-α, and IL-1β contribute to systemic inflammation and comorbidities. Chemokines and adipokines also play roles in COPD. Acute phase proteins like CRP are elevated in COPD and are linked to cardiovascular risk. Fibrinogen and serum amyloid A are also increased in COPD. Surfactant protein D is a marker of lung inflammation. Circulating cells show abnormalities, including monocytes and neutrophils, which may contribute to inflammation. Lymphocytes and natural killer cells are also affected in COPD. COPD leads to impaired functional capacity, reduced exercise capacity, and increased mortality. Functional capacity is measured by exercise tests and is important for assessing COPD severity. Pulmonary and systemic factors contribute to functional limitation. Patients with COPD are often inactive, leading to muscle wasting and malnutrition. Muscle dysfunction in COPD is associated with loss of muscle mass and strength, and is linked to poor outcomes. Mechanisms include systemic inflammation, oxidative stress, and impaired protein metabolism. Treatments like pulmonary rehabilitation can improve exercise capacity and muscle function. Cardiovascular disease is common in COPD, with increased risk of myocardial infarction and heart failure. COPD and atherosclerosis share risk factors, and systemic inflammation may contribute to both. Pulmonary arterial hypertension is also common in COPD, with increased pulmonary artery pressure and right ventricular dysfunction. Arterial stiffness and endothelial dysfunction are associated with COPD. Normocytic anaemia is common in COPD, with resistance to erythropoietin. Osteoporosis is prevalent in COPD, with risk factors including age, smoking, and systemic inflammation. Depression is common in COPD