The Importance of Chronic Bronchitis in Chronic Obstructive Pulmonary Disease

Abstract

Chronic obstructive pulmonary disease (COPD) is a common and important group of conditions characterised by airflow obstruction with related symptoms including cough, shortness of breath, expectoration and wheeze. The widely accepted Global Initiative for Chronic Obstructive Lung Disease (GOLD) has classified COPD as “a disease state characterised by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases” (1). The current GOLD definition for airflow limitation is a forced expiratory volume in 1 second (FEV1) / forced vital capacity (FVC) ratio of 80% predicted); stage 2 (FEV1 > 50 to 30 to < 50% predicted); stage 4 (FEV1 < 30 or < 50% predicted in the presence of chronic respiratory failure) (2). COPD is one of the foremost causes of chronic morbidity and mortality worldwide. Globally, it affected 44 million people in 1990 (3) and recent estimates suggest that COPD affects approximately 210 million people (4) or 10% of all adults (5) with the prevalence continuing to rise. In 2007, COPD accounted for 5% of all deaths (4) but the WHO predicts an increase in COPD-related deaths of more than 30% in the next 10 years, emphasising the continued impact this disease will have internationally (6). Cigarette smoking remains the most important risk factor for the development of COPD (7) although only approximately 20% of smokers develop clinically significant disease (8). This suggests that a combination of genetic and environmental factors interact to cause COPD, and there has been much research aiming to identify candidate genes that may confer genetic susceptibility. To date, however, only deficiency alleles on the 1AT gene have been robustly identified as predisposing to disease (9). Pathologically, COPD is characterised by widespread inflammation of the peripheral and central airways with destruction of the lung parenchyma. Oedema, fibrosis, smooth muscle hypertrophy and loss of elastic recoil lead to bronchial wall thickening, which affects airflow (10). COPD, while primarily a lung disease, is associated with increased co-morbidity including cardiovascular disease, type 2 diabetes, osteoporosis and systemic pathology such as muscle wasting and dysfunction. It has been hypothesised that persistent low-grade inflammation may drive the co-morbidity and the systemic effects noted with this disease (11). The systemic manifestations of COPD are important, as they are not only associated with