Chronic obstructive pulmonary disease (COPD) is defined and characterized by the limitation of expiratory airflow. There are several factors that contribute to the limitation of airflow. Historically, COPD was thought to result primarily from physiological mechanist from disease of either airways or the pulmonary parenchyma. Based on the current concepts, cellular and biochemical pathways involved, suggesting an overlap in historical hypothesis with the current concepts. The concept of tissue damaged is also regarded as one of the main causes of COPD.
In order to unearth the mysteries surrounding the disorder, a study was done after it was evident that the elastate released from neutrophils exceeded the protective effect of alpha 1 anti-typsin and resulted in tissue damage. This study shows that for a smoking individual, the inflammation and inflammatory mediators in the lungs of COPD patients respond to cigarette smoking. Based on the fact that there are a wide range of causes of the condition, there varied clinical characteristic in COPD patients.
The studies show that multiple pathogenic mechanisms are responsible for the initiation and progression of COPD. Smoking cigarette being the most risky factor since it also affects the lungs. The results from the studies show that other factors contributing to the same include both genetic and acquired characteristics in determining the extent of variable susceptibility of people and their effect to cigarette and other exposures.
The results mean that COPD is a systemic disease that clinically is prominently affected by other aspects of the disease other than airflow limitation. The discovery has in itself offered an avenue for identifying and developing new therapeutic targets that could help mitigate against the devastating effects of the disease.