COPD is a disease of increasing social importance, as it is widespread worldwide. Its morbidity is rising, and it is the only leading cause of death with increasing mortality. More than 350 million people are affected by COPD globally, accounting for approximately 10% of the population over 40 years old.
The percentage of non-smokers with COPD is increasing, reaching 50% today, due to the widespread use of biomass fuels in the Asian region and underdeveloped countries, where the percentage of non-smokers with COPD continues to rise. Approximately 3 billion people on Earth are exposed to biomass burning smoke, which constitutes around 50% of the global population.
Around 1 billion people are smokers worldwide. COPD affects 20% of smokers, ranking fifth in terms of prevalence and fourth in terms of mortality worldwide, with a tendency to climb to the third position in the next few years.
In Bulgaria, due to the still high percentage of smokers and increased use of biomass fuels during the winter months, the prevalence of the disease is closer to the higher percentages reported in the literature. According to data from the National Statistical Institute over the past 10 years, the number of people with COPD in Bulgaria ranges between 450,000 and 500,000, which represents about 13% of the population – a significant prevalence rate.
Each year, at least 15,000 new cases are added to the total number of affected individuals. Even more concerning is the statistic regarding the percentage of patients receiving therapy for their condition, which is no more than 30% of all affected individuals.
Chronic obstructive pulmonary disease (COPD) is a group of diseases (mainly emphysema, chronic bronchitis, bronchial asthma, and bronchiectasis) characterized by chronic or recurrent obstruction of the airways. The main symptoms include shortness of breath and cough with sputum production. It is a progressive disease that worsens over time.
The primary cause of COPD is tobacco smoke, with occupational exposures being significant factors in some countries. Usually, these exposures need to occur for several decades before the onset of symptoms. Genetic predisposition also influences the risk. Intensive and prolonged exposure to dust, chemicals, and fumes in the workplace increases the risk of the disease in both smokers and non-smokers.
COPD is a type of obstructive lung disease characterized by chronic, partially reversible airflow limitation and an inability to fully exhale. The airflow limitation results from the breakdown of lung tissue (known as emphysema) and small airway diseases (known as obstructive bronchiolitis). The relative contribution of these two factors varies among individuals. Severe destruction of small airways can lead to the formation of large air pockets called bullae, which replace lung tissue. This form of the disease is called bullous emphysema.
COPD develops as a significant and chronic inflammatory response to inhaled irritants. Chronic bacterial infections can also contribute to this inflammatory state. Inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells. Smokers additionally have Tc1 lymphocyte involvement, and some individuals with COPD have eosinophilic involvement similar to that seen in asthma.
Part of this cellular response is triggered by inflammatory mediators such as chemotactic factors. Other processes related to lung damage include oxidative stress caused by high concentrations of free radicals in tobacco smoke and released by inflammatory cells, as well as breakdown of lung connective tissue by proteases inadequately inhibited by protease inhibitors.
Destruction of lung connective tissue leads to emphysema, which contributes to airflow limitation and ultimately to impaired uptake and release of respiratory gases.
The narrowing of the airways is due to inflammation and scarring within them, contributing to the inability to breathe fully. The greatest reduction in airflow occurs during exhalation, as the pressure in the chest compresses the airways at that time. This can lead to a larger volume of air remaining in the lungs from the previous breath, known as air trapping, which results in an increased overall volume of air in the lungs at any given moment – a process called hyperinflation.
Low levels of oxygen and potentially high levels of carbon dioxide in the blood can result from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation, and decreased respiratory drive. During exacerbations, inflammation of the airways is further increased, leading to heightened hyperreactivity, decreased airflow during exhalation, and worsening gas exchange. This can result in inadequate ventilation and, ultimately, low levels of oxygen in the blood.
Prolonged low levels of oxygen can lead to constriction of the arteries in the lungs, while emphysema leads to the breakdown of capillaries in the lungs. Both changes contribute to increased blood pressure in the pulmonary arteries, which can cause “cor pulmonale”.
The predominant pathological changes in chronic obstructive pulmonary disease (COPD) are found in the airways, but changes are also observed in the lung parenchyma and pulmonary vasculature. The pattern of pathological changes depends on the underlying condition (such as chronic bronchitis, emphysema, or alpha-1 antitrypsin deficiency), individual sensitivity, and disease severity.
Airway abnormalities in COPD include chronic inflammation, increased goblet cells, hyperplasia of the lining, fibrosis, narrowing, and decreased number of small airways, as well as collapse of the airways due to destruction of the alveolar walls in emphysema. Patients with chronic bronchitis and excessive mucus secretion typically exhibit increased numbers of goblet cells and enlarged submucosal glands.
Chronic inflammation in chronic bronchitis and emphysema is characterized by the presence of CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages in the airways. Changes in the pulmonary vasculature include intimal hyperplasia and smooth muscle hypertrophy/hyperplasia, believed to be due to chronic hypoxic vasoconstriction of the small pulmonary arteries.
Destruction of alveoli, caused by emphysema, can lead to loss of the capillary bed associated with the alveoli and loss of the distal vasculature.
Based on the localization of the changes within the lung lobules, which can be accurately assessed on histotopographic sections of the entire lung, the following main morphological forms of emphysema are distinguished:
Over the past 15 years, the clinical research team at Convex has participated in more than 40 clinical trials involving patients in phases I-IV with COPD. We have successfully enrolled over 500 patients, meeting the required number for each clinical trial protocol.
If you require any information for planning a clinical trial involving COPD patients, please do not hesitate to contact us and ask your questions at firstname.lastname@example.org