subject: Emphysema aetiology and prevalence [print this page] Emphysema is denned by its pathology and is characterizedby the destruction of respiratory tissue and permanentenlargement of the unit of the lung distal to the terminalbronchiole (the acinus). The injury to alveolar septa iscaused by proteolysis. Lung tissue is normally protectedby a shield of proteinase inhibitors, derived fromthe blood but also synthesized locally. When the proteinase-antiproteinase balance is disturbed, favouringproteolytic activity, elastin destruction and septal digestionoccur. The consequences of this are loss of the 'tethering'support of airways, leading to collapse on expiration andreduction of lung elastic recoil and pulmonary capillarybed.In the past much importance has been placed on the distinction between chronic bronchitis and emphysema.In the majority of patients both conditions coexist, usuallyin heavy cigarette smokers, and the physician thereforemakes a clinical diagnosis of chronic bronchitis andemphysema.
Aetiology and prevalence
Chronic bronchitis and emphysema are responsible forthe personal disability and misery of tens of thousands ofpatients and impose a huge social and economic burden onsociety. Respiratory disorders are an important cause ofdeath in the UK and, of these, chronic bronchitis andemphysema constitute a large proportion. In the UK 10%of absences from work are caused by chronic bronchitisand emphysema, and approximately 10% of occupancy ofacute general medical hospital beds is the result of thesediseases.Atmospheric pollution and occupational dust exposureare minor aetiological factors in chronic bronchitis; thedominant causal agent is cigarette smoke. For symptomsand physiological changes to be demonstrated it probablyneeds a smoking history of 20 pack years.
Smoking alsocauses emphysema, probably damaging the lung by therelease of proteolytic enzymes. Smoke-affected pulmonaryalveolar macrophages, present in greater numbers thanusual, release neutrophil chemotactic factor and theattracted neutrophils are damaged by smoke and releaseproteolytic enzymes, especially elastase, capable of lysingelastin, collagen and basement membranes. The effectivenessof oci-antitrypsin is impaired by smoking and theunchecked proteolysis results in centrilobular emphysema.This process is particularly rapid in patients who are deficientin aj-antitrypsin. Overall severity of airways obstructionis related to the number of cigarettes smoked.
