Emphysema Treatment

By Jorge A LLontop

The word emphysema is derived from the Greek word for inflation, is an anatomic alteration of the lung characterized by an abnormal enlargement of the air spaces distal to the terminal, non-respiratory bronchiole, accompanied by destructive changes of the alveolar walls. Pulmonary emphysema has been defined as enlargement and destruction of the alveolar containing portions of the lung. The disease occurs most commonly in smokers and people exposed to polluted air, dust or irritants.

Disorders of this protein include alpha 1-antitrypsin deficiency, a hereditary disorder in which a deficiency of alpha 1-antitrypsin leads to a chronic uninhibited tissue breakdown. This causes the degradation especially of lung tissue, and eventually leads to characteristic manifestations of pulmonary emphysema. Evidence has shown that cigarette smoke can lead to oxidation of methionine 358 of α1-antitrypsin, a residue essential for binding elastase; Elastase is an enzyme that digests and degrades a number of proteins including elastin, an elastic substance in the lungs and some other organs that supports their structural framework. Elastase is specifically inhibited by alpha-1 antitrypsin. This is thought to be one of the primary mechanisms by which cigarette smoking can lead to emphysema. Lungs of smokers who developed emphysema seem more prone to the central lobular form, where patients with alpha 1-antitrypsin deficiency usually demonstrate the Panlobular form.

A deficiency in a protein in the liver called alpha 1- antitrypsin has been found in some patients to produce emphysema. Antitrypsin counteracts trypsin, an enzyme produced by many types of bacteria that destroy tissue. Oxidation of the methionine active center in the 1-alpha antitrypsin molecule results in a loss of inhibitory function of the protein for elastase. Patients exposed to tobacco smoke could inactivate the alpha 1-antitrypsin in the alveolar lining and thereby increase the elastase burden on alveolar septal tissue. The level of alpha 1- antitrypsin may be a factor when smoke is involved to developed emphysema.

Emphysema in humans takes several different forms and can be classified as Centrilobular, Panlobular, Paraseptal, and airspace enlargement with fibrosis. The two main types of emphysema are Panlobular, involving all of a secondary lobule, and Centrilobular, involving the central area of a secondary lobule. Panlobular emphysema is relatively unusual, with no more than 1 individual for every 20 with Centrilobular emphysema. Centrilobular emphysema is the more common form of emphysema and is more severe in the upper lobes and is much more common in men than women.

Centrilobular emphysema is associated with cigarette smoking because the products of cigarette smoke produce a reaction that release proteolytic enzymes increasing elastase activity in the airways. Cigarette smoke destroys the delicate structure of the air sacs in the lung, preventing the efficient exchange of oxygen and carbon dioxide. Cigarette smoke contains carcinogens that damaged and distended the air sacs in the lungs. As a result, the lungs are less able to supply the oxygen that the body requires. Alveoli are the tiny sacs at the end of the bronchioles where blood gives up carbon dioxide and takes on fresh oxygen from inhaled air. As the alveoli become less efficient the air is trapped in the lungs decreasing the volume of fresh air that can be inhaled. In emphysema the patient's greatest problem is to exhale enough residual air because the lungs are partially inflated all the time.

Cigarette smoke produce irritants that stimulate mucus production and impair ciliary function. Excess mucus production increases an individual's vulnerability to respiratory tract infection and interferes with recovery from infection. The great quantity of mucus leads to persistent coughing and a greater susceptibility to colds, which can lead to chess infections. It is clear that cigarette smoke produce an impairment of gas distribution related to long term smoking.

Cigarette smoking is associated with a marked increase in the number of alveolar macrophages and phagocytes. Macrophages participate in a variety of phagocytic, immune, and inflammatory processes and play a role in the degradation and remodeling of the extracellular matrix.

The lung has developed a sophisticated defense system to deal with inhaled antigens and bacteria. When the bacterial load entering the lung is small these organisms are removed by mechanism including mucociliary clearance, local immunoglobulin binding, and ingestion by resident phagocytes. However, as the bacterial rises, the organisms are able to overcome these defense mechanisms and a symptomatic infection results. This is characterized by inflammatory response associated with recruitment and activation of circulating phagocytes such as monocytes and neutrophils, increased transudation of plasma proteins, and often the expectoration of purulent secretions. A major consequence of inhaled particles is an increase of macrophages in the lung. Then, if normal pulmonary defenses are limited and an increasing level of proteolytic enzymes is not activated, alveolar destruction may occur.

Macrophages promote elastin degradation through the production and release of elastolytic enzymes. Elastin is a protein in connective tissue that is elastic and allows many tissues in the body to resume their shape after stretching or contracting.

Phagocytes express a changing profile of proteinases that may participate in the degradation of elastin and other extracellular matrix components. Elastin degradation is an important component of the alveolar destruction in emphysema, and once the destruction of elastin had occurred, the anatomic and physiologic abnormalities might remain because of an inability to restore elastin continuity.

Pulmonary emphysema, characterized by destruction of alveolar structures, is the result of an unrestrained in the lung of proteinases, especially elastase originating from neutrophils. Recent findings suggest that cigarette smoking causes retention of neutrophils in the lung and that these cells contain at least two enzymes that affect the normal proteinase inhibitor defense mechanism and destroy lung tissue. Cigarette smoking recruits neutrophils into the airways, increase human neutrophil elastase from neutrophils, and inactivate proteinase inhibitor. Neutrophils are found in increased number in the alveolar region of individuals who smoke cigarettes, and the release of proteinase by these cells in the alveolar region is considered to play an important role in the subsequent development of emphysema in a proportion of individuals who smoke. The increase in the number of neutrophils in the lung and in the number of alveolar macrophages produces an increase in the concentration of proteinases, including neutrophil elastase.

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