The high prevalence of asthma in the developed world and its rapid increases in the developing world call for a strategy for primary prevention. Strict antigen avoidance during infancy, once thought to be sensible, has now been shown to be ineffective. In fact, growing up from birth on a farm with domestic animals or in a household where cats or dogs are kept as pets appears to protect against developing asthma. The best hope seems to lie in understanding the mechanisms by which microbial exposures during infancy foster development of a balanced immune response and then mimicking the effects of natural environmental exposures through administration of harmless microbial commensals (probiotics) or of nutrients that foster their growth (prebiotics) in the intestinal tract during the critical period of immune development in early infancy. Identifying the particular microbes whose growth should be fostered, or the microbial products responsible for inducing appropriate maturation of immune function, has become an active focus of epidemiologic, basic, and translational research.
COPD is now the third most common cause of death in the United States and accounts for more than $40 billion per year in direct and indirect health care costs. COPD resembles asthma in that it is also characterized by airflow limitation, although the obstruction of COPD is not fully reversible with treatment. The airflow limitation of COPD, believed to reflect an abnormal inflammatory response of the lung to noxious particles or gases, especially to cigarette smoke, absolutely progresses if the exposure continues and appears to progress, albeit more slowly, even if the exposure ceases. The belief that COPD develops in only 15–30% of habitual smokers is now challenged by radiographic demonstration of important, progressive changes in bronchial wall thickness and loss of lung tissue even in smokers with measures of pulmonary function in the normal range. Although COPD differs from asthma, many of the same drugs are used in its treatment. This section discusses the drugs that are useful in both conditions; a more comprehensive guide to their use is available in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines for classification and treatment of COPD (http://goldcopd.org).
Although asthma and COPD are both characterized by airway inflammation, reduction in maximum expiratory flow, and episodic exacerbations of airflow obstruction, most often triggered by viral respiratory infection, they differ in many important respects. Compared to asthma, COPD occurs in older patients, is associated with neutrophilic rather than eosinophilic inflammation, is poorly responsive even to high-dose ICS therapy, and is associated with progressive, inexorable loss of pulmonary function over time, especially with continued cigarette smoking.
Despite these differences, the approaches to treatment are similar, although the benefits expected (and achieved) are less for COPD than for asthma. For relief of acute symptoms, inhalation of a short-acting β agonist (eg, albuterol), of an anticholinergic drug (eg, ipratropium bromide), or of the two in combination is usually effective. For patients with persistent symptoms of exertional dyspnea and limitation of activities, regular use of a long-acting bronchodilator, whether an LABA or a long-acting anticholinergic, or the two together, is indicated. Theophylline may have a particular place in the treatment of COPD, as it may improve contractile function of the diaphragm, thus improving ventilatory capacity. The nonmethylxanthine, roflumilast, a selective phosphodiesterase inhibitor that improves pulmonary function and reduces exacerbation frequency, is now approved as a treatment for COPD.
The place of ICS therapy is less central to treatment of COPD than of asthma, in part because of its lower efficacy for this condition and in part because of reports of its use being associated with heightened risk of bacterial pneumonia. Its use is thus recommended only for patients with severe airflow obstruction or with a history of prior exacerbations.