title: Future treatment to lessen exacerbations of chronic obstructive pulmonary disease.
abstract: Therapies currently used to reduce exacerbations of chronic obstructive pulmonary disease (COPD) are compounds used almost entirely for asthma therapy. A notable exception is tiotropium, a long-acting parasympatholytic agent. This compound and its precursor, iprotropium, are only occasionally used for asthma therapy. Likewise, leukotriene-modifying drugs are used occasionally for the treatment of COPD. In neither circumstance is there agency-approved indication for these particular cross-over therapies, but the use of long-acting beta(2)-adrenergic compounds and high-solubility inhaled steroids is a mainstay for therapy in both asthma and COPD. Similarly, theophylline, although less often used for either process, is therapeutically applicable to both asthma and COPD. Although overlap syndromes point to the occurrence of a common pathway in some cases, the inflammatory process for asthma and chronic obstructive pulmonary disease (COPD) differs substantially in most cases. Hence, the application of therapies designed to relax airway smooth muscle and ameliorate asthmatic inflammation lacks a therapeutic rationale for a disease characterized by predominant neutrophilic inflammation occurring in the small airways and alveoli. By definition, COPD is poorly reversible airflow obstruction; hence, the use of drugs designed to relax airway smooth muscle is somewhat counterintuitive and does not address the pathophysiological process of the disease.
authors: Department of Medicine, University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637, USA. aleff@medicine.bsd.uchicago.edu
authors: Alan R
authors: AR
authors: Leff
authors: Nilda M
authors: NM
authors: Muñoz
mesh_terms: D017305:Annexin A1 / Q000378:metabolism; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D054513:Group IV Phospholipases A2 / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D016023:Integrins / Q000502:physiology; D009504:Neutrophils / Q000378:metabolism; D054467:Phospholipases A2 / Q000378:metabolism; D010766:Phosphorylation; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism*; D014161:Transduction, Genetic; D018631:ras Proteins / Q000008:administration & dosage; D054322:tat Gene Products, Human Immunodeficiency Virus / Q000378:metabolism
chemical_list: D017305:Annexin A1; D000893:Anti-Inflammatory Agents; D016023:Integrins; D054322:tat Gene Products, Human Immunodeficiency Virus; D054513:Group IV Phospholipases A2; D054467:Phospholipases A2; D018631:ras Proteins