Airway remodeling and persistent airway obstruction in asthma.
There is growing recognition that some patients with long-standing asthma may possess a component of irreversible airflow obstruction despite optimal therapy. This persistent airflow obstruction is thought to be the result of structural changes in the airways that occur as a result of airway remodeling. The structural changes that lead to chronic obstruction are not known, nor are the intricacies of the remodeling process. Hence airway remodeling and its role in the evolution of irreversible airflow obstruction remain conceptual. Much work has been carried out to better define the histopathologic characteristics of asthma, including the characteristic features of airway inflammation. However, attempts to delineate the physiologic consequences of specific histologic findings are at an early stage of development. The thesis that airway remodeling is driven by chronic inflammatory processes has important implications for the way we make treatment decisions, especially in the patient with mild asthma. Abounding interest in airway remodeling has led to a growing literature on the subject, a literature that is largely speculative and perhaps too tautologic in the sense that remodeling is frequently defined by any observed histologic change, irrespective of its physiologic consequences. Careful attempts to link histologic observations with clinical, demographic, and physiologic findings will be necessary to unravel the causes of remodeling and identify who is at risk for development of irreversible airway obstruction.
Fish
J E
JE
Division of Critical Care, Pulmonary, Allergic, and Immunologic Diseases, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107, USA.
Peters
S P
SP
D000402:Airway Obstruction / Q000188:drug therapy / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D000818:Animals; D001249:Asthma / Q000188:drug therapy / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D008168:Lung / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology