Melvin Berger1, Bob Geng2, D William Cameron3, Ladonna M Murphy4, Edward S Schulman5. 1. CSL Behring, 1020 First Avenue, King of Prussia, PA 19406, USA. Electronic address: mel.berger@cslbehring.com. 2. Department of Medicine, University of California at San Diego, 200W Arbor Dr Frnt, San Diego, CA 92103, USA. Electronic address: geng.bob@gmail.com. 3. Department of Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, K1H 8M5, Canada. Electronic address: d.william.cameron@gmail.com. 4. CSL Behring, 1020 First Avenue, King of Prussia, PA 19406, USA. Electronic address: ladonna.murphy@cslbehring.com. 5. Department of Medicine, Drexel University College of Medicine, 219 N. Broad Street, The Arnold T. Berman MD Building, 9th Floor, Philadelphia 19107, USA. Electronic address: edward.schulman@drexelmed.edu.
Abstract
BACKGROUND: More than half of all primary immune deficiency diseases (PIDD) affect antibody production and are well known as causes of recurrent sinusitis and lung infections. Chronic and recurrent infections of the upper and/or lower airways can contribute to inflammatory and obstructive processes in the lower airways which are initially reversible and considered "asthma", but can eventually cause irreversible remodeling and chronic obstructive pulmonary disease (COPD). Conversely, several lines of evidence suggest that many patients who present with a diagnosis of asthma have an increased incidence of infection, suggesting underlying host-defense defects. Asthma and respiratory infections in the first decades of life are recognized as risk factors for development of COPD, but when patients present with COPD as adults, underlying primary immune deficiency disease may be unrecognized. MAIN FINDINGS AND CONCLUSIONS: Detection of PIDD as a potentially treatable underlying contributor to recurrent/acute exacerbations and morbidity of COPD, and provision of immunoglobulin (Ig) G replacement therapy, when appropriate, may decrease the progression of COPD. Decreasing the severity and rate of exacerbations and admissions should improve the quality of life and longevity of an important subset of patients with COPD, while decreasing costs. Major steps toward achieving these goals include developing a high index of suspicion, more frequent use and appropriate interpretation of screening tests such as quantitative immunoglobulins and vaccine responses, and prompt institution of IgG replacement therapy when antibody deficiency has been diagnosed.
BACKGROUND: More than half of all primary immune deficiency diseases (PIDD) affect antibody production and are well known as causes of recurrent sinusitis and lung infections. Chronic and recurrent infections of the upper and/or lower airways can contribute to inflammatory and obstructive processes in the lower airways which are initially reversible and considered "asthma", but can eventually cause irreversible remodeling and chronic obstructive pulmonary disease (COPD). Conversely, several lines of evidence suggest that many patients who present with a diagnosis of asthma have an increased incidence of infection, suggesting underlying host-defense defects. Asthma and respiratory infections in the first decades of life are recognized as risk factors for development of COPD, but when patients present with COPD as adults, underlying primary immune deficiency disease may be unrecognized. MAIN FINDINGS AND CONCLUSIONS: Detection of PIDD as a potentially treatable underlying contributor to recurrent/acute exacerbations and morbidity of COPD, and provision of immunoglobulin (Ig) G replacement therapy, when appropriate, may decrease the progression of COPD. Decreasing the severity and rate of exacerbations and admissions should improve the quality of life and longevity of an important subset of patients with COPD, while decreasing costs. Major steps toward achieving these goals include developing a high index of suspicion, more frequent use and appropriate interpretation of screening tests such as quantitative immunoglobulins and vaccine responses, and prompt institution of IgG replacement therapy when antibody deficiency has been diagnosed.
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