Persistent Childhood Asthma Linked to Early COPD

Veronica Hackethal, MD

May 12, 2016

Persistent childhood asthma may be linked to earlier development of chronic obstructive pulmonary disease (COPD), according to results from the Childhood Asthma Management Program (CAMP) study published in the May 12 issue of the New England Journal of Medicine.

Although COPD rarely develops before the fourth decade of life and typically affects current or former smokers, 11% of the children in this study met Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria for COPD by age 30 years. Children with a decreased pattern of lung growth or decreased lung function at study entry and males were at increased risk.

"Our data support the hypothesis that both reduced growth and an early decline are trajectories leading to an asthma–COPD overlap syndrome and complement the recent observation that in older patients, a rapid decline in lung function can lead to COPD," write Michael J McGeachie, PhD, from Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, and colleagues.

Past studies have linked early decline in lung function and a pattern of decreased lung growth to the development of COPD. A recent study found that poorer lung function in early adulthood is associated with the development of COPD later in life. However, long-term data on the issue are limited in children with asthma, who are already at increased risk for airflow obstruction.

The current analysis was part of the randomized placebo-controlled CAMP study, which enrolled children aged 5 to 12 years with mild to moderate asthma and followed them into the third decade of life. The larger CAMP study found that inhaled anti-inflammatory agents were no better than placebo in terms of their long-term effects on lung function growth. During the study, participants underwent annual spirometry lung function assessments.

Researchers identified 684 CAMP participants who had mild to moderate persistent asthma despite medication use. They separated these children into four groups, based on their trajectories of lung growth and decline in lung function, as measured by forced expiratory volume in 1 second (FEV1). FEV1 is a measure of lung function that usually peaks in late adolescence or early adulthood, but then remains stable for many years before starting a gradual decline. The four categories included normal growth with normal peak, normal growth and early decline, reduced growth and normal peak, and reduced growth and early decline.

Results showed that 75% (n=514) of children showed abnormal patterns of lung growth before their early twenties: 26% (n=176) showed reduced lung growth along with early decline, 23% (n=160) had reduced lung growth alone, and 26% (n=178) had normal lung growth and early decline.

Decreased lung function at baseline and male sex were the strongest predictors of impaired lung function later in life. Reasons why males might be at increased are unknown, although they were a little more than eight times more likely to have a reduced pattern of lung growth compared with those with normal growth (odds ratio, 8.18; P < .001).

Other factors associated with decreased lung growth included less bronchodilator response, airway hyperresponsiveness, young age at study entry, maternal smoking during gestation, lower level of parental education, vitamin D insufficiency, number of courses of prednisone, and more positive skin tests.

By about age 26 years, 11% (n = 73) of participants had lung impairment suggestive of COPD, as defined by the GOLD criteria. Thirty-six percent of participants with a reduced lung growth pattern and 8% of those with a normal growth pattern met GOLD criteria for COPD (P < .001).

The study could not conclusively assess smoking exposure, a known risk factor for COPD. It also could not look at genetic risk factors, prematurity, childhood respiratory infections, and other environmental exposures.

The length of follow-up was also too short to assess the full extent to which early decline in lung function in patients with asthma contributes to COPD, Stefano Guerra, MD, PhD, associate professor of medicine at the University of Arizona in Tucson, told Medscape Medical News.

Nevertheless, he commented: "These findings have critical implications in terms of tertiary prevention because they indicate that interventions aimed at reducing the long-term sequelae of childhood asthma need to start early in life and to target patients years before they enter adulthood."

The authors note that more studies are needed to identify interventions that could improve outcomes in children with mild to moderate persistent asthma.

One or more authors reports receiving grants, fees, or other support from one or more of the following: National Institutes of Health, Alpha-1 Foundation, National Heart Lung Blood Institute, Roche, Merck, GlaxoSmithKline, AstraZeneca, Brigham and Women's Hospital, Agency for Healthcare Research and Quality, ICON Medical Imaging, Novartis, Dutch Lung Foundation, Teva, Ubbo Emmius Foundation, Stichting Astma Bestrijding, Parker B. Francis Foundation, Boehringer Ingelheim, Takeda, Chiesi, UpToDate, Genentech, Aerocrine, Mylan, Sunovion, Pfizer, Pulmonx, Spiration, Vertex, Verona, Bristol-Myers Squibb, Janssen, Theravance, and MedImmune. Dr Guerra has disclosed no relevant financial relationships.

N Engl J Med. 2016;374:1842-1852. Abstract

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