A drug widely prescribed as the sole treatment for asthma has been found to be
incapable by itself of preventing asthma attacks or controlling the airway
inflammation thought to lead to deteriorated lung function and gradual
worsening of asthma.
While the popular drug, known as a long-acting beta agonist, provides effective
and satisfying relief of asthma symptoms, it does not attack the inflammation
nearly always present in the airways of people with asthma, the study found.
“Most asthma experts have concluded that long-acting beta agonists alone do not
provide enough protection,” said Stephen Lazarus, MD, professor of medicine at
the University of California, San Francisco and leader of the national study.
“This is the first clear-cut clinical study confirming this impression.”
“People with mild to moderate persistent asthma - and that is about 75 percent
of asthma patients - need medication that addresses the underlying inflammation
if they are to keep their asthma under control.”
The research is published in the current (May 23) issue of The Journal of the
American Medical Association (JAMA).
The federally funded study of people with mild to moderate asthma compared patients’ progress on either a long-acting beta agonist or an inhaled corticosteroid. Researchers found that most patients were satisfied with how well the beta agonist controlled their symptoms, but the study showed that they suffered more asthma attacks and had more airway inflammation than did patients using the inhaled corticosteroid.
The 28-week study of 164 asthma patients was carried out at the six university
hospitals across the country that make up the Asthma Clinical Research Network
funded by the National Heart, Lung, and Blood Institute of the NIH.
Patients with mild to moderate asthma - symptoms more than three times a week -
were treated for six weeks with the inhaled corticosteroid triamcinolone to
control their asthma and then split into three groups: those who continued this
treatment for 16 more weeks; those who switched to the long-term beta agonist
salmeterol; and a group who received only placebo. Throughout the study
patients kept daily diaries of asthma symptoms and quality of life, and were
assessed every two to four weeks for lung function and airway inflammation.
Although the long-acting beta agonist was effective at improving symptoms of
asthma, it was no more effective than placebo at preventing asthma attacks.
Beta agonists are popular because they dilate constricted bronchial airways,
providing relief of wheezing and shortness of breath. Inhaled steroids, on the
other hand, don’t act as quickly, but they reduce inflammation. Because their
effects are not obvious over the short term, patients often use inhaled
steroids inconsistently or stop them completely. Some patients and physicians
also remain concerned about the safety of using inhaled steroids, even in low
“Inhaled steroids are widely underutilized,” Lazarus concludes. “In low doses
they are safe, and they are the most proven method of attacking the
inflammation that is asthma’s greatest long-term danger.”
Lazarus is co-author of a companion article in the same issue of JAMA which
found that once their asthma was brought under control with inhaled steroids
and long-acting beta agonists, most patients with more severe asthma could cut
their steroid dosage in half with no ill effects. But if the steroids were
dropped completely, the asthma could not be adequately controlled.
Taken together, the two studies clarify and underscore the importance of an
effective anti-inflammatory drug such as the inhaled corticosteroids in
treating asthma, Lazarus said. Newer non-steroid drugs have also been approved to control airway inflammation, he pointed out. So-called leukotriene receptor antagonists such as montelukast and zafirlukast are an alternative to inhaled steroids for some patients.
In addition, he said,“In the near future we likely will have medicines that
allow us to stop the allergic inflammatory cascade before it starts.” A
monoclonal antibody directed against another antibody, IgE,—a kind of
anti-missile missile—is currently undergoing clinical trials, Lazarus said.
Co-authors on the JAMA paper and collaborators in the study are Homer Boushey,
MD and John Fahy, MD, UCSF; Vernon Chinchilli, PhD, Timothy Craig, DO, and
Elizabeth Mauger, PhD, Hershey Medical Center, Hershey, Pa; Robert Lemanske,
Jr., MD, and Christine Sorkness, PharmD, University of Wisconsin Medical
School and School of Pharmacy, respectively.
Also: Monica Kraft, MD, Richard Martin, MD, Joseph Spahn, MD, and Stanley
Szefler, MD, National Jewish Medical and Research Center, Denver; James Fish,
MD and Stephen Peters, MD, PhD, Thomas Jefferson University, Philadelphia;
Jeffrey Drazen, MD, and Elliot Israel, MD, Brigham and Women’s Hospital and
Harvard Medical School, Boston.
The authors have research funding and other affiliations with a number of
pharmaceutical companies, noted at the end of the JAMA article.
The study was funded by the National Heart, Lung and Blood Institute.