Asthma drug may do more harm than good.
A bronchodilator drug used to open airways may actually exacerbate asthma when used routinely, according to a yearlong study of asthma patients in New Zealand. If related drugs cause similar effects, the finding may help explain a widespread increase in asthma deaths over the past few decades, the researchers say.
Asthma's death toll has risen alarmingly in the United States, England, Germany, Ireland, Belgium and particularly Jes Zealand, where researchers have reported "epidemics" of asthma deaths. Respiratory specialists don't know what's causing the trend, but several have speculated that some aspect of asthma treatment might play a contributing role.
Malcolm R. Sears of McMaster University in Hamilton, Ontario, and his co-workers at the University of Otago Medical School in Dunedin, New Zealand, now report evidence linking the bronchodilator drug fenoterol with worsening symptoms in some asthmatics.
Fenoterol belongs to a class of drugs called beta-agonists, which ease breathing by relaxing constricted muscles surrounding the narrowed airways. Fenoterol is not available in the United States, butmany U.S. asthma patients inhale similar beta-agonist drugs, such as salbutamol or terbutaline, notes asthma researcher A. Sonia Buist of the Oregon Health Sciences University in Portland. Buist says the new study raises concerns that fenoterol and other beta-agonists may, over the long run, do asthma patients more harm than good.
Sears' team studied 64 New Zealanders with moderate asthma. Half the volunteers inhaled a dry-powder form of fenoterol four times daily, while the rest inhaled a placebo powder. After six months, the two groups traded treatments. Throughout the study, volunteers were permitted to use their regularly prescribed beta-agonist inhalers as needed to control breathing difficulties. Each made twice-daily entries in a log, describing all medication taken and any symptoms of wheezing, coughing, respiratory secretions or tightness of chest.
"We broke the code [of the double-blind study] in July and were astonished at the results," Sears says.
Statistical analysis of data from the logs revealed that 57 of the 64 volunteers experienced clear improvements or declines in asthma control after switching from one test treatment to the other, the researchers report in the Dec. 8 LANCET. Seventeen of those individuals (30 percent) reported more asthma symptoms during placebo treatment than during fenoterol treatment. But the remainder -- 70 percent -- fared better on the placebo than on fenoterol. These 40 volunteers reported more symptoms -- and in some cases more puffs on their as-needed inhalers -- during the fenoterol phase.
Sears speculates that reliance on fenoterol may contribute to an insidious decline in some asthmatics, perhaps by triggering a cycle in which airway muscles relax right after drug inhalation but constrict again when treatment wears off. To keep airways open, many asthmatics routinely inhale beta-agonists several times a day. But while these drugs do offer short-tern relief, they do not treat the underlying airway inflammation. Sears suggests that the cumulative effects of their routine use may increase local inflammation and lead to permanent scarring that further narrows the airways, perhaps heightening the risk of death from a future attack.
Whether beta-agonist inhalers commonly used in the United States cause such adverse effects remains unknown, notes Albert L. Sheffer, an asthma expert at Harvard Medical School in Boston. Sears says he believes fenoterol is not alone, but he agrees that further research must confirm that suspicion. "I'm certainly not saying these drugs should be banned," Sears says. However, both the and Sheffer advise physicians to steer asthma patients away from heavy use of beta-agonist inhalers, and instead recommend occasional use of bronchodilators combined with a regimen of inhaled steroids, which fight inflammation and thus offer the prospect of getting asthma under long-term control.
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|Author:||Fackelmann, Kathy A.|
|Date:||Dec 15, 1990|
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