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Home > Health Information > Health News Archive 

New Guidelines for Asthma Treatment Contain Some Changes

< June 26, 2002 > Combining two drugs to treat persistent asthma is better than just increasing the dose of one drug.

And you can rest reassured the newest drugs are safe for children.

These are among the findings of the National Asthma Education and Prevention Program (NAEPP), which has just updated its guidelines for asthma treatment. The guidelines, first established in 1991, are coordinated by the National Heart, Lung, and Blood Institute (NHLBI).

"The new recommendations reinforce the previous guidelines and offer new treatments," says Dr. James Kiley, director of the NHLBI's Division of Lung Diseases.

The new guidelines also state that inhaled corticosteroids, the primary drug used to treat asthma, are safe for children. And they do not stunt growth, a particular worry for parents.

"This should reassure the parents of patients of the safety of giving medicine to children," Kiley says. "Any delay in their growth is temporary."

Kiley says the biggest change in the guidelines is that inhaled corticosteroids are the preferred treatment for asthma. But if symptoms persist, corticosteroids should be combined with longer-acting inhalant drugs, called beta2-agonists, for optimal treatment. Previous guidelines recommended simply upping the dose of corticosteriods, rather than combining them with a second drug.

He adds, however, that this combination therapy has not been thoroughly studied in children under 5 years of age and needs further research.

Dr. Paul Williams, a Seattle pediatrician who specializes in asthma, says the new guidelines reinforce what he has been doing in his own clinical practice.

"As a pediatrician, I am reassured by the latest literature that the medicines are safe at the dosages I use," he says.

With the guidelines, he says, "I feel like I can do what I do with less concern."

According to the American Academy of Allergy, Asthma and Immunology (AAAAI), asthma affects more than 17 million Americans, including 5 million children. It is a chronic disease that inflames the airways. The bronchial tubes swell and constrict, making it hard for air to flow easily in and out of the lungs.

The guidelines were prepared by an 11-member NAEPP panel of health professionals involved in asthma treatment. They reviewed all the latest scientific evidence to make their recommendations. The NAEPP was established in 1989 to reduce asthma-related illness and death and to enhance the quality of life of people with asthma.

Among the panel's other findings was that corticosteroids did not increase the risks of other potential health problems, like reduced bone mineral density, suppressed adrenal function, and increased incidence of cataracts.

Kiley says that while research has led to numerous medications for asthma treatment, more study is needed to find out what causes the disease, what makes it progress, and how treatment could prevent the progression. Also important is further study into asthma therapies for children 5 and under. These areas, he says, are targeted for future studies.

"We have a full spectrum of research from the laboratory bench to the bedside," he says.

Always consult your physician for more information.



Online Resources:

American Academy of Allergy, Asthma, and Immunology

National Heart, Lung, and Blood Institute (NHLBI)

 

 

For more information on asthma, please visit our adult respiratory health pages or our pediatric respiratory health pages.


For physician referral information, please call 314-FOR-DOCS or 1-888-700-7171.
Moving one step closer to the use of genetics in treating asthma, researchers have identified another gene that plays a role in the ailment.

The gene, called T-bet, controls the production of interferon-gamma, a molecule in the family of cytokines, which act as growth factors. Interferon-gamma stimulates the T-cells that are active in the immune system.

Genetically engineered mice that lack the T-bet gene have the kind of inflammation of the airways seen in human asthma, a group at Harvard Medical School reports in the January 2002 Science. In addition, tests of seven humans with asthma showed significantly reduced T-bet activity, the researchers say.

"These data suggest that T-bet might be an attractive target for the development of anti-asthmatic drugs," they write.

The discovery is part of an emerging field linking specific genes with asthma, says Dr. Lanny Rosenwasser, head of adult allergy at the National Jewish Medical and Research Center in Denver. He has identified some genes, and has done collaborative work with the Harvard group.

"This study demonstrates that one of a class of genes that control T-cell activation are involved in asthma," Rosenwasser says. "It's a good paper because it has human correlates to the animal model."

Rosenwasser ticks off the names of other molecules that have similar activity and are involved in asthma: GATA3, CMAF, NATF 1 through 4.

Half a dozen of these genes, including T-bet, look promising, Rosenwasser says, "but direct treatment is at least five years in the future." And no one gene plays a dominant role; each "contributes a little bit," with the mix varying from patient to patient, he adds.

"Eventually, what we will be doing in this area is to profile more than a dozen genes in a patient to identify which treatments are most effective, a pattern that says this kind of patient should get inhaled steroids, or other kinds of treatment," Rosenwasser says.

Asthma is not the only disease in which genetic patterning will move into medical practice, he adds. The same kind of complex genetic interplay with environmental factors is to be found in a number of chronic conditions, Rosenwasser says.

It is too early to know how important T-bet is in human asthma, says Dr. Jeffrey M. Drazen, professor of medicine at Harvard Medical School and leader of the research team.

"It looks interesting, but we don't know its role for sure," Drazen says. "We know that humans with asthma have diminished expression of T-bet, but that doesn't mean that human asthma is characterized by a deficiency of T-bet."

The next step, he says, is to find out whether "if you did something to enhance expression of T-bet, would you make asthma better." That would require "something that works on that specific pathway, and we don't have it yet," Drazen says. His group will be looking for that something, he says.

Dr. Stephen Wasserman, chief of the allergy section at the University of California, San Diego, calls the finding "excellent work by a first-rate group," but adds a caution: "Mice ain't humans."

"We don't know whether we can interfere with this gene in humans," Wasserman, a past president of the American Academy of Allergy, Asthma, and Immunology, says. "And we don't know whether we can interfere without causing mischief."

 

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