New
Guidelines for Asthma Treatment Contain Some Changes
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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)
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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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