Large Trial of Drug Therapy for COPD Offers New Hope
for Those with This Lung Problem
It did not abolish the accelerated decline in lung
function but did make substantial improvement
Shows the
respiratory system and cross-sections of healthy alveoli and
alveoli with COPD
Aug. 18, 2008 - For the first time, a drug therapy
appears to reduce lung function loss in patients with moderate to severe
chronic obstructive pulmonary disease (COPD), the fourth leading cause
of death in the U.S., which is primarily diagnosed in older people.
In a randomized, double-blind, placebo-controlled
trial in 42 countries, the Toward a Revolution in COPD Health (TORCH)
study investigated the effects of combined salmeterol, a ß-agonist, and
fluticasone propiniate, an inhaled cortical steroid, either alone or in
combination.
Note:Salmeterol is a
long-acting beta2-adrenergic receptor agonist drug that is currently
prescribed for the treatment of asthma and chronic obstructive pulmonary
disease (COPD). It is currently available as a metered-dose inhaler
(MDI) or a proprietary "disk-styled" inhaler that releases a powdered
form of the drug. (more at Wikipedia,
click here).
Fluticasone nasal spray is used to
treat the symptoms of seasonal (occurs only at certain times of year),
and perennial (occurs all year round) allergic rhinitis and perennial
nonallergic rhinitis. These symptoms include sneezing and stuffy, runny,
or itchy nose. Fluticasone is in a class of medications called
corticosteroids. It works by preventing and decreasing inflammation
(swelling that can cause other symptoms) in the nose. (more at
MedlinePLUS,
click here).
The tests were run on
> mortality,
> exacerbations (making condition worse),
> health-related quality of life and
> rate of decline in lung function as measure by forced
expiratory volume in one second (FEV1) in patients with COPD.
About COPD
(Chronic Obstructive Pulmonary Disease)
Chronic Obstructive Pulmonary Disease (COPD)
makes it hard for you to breathe. Coughing up mucus is often the
first sign of COPD. Chronic bronchitis and emphysema are common
COPDs.
Your airways branch out inside your lungs
like an upside-down tree. At the end of each branch are small,
balloon-like air sacs. In healthy people, both the airways and
air sacs are springy and elastic.
When you breathe in, each air sac fills
with air like a small balloon. The balloon deflates when you
exhale. In COPD, your airways and air sacs lose their shape and
become floppy, like a stretched-out rubber band.
Cigarette smoking is the most common
cause of COPD. Breathing in other kinds of irritants, like
pollution, dust or chemicals, may also cause or contribute to
COPD. Quitting smoking is the best way to avoid developing COPD.
COPD develops slowly, and it may be many
years before you notice symptoms like feeling short of breath.
Most of the time, COPD is diagnosed in middle-aged or older
people.
COPD is a major cause of death and
illness, and it is the fourth leading cause of death in the
United States and throughout the world.
Treatment can make you more comfortable,
but there is no cure.
National Heart, Lung, and Blood Institute
(Click
for more)
The results are published in the second issue for
August of the American Journal of Respiratory and Critical Care
Medicine, published by the American Thoracic Society.
"Pharmacotherapy with salmeterol plus fluticasone
propionate, or the components, reduces the rate of decline on FEV1 in
patients with moderate to severe COPD, thus slowing disease
progression," wrote Bartolome R. Celli, M.D., lead author of the study
and professor at Tufts University School of Medicine.
"To date, smoking cessation is the only
intervention that has conclusively been shown to alter the rate of
decline in FEV1," remarked Dr. Celli.
This is the first demonstration of an effective
pharmacotherapy (the use of drugs to treat condition) in COPD.
The TORCH study randomized more than 6,000 patients
with moderate to severe COPD from 42 countries to g), fluticasone
propionate (FP; 500mreceive
either salmeterol (SAL; 50 g), or placebo. After baselinemg),
the two in combination (SFC; 50/500m
FEV1 was recorded, patients were re-evaluated every 24 weeks to
determine the rate of decline in FEV1.
"The rate of decline in FEV1 was slowest in
patients on SFC and fastest in those randomized to the placebo arm,"
wrote Dr. Celli. "From week 24 onward, the adjusted rate of decline in
FEV1 was 39ml/year for SFC, 42 ml/year for both SAL and FP and 55
ml/year for placebo."
Although the study was not formally powered to
detect differences in rate of decline of FEV1, the results were highly
significant (p<0.001.) The rate of decline in treatment groups was
similar across a number of variables, including sex, age, ethnicity and
body mass index. Furthermore, the slower rate of decline in FEV1
appeared to be associated with a lower risk of exacerbation.
"Although treatment did not abolish the accelerated
decline in lung function [that occurs with COPD], it did ameliorate it
substantially," wrote Dr. Celli, while noting that "the mechanism
responsible for the effect on rate of decline is not clear, as all
treatments have potentially significant nonbronchodilator effects."
Clarifying those mechanisms is the goal of the next
phase of the research, with the comparison between a long-acting
bronchodilator drug and placebo with respect to FEV1 decline.
In the meantime, "the TORCH study brings some
clarity to the treatment picture and provides some hopeful signs for
patients with COPD," wrote Samy Suissa, Ph.D., of McGill University, in
the accompanying editorial. "This study also demonstrates that no
treatment [placebo] is not an option for patients with moderate to
severe COPD."
