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Three years ago, Doris Rheaume, a retired addiction counselor who lives in Needham, could barely breathe. “I was on oxygen 24 hours a day,” she says. “If I turned my head without it, I huffed and puffed.” There is no mystery about why Rheaume was so sick. Now 71, she had smoked “a few packs a day for many, many years.” And, like 15 to 20 percent of smokers, Rheaume has paid a terrible price for her habit: COPD, chronic obstructive pulmonary disease. People with COPD have chronic bronchitis (inflammation of bronchial tubes), emphysema, destruction of the tiny air sacs in the lungs, or both. Better drugs, daring surgery – the subject of a just-released report - and better pulmonary rehabilitation are significantly improving the outlook and quality of life for many people with COPD. But it remains a miserable condition in which sufferers slowly suffocate to death, breath by breath, over many years. The lungs swell and lose their normal elasticity. Stale air gets trapped in over-inflated air sacs. By using accessory muscles, people still inhale, with effort, but exhaling is nearly impossible. Instead of looking healthy and sponge-like, the lungs begin to resemble cotton candy. People with severe COPD “can’t get a whole sentence out without taking a breath,” says Dr. Gail Weinmann, director of the airways biology and disease program at the National Heart, Lung and Blood Institute. “They have to rest after putting on a sock.” According to the federal Centers for Disease Control and Prevention in Atlanta, 10 million Americans have diagnosed COPD and an additional 14 million have somewhat impaired lung function. The death toll is currently 120,000 Americans a year – and rising. “COPD is the only cause of death that is rising in the US and in the world,” says one world expert, Dr. Bartolome Celli, chief of pulmonary and critical care medicine at Caritas St. Elizabeth’s Medical Center in Boston. It now ranks as the fourth leading cause of death in the US, and is expected to be number three in the US and worldwide by 2020. Moreover, the death rate is rising fastest in women. Men in the US have begun responding to anti-smoking campaigns but in general, women have not. Worldwide, the surge in COPD stems from tobacco companies “trying to get women in developing countries to smoke,” says Dr. Sonia Buist, professor of medicine at Oregon Health & Sciences University. In the US, even teenaged smokers show “unmistakable evidence” of early COPD, says Dr. Donald Tashkin, a professor of medicine and specialist in pulmonary critical care at the University of California, Los Angeles, citing data from lung function tests and autopsies of teens who died in car crashes. In COPD, as in asthma, the big culprit is inflammation of the lungs and airways. White blood cells pump out chemicals called cytokines that cause mucus glands to produce excess mucus. Inflammation also leads to scar tissue that makes the windpipe more rigid, which makes breathing harder. In the delicate air sacs of the lungs, inflammatory cells pump out digestive enzymes such as elastase, collagenase and some metalloproteinases that eat away lung tissue. “The air sacs get larger and larger and their number decreases,” notes Celli. “The result is a net decrease in surface area, and air gets trapped inside.” . So, what to do? First, if you smoke, stop. Some loss of lung function is normal with aging, but COPD speeds up that decline, says Dr. Gregory Diette, assistant professor of medicine and epidemiology at Johns Hopkins University. “People who quit smoking return to a normal rate of lung function decline within weeks.” Second, get influenza and pneumococcus vaccinations to avoid bronchial infections. Third, exercise, but judiciously - when air quality is good. Beyond that, watch for signs of signs of COPD and ask your doctor for a lung function test called spirometry if you’re worried. Worrisome signs include shortness of breath without much exertion, chronic cough or excess mucus production. If you are diagnosed with COPD, don’t despair; treatments are getting somewhat better. Among medications, there are three main options, which can be used together. Inhaled bronchodilators (drugs that keep airways open) are key, and there are three main types: beta-agonists, anti-cholinergics and theophylline-based drugs. The beta-agonists stimulate receptors on the muscle cells that line the airways, causing the airway to dilate. Short-acting beta-agonists like Albuterol last a few hours; longer-acting ones like Salmeterol and Formoterol act for about 12 hours. The anti-cholinergics work differently, by blocking a substance called acetylcholine, thus relaxing bronchial muscles. Short-acting drugs like Ipratropium dilate airways for a few hours; a new longer-acting drug called Tiotropium is on the market elsewhere and may be approved for the US market within months. The third type of bronchodilators contains theophylline, found in coffee and chocolate. These drugs, such as Uniphyl, inhibit the destruction of a natural substance called cyclic AMP, which keeps airways open. A totally different approach is to use anti-inflammatory drugs such as the inhaled corticosteroids Budesonide, Fluticasone and Beclomethasone. Yet another approach is to use anti-oxidants, which combat the dangerous free radicals triggered by inflammation. One anti-oxidant drug (N-acetylcysteine) has been shown helpful in European studies, but is not approved for use in COPD in the US yet. There’s also a 5-center study going on now to see whether some forms of retinoid (Vitamin A) can induce new lung tissue growth in people, as it does in rats. Portable oxygen tanks also can make life more livable for people with COPD, as can pulmonary rehabilitation, which involves learning how to conserve energy while dressing, talking, climbing stairs and how to exercise without undue shortness of breath. Lung transplants are a last resort, but donor lungs are in short supply. That has led surgeons to try a radical alternative – cutting away parts of the diseased lungs to reduce overall lung size so that there is more room in the chest cavity for the remaining lung tissue to deflate and inflate properly. One new study on lung-reduction surgery combined data on 150 patients (from studies in Massachusetts and Canada). It showed that the surgery works better than medications at improving lung function, says Celli, who was part of the study. Another study called NETT (the National Emphysema Therapy Trial) is being released today [Tuesday, May 20]. It was set up in 1996 after Medicare stopping pay for lung reduction surgery, following questions about its benefits. The new study found that “patients with severe emphysema who undergo lung volume reduction surgery along with medical management are more likely to function better and face no increased risk of death after two years compared to those treated with medical management alone,” according to a prepared statement from Johns Hopkins researchers, who led the study. But some patients fared worse with the surgery – those whose disease was located primarily in the upper lobes of the lungs and who had relatively good exercise capacity before surgery. The study is expected to impact Medicare coverage. Though the
operation is clearly not for everyone, some patients who’ve had it
swear by it, among them Doris Rheaume. “I can’t do like I used to
do,” she says. “But at least I can go around with oxygen and go
places. That is most important.”
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