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American Thoracic Society Journal news tips for August 2005 (second issue)

American Thoracic Society

Investigators Reveal a Key to Viral-Induced Asthma

Researchers have discovered a new way to distinguish virus-induced asthma from that of allergen-caused disease based on a study of 59 asthma patients who were experiencing an acute exacerbation.

The investigators compared sputum cellular profiles of the 59 acute asthmatics against those of 45 controls. The control groups included 14 patients with stable asthma and no viral infection, 15 subjects without asthma but with a viral infection, and 16 healthy, uninfected persons. To establish infection status along with pulmonary status/history, participants completed common cold and asthma questionnaires, microbiological tests, and lung function and allergy (atopy) tests.

A respiratory virus was detected in 46 subjects, or 78 percent, of those with acute asthma.

In both children and adults, asthma exacerbations are caused by viral respiratory infections. Eighty three percent of the cases were infected with rhinovirus.

Expression of interleuken 10 (IL-10), a potent immunoregulator that functions to suppress immune responses broadly, was significantly increased in acute asthma with viral infections when compared with the control groups. Upon recovery from acute asthma, IL-10 gene expression returned to normal levels.

Consequently, according to the authors, IL-10 gene expression from airway cells appears to be a feature of virus-induced acute asthma. They said that their results reveal different mechanisms at work in virus-induced asthma patients than those described in allergen-induced asthma.

The study appears in the second issue for August 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

Study Shows Benefits of Inhaled Corticosteroids in Chronic Obstructive Pulmonary Disease

Researchers who designed two different studies to reduce potentially biased results among chronic obstructive pulmonary disease (COPD) patients who used inhaled corticosteroids (ICS) reported a 30 percent reduction in risk for either rehospitalization or death from the disease.

In an effort to avoid "immortal time bias," the authors created 2 matched sets of patients, based on a cohort from the United Kingdom's General Practice Database. All patients had been hospitalized for a COPD-related condition between 1990 and 1999. In the first study, each group of matched patients numbered 393 individuals. One set had been treated with ICS and the other was untreated. In the second study, also free of potential bias, a case-control analysis of 2,222 patients was designed without regard to ICS exposure status. Both resulted in approximately a 30 percent reduction in the risk for either rehospitalization or death for patients who used ICS over a one-year follow-up period.

COPD is a lung disease characterized by airflow obstruction that interferes with normal breathing. The two most frequent disease conditions that underlie COPD are severe emphysema and chronic bronchitis. Years of smoking are the primary cause for these illnesses.

According to the authors, COPD is currently the fourth leading cause of death worldwide, causing more than 2.5 million deaths per year. Also, the illness is the leading cause of hospitalization in the U.S., particularly among older patients.

With different study designs reducing potential bias, the study's results consistently showed an association between ICS use and the reduction of risk of hospitalization and death, the investigators concluded.

The study appears in the second issue for August 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.


For the complete text of these articles, please see the American Thoracic Society Online Web Site at http// For either contact information or to request a complimentary journalist subscription to ATS journals online, or if you would like to add your name to the Society's twice monthly journal news e-mail list, contact Brian Kell at 212-315-6442, or by e-mail at

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