News Release

American Thoracic Society journal news tips for January 2005 (first issue)

Peer-Reviewed Publication

American Thoracic Society

AIRFLOW OBSTRUCTION IN SURVIVORS OF BRONCHOPULMONARY DYSPLASIA

In a study of school-age children who were survivors of bronchopulmonary dysplasia (BPD), the chronic lung disease of prematurity, researchers uncovered long-term airflow limitation as demonstrated by impaired lung function test results, while at the same time finding low levels of a marker of pulmonary cellular dysfunction, exhaled nitric oxide. The investigators studied 31 school-age survivors of BPD, comparing their test results with 31 patients with asthma, 31 preterm children without BPD, and 31 healthy control children born at term. (BPD was first described in premature neonates in neonatal intensive care units who survived respiratory distress syndrome after suffering chronic lung injury induced by mechanical ventilation and exposure to high oxygen concentrations.) According to the researchers, the children with BPD in the study had significantly lower exhaled nitric oxide levels than did either the healthy control subjects or the preterm children without BPD. For their individual lung function test values, 9 of the subjects with BPD had results that were 70 percent or less of the normal predicted value. The children with asthma had a similar degree of airflow limitation. The authors said that although BPD survivors and those with asthma share some clinical and functional features, the remarkable difference in exhaled nitric oxide values suggests that airflow limitation in the two obstructive lung diseases is related to distinctive individual pathophysiologic pathways that ought to be properly identified. Unfortunately, to date, studies on the problem beyond infancy are lacking. The research appears in the first issue for January 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

BERYLLIUM SENSITIZATION PROGRESSES TO CHRONIC BERYLLIUM DISEASE

In a clinical follow-up study lasting almost 5 years, researchers have shown that individuals who are beryllium sensitive progress to chronic beryllium disease at a rate of 6 to 8 percent per year. Seventeen of 55 persons identified over 10-year period with beryllium sensitization who had had no evidence of chronic beryllium disease on initial lung biopsy showed diseased tissue on later clinical evaluations. The investigators found that 38 of the 55 remained beryllium sensitized after an average follow-up of 4.8 years. (Chronic beryllium disease is a lung inflammation caused by inhaling dust or fumes that contain beryllium. Beryllium is a silvery-white metallic chemical element that forms strong, hard alloys with several metals, including copper and nickel. Today, the metal is used in the aerospace industry and in the atomic energy and weapons industries.) The researchers studied 55 individuals who showed beryllium sensitization during tests at their institution. Eighty percent were employed in the nuclear weapons field. On average, it had been almost 25 years since their first exposure to beryllium. Beryllium sensitization was defined as beryllium-specific immune response demonstrated by two or more abnormal beryllium lymphocyte proliferation test results, with no evidence of nodular granulated tissue from a lung biopsy. Chronic beryllium disease was defined as abnormal blood test results plus cell infiltrates in lung tissue from a biopsy. The investigators said that it would be important to monitor this cohort over future years in order to determine whether all individuals with beryllium sensitization would eventually develop granulomatous disease. They also wanted to expand their follow-up to more recently identified sensitized individuals. The study appears in the first issue for January 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

A PROGNOSTIC MARKER FOR OUTCOME IN VENTILATOR-ASSOCIATED PNEUMONIA

Higher procalcitonin levels on days 1, 3, and 7 following diagnosis are strong predictors of unfavorable outcome in microbiologically confirmed ventilator-associated pneumonia (VAP), the most frequent hospital-acquired infection in patients on mechanical ventilation. The investigators studied procalcitonin as a prognostic marker in VAP among 63 patients enrolled in the study. Among the 63 patients, 38 (60 percent) had unfavorable outcomes. There were 14 deaths, 21 recurrences, and 3 documented extra-pulmonary infections, with the average time to unfavorable outcome at about 16 days. Their results showed that serum procalcitonin concentrations decreased during the clinical course of VAP but were higher in patients with unfavorable outcomes than in those with favorable results. (Procalcitonin is the precursor molecule of calcitonin, which regulates calcium concentrations in the blood. Procalcitonin levels rise during bacterial infections but not during either viral infections or inflammatory reactions of a non-infectious origin. Serum levels of procalcitonin are very low in healthy individuals.) Other clinical and biologic factors, such as white blood cell counts or C-reactive protein, were not able to discriminate between patients whose outcome would be unfavorable, as compared with favorable outcomes. The investigators commented that early identification of patients at high risk of death or VAP recurrence could provide an opportunity to change the treatment strategy to improve outcome. The study appears in the first issue for January 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

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For the complete text of these articles, please see the American Thoracic Society Online Web Site at http://www.atsjournals.org. 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 Cathy Carlomagno at 212-315-6442, or by e-mail at ccarlomagno@thoracic.org.


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