American Thoracic Society Journal news tips for November (second issue)

November 18, 2002

HALTING INHALED CORTICOSTEROID TREATMENT AFFECTS CHRONIC OBSTRUCTIVE PULMONARY DISEASE PATIENTS

Halting treatment with inhaled corticosteroids in patients with chronic obstructive pulmonary disease (COPD) is associated with both a higher risk and more rapid onset of exacerbations, together with a significant deterioration in health-related quality of life. The Dutch researchers studied 244 patients who received a high dose of inhaled corticosteroid (ICS) for four months during a run-in phase. The group was then randomized either to continue ICS treatment or to receive placebo for six months. In the ICS group of 123 individuals, 58 patients (47 percent) developed at least one exacerbation compared with 69 (57 percent) in the 121-person placebo group. In the placebo group, 26 patients experienced rapid recurrent exacerbations and had to be placed on ICS therapy again. Among the patients receiving ICS, only six were affected in this way. With regard to the health-related quality of life in the placebo group, those participants showed a significant deterioration in the total score, symptoms, and activity domains on a respiratory questionnaire. The research appears in the second issue for November 2002 of the American Journal of Respiratory and Critical Care Medicine.

LONGER AIRWAY IN MEN RAISES POTENTIAL FOR PHARYNGEAL COLLAPSE

Because of a substantially longer airway, men are much more predisposed to pharyngeal collapse than women, which investigators believe could explain their much higher risk of obstructive sleep apnea. In addition to their substantially longer pharyngeal airways, men also had an increased cross-sectional area of soft palate and increased airway volume. Based on an in-depth study of 19 males and 20 females to determine the anatomic and physiologic variables that are mechanistically important in pharyngeal behavior, the researchers constructed a model of a human upper airway. Then they used this model to assess the impact of specific anatomic features in upper airway mechanics. The investigators believe that the anatomic differences observed can significantly impact airway collapsibility and could explain, in part, the male predisposition to obstructive sleep apnea. They said that the fact the male airway is longer, even when length is normalized for body height, suggests that the observed length differences are sex-specific rather than a function of men being taller than women. The study appears in the second issue for November 2002 of the American Journal of Respiratory and Critical Care Medicine.

BRAIN GRAY MATTER DECLINES IN SLEEP APNEA PATIENTS

Researchers have shown that the volume of gray matter in the brains of patients with obstructive sleep apnea (OSA) was reduced by up to 18 percent compared with normal controls. The amount of the reduction increased as the syndrome became more severe. The investigators analyzed three-dimensional images done on the brains of 21 patients with OSA and 21 healthy control subjects. They reported that OSA patient gray matter losses occurred in such brain regions as the left frontal cortex, in an area that modulates upper airway motor function, and the cerebellum, which is a brain structure that plays a major role in cardiovascular and respiratory control. The researchers said that a portion of the volume changes may have been present before the onset of OSA and may have contributed to the characteristics of the syndrome. In an editorial in the same issue on the research, David Gozal, M.D., of Kosair Children's Hospital Research Institute, University of Louisville, Louisville, Kentucky, noted that these research findings "raise the tantalizing possibility that changes in gray matter hint at mechanisms for the genesis of the sleep disordered breathing syndrome, likely in concert with anatomic features but certainly playing a role in the progression of a compromised oral airway environment leading to a condition of certain upper airway failure." He points out that, to date, neural deficits have been justifiably assumed to represent a consequence of sleep-disordered breathing rather than to precede the syndrome. "Perhaps the time has come to reverse our thinking," he said. The research and editorial appear in the second issue for November 2002 of the American Journal of Respiratory and Critical Care Medicine.
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For the complete text of these articles and editorial, please see the American Thoracic Society Online Web Site at http://www.atsjournals.org. For 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 mailing list (please select either postal or electronic delivery), contact Cathy Carlomagno at (212) 315-6442, or by e-mail at ccarlomagno@thoracic.org.

American Thoracic Society

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