In the first, double-blind, placebo-controlled study to investigate the effect of inhaled corticosteroids (ICS) on the immunopathology of bronchial biopsies in COPD, researchers found that ICS treatment had no effect on major inflammatory cell types, but did significantly improve disease symptoms and seriously reduce patient exacerbations. COPD is a slowly progressive airway disease caused by cigarette smoking that produces a major, non-reversible decline in lung function. In the 14-person placebo group of patients with advanced disease, there were a total of 10 exacerbations, compared with three among the 16 individuals in the treatment group. In addition, those persons who received ICS showed significant reductions in cough symptoms and sputum production, as well as exhibited less use of reliever medication. However, ICS patients did not demonstrate improvement in breathlessness, wheezing, exercise tolerance, or in a general feeling of well being. There was no significant change in lung function in either group. The investigators believe that ICS use does affect selected aspects of airway inflammation in COPD. The research appears in the second issue for June 2002 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
Expert points up value of use in advanced COPD
In an editorial, COPD expert Romain Pauwels, M.D., of the Department of Respiratory Disease, Ghent University Hospital, Ghent, Belgium, confirmed that the major benefits from ICS use in COPD are fewer exacerbations, less progressive decline in health, and an additive effect to long-term ß2 agonists on lung function and symptoms. In addition, he noted that there was indirect evidence of improved mortality rates for patients. However, Dr. Pauwels pointed out that the bronchial biopsies taken in the COPD study were unlikely to reflect the pathological abnormalities at the disease's principal peripheral site in the small airways of the lung. He notes that the medical research community does not understand the pathogenics of COPD, and has not identified the responsible cells and molecules. He said that airway inflammation in COPD is clearly different from that in asthma. In regard to the use of ICS in COPD, he personally regards the clinical data as sufficiently convincing to justify its use in patients with advanced disease. He defines advanced COPD as an individual demonstrating a standard lung function test result of less than 50 percent of the normal level predicted for that person's age. He points out that physicians have very little to offer those with advanced COPD, although they should repeatedly try to convince such patients to stop smoking. Dr. Pauwels also notes that regular treatment with long-acting bronchodilators, plus pulmonary rehabilitation, can decrease symptoms and improve exercise tolerance. The editorial appears in the second issue for June 2002 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
Blood vessel producing protein higher in sleep apnea patients
Researchers from Israel found that sleep apnea patients have significantly higher overnight plasma vascular endothelial growth factor (VEGF) concentrations than did either age-similar snorers or young healthy control subjects. VEGF is a key mediator of angiogenesis (the formation of new blood vessels). Angiogenesis is a prominent physiologic adaptive response of a tissue to hypoxia (inadequate amounts of oxygen available in the blood). Sleep apnea, involving repeated episodes of breathing cessation for longer than 10 seconds, causes hypoxia. According to the investigators, recent studies have shown VEGF may also affect the artherogenetic process itself, producing changes closely linked to the progression of atherosclerosis (narrowing of the arteries) in humans. This protein has also been shown to be higher in patients with uncomplicated hyperlipidemia (high concentrations of lipids in the blood), with or without atherosclerosis, and in those with untreated essential hypertension. Although the clinical significance of elevated VEGF concentrations in patients with sleep apnea is a matter of speculation at this stage, the researchers believe that augmented concentrations of this protein in patients who also have other disease could offer a contributory mechanism for the development of cardiovascular illness. The research is published in the second issue for June 2002 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
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