[New pharmacological options in the therapy of COPD].
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation that is not fully reversible, mostly progressive and associated with an abnormal inflammatory reaction. The course of this pulmonary disease is influenced by systemic inflammation and comorbidities. COPD is caused by inhaled gases and particles and therefore avoidance of inhalative smoking results in symptomatic relief and improvement of the course of the disease. Modulation of the characteristic pulmonary inflammation, which is present in airways, parenchyma and pulmonary vasculature is targeted by a variety of novel pharmacological approaches. Systemic inflammation associating COPD should also be influenced to improve the disease. Assessment of the benefits of these approaches is difficult since FEV (1.0) as the most popular marker to describe the functional severity of COPD does not always reflect the benefits of the novel therapeutic strategies. Therefore new therapeutic modalities must be paralleled by the development of new clinical relevant targets.
Watz
H
H
Pneumologisches Forschungsinstitut am Krankenhaus Grosshansdorf.
Kanniess
F
F
Magnussen
H
H
D000111:Acetylcysteine / Q000627:therapeutic use; D000280:Administration, Inhalation; D000305:Adrenal Cortex Hormones / Q000008:administration & dosage / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D015415:Biomarkers; D002097:C-Reactive Protein / Q000378:metabolism; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation / Q000209:etiology; D018942:Macrolides / Q000627:therapeutic use; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D012016:Reference Values
D000305:Adrenal Cortex Hormones; D000900:Anti-Bacterial Agents; D015415:Biomarkers; D018942:Macrolides; D002097:C-Reactive Protein; D000111:Acetylcysteine