title: Impact of long-term treatment with low-dose inhaled corticosteroids on the bone mineral density of chronic obstructive pulmonary disease patients: aggravating or beneficial?
abstract: OBJECTIVE
  Chronic obstructive pulmonary disease (COPD) is characterized by a low-level systemic chronic inflammatory activity that is responsible for many of the disease's extra-pulmonary manifestations, including osteoporosis and fragility fractures. These manifestations are also well-documented side-effects of oral corticosteroids. It was hypothesized that low levels of inhaled corticosteroids, due to their anti-inflammatory properties and their low circulating levels, might preserve the bone mineral density (BMD) of COPD patients.
  
  
  METHODS
  Two hundred and fifty-one male ex-smokers with COPD patients grouped on the basis of their diffusion capacity value as predominantly bronchitic or predominantly emphysematic and 313 male controls with similar age and smoking history were enrolled in the study. Each of the patient's categories was randomized into two separate subgroups. Patients enrolled in subgroups B(neg) (n = 91, 36%) and E(neg) (n = 37, 14.7%) were treated with long-acting β2-agonists and anticholinergics, while subgroups B(ICS) (n = 87, 35%) and E(ICS) (n = 38, 15.1%) were additionally receiving low-dose inhaled corticosteroids. Patients and controls were evaluated by clinical examination, lung function testing and BMD measurement every 6 months for 4 years.
  
  
  RESULTS
  According to the findings, emphysematic patients demonstrated an increased rate of BMD loss compared with bronchitic patients (P = 0.01). Furthermore, a reduction of the annual BMD loss in bronchitic patients on inhaled corticosteroids (P = 0.02) was measured, without a corresponding benefit for the emphysematics (P = not significant).
  
  
  CONCLUSIONS
  Long-term administration of low-dose inhaled corticosteroids decelerates the annual BMD loss in bronchitic patients, possibly by reducing both pulmonary and systemic chronic inflammation caused by COPD.
authors.affiliation: Respiratory Department, King's College Hospital, London, UK. a.mathioudakis@nhs.net
authors.forename: Alexandros G
authors.initials: AG
authors.lastname: Mathioudakis
authors.forename: Stavroula G
authors.initials: SG
authors.lastname: Amanetopoulou
authors.forename: Ioannis P
authors.initials: IP
authors.lastname: Gialmanidis
authors.forename: Victoria
authors.initials: V
authors.lastname: Chatzimavridou-Grigoriadou
authors.forename: Gerasimos
authors.initials: G
authors.lastname: Siasos
authors.forename: Efstathia
authors.initials: E
authors.lastname: Evangelopoulou
authors.forename: Georgios A
authors.initials: GA
authors.lastname: Mathioudakis
mesh_terms: D000280:Administration, Inhalation; D000305:Adrenal Cortex Hormones / Q000008:administration & dosage* / Q000009:adverse effects / Q000627:therapeutic use; D000368:Aged; D015519:Bone Density / Q000187:drug effects*; D018680:Cholinergic Antagonists / Q000627:therapeutic use*; D006801:Humans; D008134:Long-Term Care; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy* / Q000503:physiopathology; D013147:Spirometry
chemical_list: D000305:Adrenal Cortex Hormones; D018680:Cholinergic Antagonists