title: Oxidative damage, platelet activation, and inflammation to predict mobility disability and mortality in older persons: results from the health aging and body composition study.
abstract: BACKGROUND
  Inflammation, oxidative damage, and platelet activation are hypothesized biological mechanisms driving the disablement process. The aim of the present study is to assess whether biomarkers representing these mechanisms predicted major adverse health-related events in older persons.
  
  
  METHODS
  Data are from 2,234 community-dwelling nondisabled older persons enrolled in the Health Aging and Body Composition study. Biomarkers of lipid peroxidation (ie, urinary levels of 8-iso-prostaglandin F(2α)), platelet activation (ie, urinary levels of 11-dehydro-thromboxane B(2)), and inflammation (serum concentrations of interleukin-6) were considered as independent variables of interest and tested in Cox proportional hazard models as predictors of (severe) mobility disability and overall mortality.
  
  
  RESULTS
  The sample's (women 48.0%, whites 64.3%) mean age was 74.6 (SD 2.9) years. During the follow-up (median 11.4 years), 792 (35.5%), 269 (12.0%), and 942 (42.2%) events of mobility disability, severe mobility disability, and mortality occurred, respectively. Only interleukin-6 showed significant independent associations with the onset of all the study outcomes. Higher levels of urinary 8-iso-prostaglandin F(2α) and 11-dehydro-thromboxane B(2) independently predicted increased risk of death (hazard ratio 1.10, 95% confidence interval 1.03-1.19 and hazard ratio 1.14, 95% confidence interval 1.06-1.23, respectively). No significant interactions of gender, race, cardiovascular disease, diabetes, and antiplatelet drugs were detected on the studied relationships.
  
  
  CONCLUSIONS
  The inflammatory marker interleukin-6 is confirmed to be a robust predictor for the onset of negative health-related events. Participants with higher urinary levels of 8-iso-prostaglandin F(2α) and 11-dehydro-thromboxane B(2) presented a higher mortality risk.
authors.affiliation: Institut du Vieillissement, Université de Toulouse, 37 Allées Jules Guesde, 31000 Toulouse, France. macesari@gmail.com
authors.forename: Matteo
authors.initials: M
authors.lastname: Cesari
authors.forename: Stephen B
authors.initials: SB
authors.lastname: Kritchevsky
authors.forename: Barbara
authors.initials: B
authors.lastname: Nicklas
authors.forename: Alka M
authors.initials: AM
authors.lastname: Kanaya
authors.forename: Paola
authors.initials: P
authors.lastname: Patrignani
authors.forename: Stefania
authors.initials: S
authors.lastname: Tacconelli
authors.forename: Gregory J
authors.initials: GJ
authors.lastname: Tranah
authors.forename: Gianni
authors.initials: G
authors.lastname: Tognoni
authors.forename: Tamara B
authors.initials: TB
authors.lastname: Harris
authors.forename: Raffaele Antonelli
authors.initials: RA
authors.lastname: Incalzi
authors.forename: Anne B
authors.initials: AB
authors.lastname: Newman
authors.forename: Marco
authors.initials: M
authors.lastname: Pahor
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000502:physiology*; D001823:Body Composition / Q000502:physiology*; D002423:Cause of Death; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood; D015227:Lipid Peroxidation / Q000502:physiology; D008137:Longitudinal Studies; D008297:Male; D051346:Mobility Limitation; D018384:Oxidative Stress / Q000502:physiology*; D015539:Platelet Activation / Q000502:physiology*; D012306:Risk; D013929:Thromboxane B2 / Q000031:analogs & derivatives / Q000652:urine
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; C075750:8-epi-prostaglandin F2alpha; D013929:Thromboxane B2; C049235:11-dehydro-thromboxane B2; D015237:Dinoprost