title: Aspirin intake and the use of serum ferritin as a measure of iron status.
abstract: BACKGROUND
  Atherosclerosis, a primary cause of myocardial infarction (MI), is an inflammatory disease. Aspirin use lowers risk of MI, probably through antithrombotic and antiinflammatory effects. Because serum ferritin (SF) can be elevated spuriously by inflammation, reported associations between elevated SF, used as an indicator of iron stores, and heart disease could be confounded by occult inflammation and aspirin use if they affect SF independently of iron status.
  
  
  OBJECTIVE
  We tested the hypothesis that aspirin use is associated with reduced SF.
  
  
  METHODS
  We used analysis of covariance to investigate the relation between SF and categories of aspirin use in 913 elderly participants aged 67-96 y in the Framingham Heart Study.
  
  
  RESULTS
  After adjustment for sex, age, body mass index, smoking, alcohol use, concentrations of C-reactive protein and liver enzymes, white blood cell count, and use of nonaspirin nonsteroidal antiinflammatory drugs and other medications, subjects who took >7 aspirins/wk had a significantly lower (by 25%) geometric mean SF than did nonusers, who took <1 aspirin/wk (71 compared with 95 microg/L, respectively; P for trend = 0.004). This effect of aspirin on SF was more marked in diseased subjects than in healthy subjects (mean SF was 50% lower compared with 21% lower, respectively).
  
  
  CONCLUSIONS
  Aspirin use is associated with lower SF. We suggest this effect results from possible increased occult blood loss and a cytokine-mediated effect on SF in subjects with inflammation, infection, or liver disease. The relations between aspirin, inflammation, and SF may confound epidemiologic associations between elevated SF, as an indicator of iron stores, and heart disease risk.
authors.affiliation: Mineral Bioavailability Laboratory and the Epidemiology Program, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
authors.forename: D J
authors.initials: DJ
authors.lastname: Fleming
authors.forename: P F
authors.initials: PF
authors.lastname: Jacques
authors.forename: J M
authors.initials: JM
authors.lastname: Massaro
authors.forename: R B
authors.initials: RB
authors.lastname: D'Agostino
authors.forename: P W
authors.initials: PW
authors.lastname: Wilson
authors.forename: R J
authors.initials: RJ
authors.lastname: Wood
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000097:blood; D000894:Anti-Inflammatory Agents, Non-Steroidal; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology*; D015331:Cohort Studies; D016207:Cytokines / Q000097:blood; D005260:Female; D005293:Ferritins / Q000097:blood* / Q000187:drug effects*; D015577:Geriatric Assessment; D006304:Health Status; D006801:Humans; D007501:Iron / Q000097:blood*; D008297:Male; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000209:etiology; D012307:Risk Factors
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D005293:Ferritins; D007501:Iron; D001241:Aspirin