The American journal of clinical nutrition · 2001
Aspirin intake and the use of serum ferritin as a measure of iron status.
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Fleming D J, Jacques P F, Massaro J M, D'Agostino R B, Wilson P W, Wood R J
Аннотация
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.
DESIGN: 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.
OBJECTIVE: We tested the hypothesis that aspirin use is associated with reduced SF.
DESIGN: 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.