Observational study reveals elevated plasma aluminium in antacid users with intact renal function, indicating minimal immediate influence on biochemical markers of bone formation.
Aluminium is involved in the etiology of several complications of chronic renal failure and has been firmly established as having toxic effects on bone tissue. We have measured plasma aluminium together with serum osteocalcin, procollagen I C-terminal peptide and total alkaline phosphatase activity in healthy subjects and in a group of subjects who consumed aluminium-containing and non-aluminium containing antacid preparations, with normal renal function. Age-related healthy reference ranges for plasma aluminium are presented and the effects of chronic antacid consumption on plasma aluminium and biochemical markers of bone formation investigated. In 172 healthy subjects the mean plasma aluminium concentration was 4.4 +/- 2.9 micrograms L-1, men having a significantly greater circulating aluminium load than women (5.4 +/- 2.8 micrograms L-1 vs. 4.0 +/- 2.8 micrograms L-1 respectively (P = 0.0039)). Older men were found to have significantly higher plasma aluminium levels than younger men. Increased plasma aluminium was seen in subjects taking antacids although this was not associated with significant changes in most indices of bone formation.
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Sharp et al. (1993) studied this question.