JAMES W. WILLIAMS, M.D.; SANTIAGO R. VERA, M.D.; THOMAS G. PETERS, M.D.; ROBERT W. LUTHER, M.D.; SYMAL BHATTACHARYA, Ph.D.; HUBERT SPEARS, M.D.; ALLEN GRAHAM, M.D.; JAMES A. PITCOCK, M.D.; ALICE J. CRAWFORD, B.S.
Two patients with chronic liver disease developed elevated serum aluminum concentrations and biopsy-proven osteodystrophy. Neither patient had chronic renal failure but both had received aluminum-containing antacids for long periods. We measured biliary and urinary aluminum excretion during antacid loading in patients with normal liver function. Our studies show that biliary excretion is an important route of elimination of orally absorbed aluminum, and we suggest that long-term antacid therapy in patients with severe liver disease be monitored with periodic serum and urinary aluminum determinations to avoid aluminum osteodystrophy.
JAMES W. WILLIAMS, SANTIAGO R. VERA, THOMAS G. PETERS, ROBERT W. LUTHER, SYMAL BHATTACHARYA, HUBERT SPEARS, et al. Biliary Excretion of Aluminum in Aluminum Osteodystrophy with Liver Disease. Ann Intern Med. 1986;104:782–785. doi: 10.7326/0003-4819-104-6-782
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Published: Ann Intern Med. 1986;104(6):782-785.
Gastroenterology/Hepatology, Liver Disease.
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