Biliary excretion of aluminum in aluminum osteodystrophy with liver disease.
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.
J W
JW
Williams
S R
SR
Vera
T G
TG
Peters
R W
RW
Luther
S
S
Bhattacharya
H
H
Spears
A
A
Graham
J A
JA
Pitcock
A J
AJ
Crawford
G M
GM
Palmieri
D000328:Adult; D000535:Aluminum / Q000097:blood / Q000378:metabolism* / Q000652:urine; D000536:Aluminum Hydroxide / Q000009:adverse effects; D001646:Bile / Q000378:metabolism*; D001851:Bone Diseases, Metabolic / Q000188:drug therapy / Q000209:etiology*; D001842:Bone and Bones / Q000473:pathology; D002908:Chronic Disease; D003676:Deferoxamine / Q000627:therapeutic use; D005260:Female; D006801:Humans; D008107:Liver Diseases / Q000150:complications* / Q000378:metabolism
D000536:Aluminum Hydroxide; D000535:Aluminum; D003676:Deferoxamine