Urinary excretion of oxalate, calcium, magnesium, and uric acid in inflammatory bowel disease

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Recently, the importance of hyperoxaluria in Crohn’s disease and its relationship to urolithiasis has been emphasized. It has been known for many years that urolithiasis may be a complication of inflammatory disease and that the predominant stone is calcium oxalate; but interest in the antecedent state of hyperoxaluria in these patients has resulted from recent work.1–7 It is recognized that hyperoxaluria may be a significant factor in the urolithiasis which occasionally occurs in patients with inflammatory bowel disease.

Conflicting views on the mechanism of hyperoxaluria in inflammatory bowel disease have been expressed. Smith et al3 felt that bile salt glycine, spilling into the colon because of ileal malabsorption, was converted to glyoxylate by bacteria, was absorbed from the portal vein, and then oxidized to oxalate in the liver. This group subsequently changed their views and postulated that an excessive amount of hepatic glycine was required for bile salt conjugation with an increased production of glycine precursors in the liver, and that this included glyoxylate.4 The glyoxylate would then be converted to oxylate. Admirand et al2 suggested an acquired defect in hepatic glyoxylate metabolism. Recently, Chadwick et al6 and Stauffer et al7 suggested that increased absorption of dietary oxalate is the mechanism for hyperoxaluria in inflammatory bowel disease. All of the recent work has focused primarily on ileal disease and has been associated mainly with Crohn’s disease rather than with ulcerative colitis. The association of uric acid urinary calculi following ileostomy for treatment of ulcerative colitis was studied earlier by. . .



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