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Impaired Carboxylation of Osteocalcin in Warfarin-Treated Patients

Departments of Chemical Pathology and Human Metabolism and Haematology London, United Kingdom
Royal Free Hospital and School of Medicine London, United Kingdom

Address all correspondence and requests for reprints to: Dr. P. Dandona, Metabolic Unit, Department of Chemical Pathology and Human Metabolism, Royal Free Hospital, Pond Street, London, NW3 2QG United Kingdom.

The total circulating osteocalcin and ratio of inactive (noncarboxylated; GLU) to active (carboxylated; GLA) form of circulating osteocalcin were measured in patients receiving long term warfarin treatment (n = 20), age-matched control patients not receiving warfarin treatment (n = 10), and normal subjects before and after the administration of 30 mg warfarin (n = 7). There was no significant difference in the total osteocalcin concentrations between the control patients and the patients receiving long term warfarin treatment, and it did not significantly change after warfarin ingestion in the normal subjects.

The GLU/GLA ratio was significantly increased (P < 0.002) in the patients receiving long term warfarin treatment compared with that in the control patients. There was a significant increase (P < 0.01) in the GLU/GLA ratio after warfarin ingestion in the normal subjects.

This study demonstrates that osteocalcin carboxylation in humans is a vitamin K-dependent process and that circulating osteocalcin is structurally altered by warfarin administration. This finding has pathophysiological implications for the fetal warfarin embryopathy syndrome, bone disease associated with chronic liver diseases, and possibly for osteoporosis, in which vitamin K deficiency has been implicated.

Received March 28, 1986.

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