Effect of long-term oral anticoagulant therapy on bone mineral density and bone turnover markers: a prospective 12 month study.

INTRODUCTION

Vitamin K-dependent posttranslational modification of glutamate to gamma-carboxyglutamate is a biochemical feature of the vertebrate blood-clotting cascade. This conversion activates clotting factors and bone proteins, including osteocalcin, a widely accepted marker of osteoblastic activity. Vitamin K antagonists, such as warfarin, inhibit this process.

OBJECTIVE

This study was aimed at evaluating the effect of warfarin treatment on BMD and bone turnover markers and determining the relationship between BMD and bone turnover markers.

PATIENTS AND METHODS

Fifty-four warfarin users and 62 age- and sex-matched healthy controls were enrolled in 1-year prospective study. Bone mineral density, bone turnover markers, 25-hydroxyvitamin D, serum and urinary calcium measurements were done at baseline and after 12 months of warfarin treatment.

RESULTS

No differences were observed between warfarin-treated and control groups in Ca-S, Ca-dU, ALP-S, 25-OHD and BMD after 12 months.The concentrations of serum CTx (306.48 +/- 29 ng/l) and osteocalcin (16.54 +/- 1.06 ig/l) were significantly lower (p < 0.001 and p < 0.05 respectively) after 12 month in warfarin-treated group compared to control group (403.29 +/- 24.7 ng/l and 22.88 +/- 1.33 ig/l). A significant increase in serum and urinary Ca values (p < 0.05) was observed in patients with oral anticoagulant therapy after 12 month compared to baseline levels. Biochemical markers of bone metabolism did not correlate with BMD in either group.

CONCLUSION

The long-term use of coumarin was not associated with decreased bone mineral density in our study, but the significantly lower OC and CTx serum levels in coumarin-treated patients suggest that vitamin K has an influence on bone turnover (Tab. 3, Fig. 2, Ref. 29). Full Text in free PDF www.bmj.sk.