Oral anticoagulation does not cause bone mass loss

Abstract

Background: It is well known that chronic therapy with heparin may produce osteoporosis, but it is not established if chronic oral anticoagulant therapy produces changes in bone mineral metabolism that may lead to loose bone mass and to produce or to worsen osteoporosis. We studied the effects of an oral anticoagulant (coumarin) on bone mineral metabolism in a group of postmenopausal women and followed them up for a year. Patients and methods: Study group, comprised 38 postmenopausal caucasian women who were enrolled after receiving oral anticoagulant treatment with acenocumarol for at least one year and were followed up for another one year. Biochemical markers of bone remodelling, immunoractive parathyroid hormone (iPTH) and bone mineral density (BMD) by dual X-ray absorptiometry (DEXA, Hologic QDR 1000) and a lateral dorsolumbar X-ray were performed in every patient at the beginning of the study and repeated a year later. Results were compared with a control group composed of 82 postmenopausal caucasian women of similar age. Results: At the beginning of the study, those women receiving oral anticoagulant had lower serum osteocalcin (GLA) levels (2.8±1.8 ng/ml vs 8.5±3.7 ng/ml, p<0.001), lower serum values or tartrate-resistant acid phosphatase (FATR) (3.1±0.5 U/l vs 3.4±0.4 U/l, p<0.001) than controls. BMD showed no difference from controls. After one year of follow up, osteocalcin levels were even lower than those found at the beginning of the study (1.9±1.3 ng/ml vs 2.8±1.8 ng/ml, p<0.05), but no other parameters, either biochemical or densitometric showed any change compared to the values found at the beginning of the study. No one patient or control presented new vertebral fractures. Conclusions: Our results suggest that prolonged oral anticoagulant treatment produces some biochemical changes in postmenopausal women, mainly decrease of serum GLA and serum FATR, that may reflect a low bone turnover rate, but these changes do not lead either to bone loss, because BMD shows no difference from controls and remains unchanged after a year of follow up, or to the appearance of new vertebral fractures.