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CLINICAL STUDIES |
B ligand levels in women with established osteoporosis treated with teriparatideDepartment of Endocrinology, Hippocration General Hospital, 54642 Thessaloniki, Greece1 Unit of Reproductive Endocrinology, First Department of Obstetrics and Gynecology, Aristotle University of Thessaloniki, 54603 Thessaloniki, Greece2 Analysis Laboratories, 54623 Thessaloniki, Greece and 3 Department of Internal Medicine, University of Thessalia, 41222 Larissa, Greece
(Correspondence should be addressed to A D Anastasilakis who is now at Soulini 4, 566 25 Sykies, Greece; Email: anastath{at}endo.gr)
Objective: The mechanisms regulating the anabolic response of the skeleton to intermittent exogenous parathyroid hormone (PTH) administration are not fully elucidated. The aim of this prospective study was to evaluate the acute effect (up to 1 month) of teriparatide (TPTD; human recombinant PTH 1–34) on serum levels of osteoprotegerin (OPG) and receptor activator for nuclear factor-
B ligand (RANKL) in women with established osteoporosis.
Design: Twenty-three postmenopausal Caucasian women with established osteoporosis (mean age 66.7±1.6 years) received daily injections of 20 µg TPTD for 12 months.
Methods: Serum samples for total calcium (Ca), phosphate, alkaline phosphatase, N-terminal propeptide of type I collagen, intact PTH (iPTH), OPG, and RANKL were obtained at baseline, 1 h, 1 day, and 1 month after initiation of therapy. Lumbar spine bone mineral density (BMD) was measured before and 12 months after TPTD treatment.
Results: Serum total Ca increased and iPTH gradually decreased with TPTD treatment. Serum OPG levels remained unchanged, while RANKL increased gradually during the study (P<0.001). There was no correlation between OPG or RANKL and BMD changes or iPTH levels.
Conclusions: TPTD therapy in women with postmenopausal osteoporosis results in acute increase in serum RANKL levels but does not affect serum OPG. These changes may reflect an increase in the number of active osteoblasts with therapy and might be responsible for the acceleration of bone turnover rate that characterizes TPTD.
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