UNLABELLED: Women with osteoporosis onraloxifene were randomized to 1-34hPTH + raloxifene or raloxifene alone for one year. In the PTH + raloxifene group, bone turnover increased 125-584%, spine BMD increased 9.6%, hip BMD increased 1.2-3.6% and radius BMD declined 4.3%. During the follow-up year, on continued raloxifene, BMD declined slightly at all sites except the femoral neck. INTRODUCTION: The influence of prior antiresorptives on response to 1-34PTH and the ability to maintain BMD gains might differ for antiresorptive agents with different potencies. The objectives were to evaluate biochemical and bone density responses to 1-34PTH in patients on prior and ongoing raloxifene and to determine whether raloxifene maintains bone gains. METHODS:Forty-two postmenopausal women with osteoporosis onraloxifene were randomized to raloxifene alone or 1-34PTH daily for 12 months (continuing raloxifene). Women were then followed for 12 months on raloxifene alone. Bone turnover markers and BMD were measured at baseline and at 3, 6, 12, 18 and 24 months. RESULTS: Biochemical indices increased rapidly during PTH treatment with peak increments of 125-584% for the three markers (p<0.001 vs. baseline). After one year of PTH, mean BMD increases were 9.6% for spine, 2.7% for total hip, 3.6% for trochanter (all p<0.005) and 1.2% in femoral neck (NS), while BMD declined 4.3% in the radius (p=0.003). After PTH withdrawal, on continued raloxifene, BMD declined slightly (0.7-2.9% losses; NS) at all sites, except the femoral neck, where BMD increased modestly (p=0.04). At 24 months, spine and femoral neck BMD remained significantly higher than baseline, while radius BMD remained significantly lower (all p<0.04). CONCLUSION: Substantial gains in BMD of the spine and hip, but not the radius, are seen with one year of PTH treatment in patients on prior raloxifene. After PTH is discontinued, raloxifene partially maintains PTH-induced BMD gains in the spine and hip.
RCT Entities:
UNLABELLED: Women with osteoporosis on raloxifene were randomized to 1-34hPTH + raloxifene or raloxifene alone for one year. In the PTH + raloxifene group, bone turnover increased 125-584%, spine BMD increased 9.6%, hip BMD increased 1.2-3.6% and radius BMD declined 4.3%. During the follow-up year, on continued raloxifene, BMD declined slightly at all sites except the femoral neck. INTRODUCTION: The influence of prior antiresorptives on response to 1-34PTH and the ability to maintain BMD gains might differ for antiresorptive agents with different potencies. The objectives were to evaluate biochemical and bone density responses to 1-34PTH in patients on prior and ongoing raloxifene and to determine whether raloxifene maintains bone gains. METHODS: Forty-two postmenopausal women with osteoporosis on raloxifene were randomized to raloxifene alone or 1-34PTH daily for 12 months (continuing raloxifene). Women were then followed for 12 months on raloxifene alone. Bone turnover markers and BMD were measured at baseline and at 3, 6, 12, 18 and 24 months. RESULTS: Biochemical indices increased rapidly during PTH treatment with peak increments of 125-584% for the three markers (p<0.001 vs. baseline). After one year of PTH, mean BMD increases were 9.6% for spine, 2.7% for total hip, 3.6% for trochanter (all p<0.005) and 1.2% in femoral neck (NS), while BMD declined 4.3% in the radius (p=0.003). After PTH withdrawal, on continued raloxifene, BMD declined slightly (0.7-2.9% losses; NS) at all sites, except the femoral neck, where BMD increased modestly (p=0.04). At 24 months, spine and femoral neck BMD remained significantly higher than baseline, while radius BMD remained significantly lower (all p<0.04). CONCLUSION: Substantial gains in BMD of the spine and hip, but not the radius, are seen with one year of PTH treatment in patients on prior raloxifene. After PTH is discontinued, raloxifene partially maintains PTH-induced BMD gains in the spine and hip.
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