Cosman F, Nieves J W, Zion M, Barbuto N, Lindsay R
Clinical Research Center, Helen Hayes Hospital, West Haverstraw, NY 10993, USA.
Osteoporos Int. 2008 Apr;19(4):529-35. doi: 10.1007/s00198-007-0475-0. Epub 2007 Oct 11.
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.
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.
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.
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).
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.
正在服用雷洛昔芬的骨质疏松症女性被随机分为两组，一组接受1-34hPTH联合雷洛昔芬治疗，另一组仅接受雷洛昔芬治疗，为期一年。在PTH联合雷洛昔芬组中，骨转换增加了125%-584%，脊柱骨密度增加了9.6%，髋部骨密度增加了1.2%-3.6%，而桡骨骨密度下降了4.3%。在随访的一年中，继续服用雷洛昔芬时，除股骨颈外，所有部位的骨密度均略有下降。
不同效力的抗吸收药物，先前使用抗吸收药物对1-34PTH反应及维持骨密度增加能力的影响可能不同。目的是评估正在服用雷洛昔芬的患者对1-34PTH的生化和骨密度反应，并确定雷洛昔芬是否能维持骨量增加。
42名正在服用雷洛昔芬的绝经后骨质疏松症女性被随机分为两组，一组仅服用雷洛昔芬，另一组每天服用1-34PTH，为期12个月（继续服用雷洛昔芬）。之后这些女性仅服用雷洛昔芬再随访12个月。在基线以及第3、6、12、18和24个月时测量骨转换标志物和骨密度。
PTH治疗期间生化指标迅速升高，三种标志物的峰值增量为125%-584%（与基线相比，p<0.001）。PTH治疗一年后，脊柱平均骨密度增加9.6%，全髋增加2.7%，大转子增加3.6%（均p<0.005），股骨颈增加1.2%（无统计学意义），而桡骨骨密度下降4.3%（p=0.003）。停用PTH后，继续服用雷洛昔芬时，除股骨颈骨密度略有增加（p=0.04）外，所有部位的骨密度均略有下降（损失0.7%-2.9%；无统计学意义）。在24个月时，脊柱和股骨颈骨密度仍显著高于基线，而桡骨骨密度仍显著低于基线（均p<0.04）。
先前服用雷洛昔芬的患者接受一年PTH治疗后，脊柱和髋部骨密度显著增加，但桡骨未增加。停用PTH后，雷洛昔芬可部分维持PTH诱导的脊柱和髋部骨密度增加。
