Increased Serum 25(OH)D3 Levels in Post-Menopausal Japanese Women with Osteoporosis after 3-Year Bisphosphonate Treatment
Increased Serum 25(OH)D3 Levels in Post-Menopausal Japanese Women with Osteoporosis after 3-Year Bisphosphonate Treatment
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DOI：
10.1620/tjem.242.241
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发表时间：
2017-07-01
影响因子：
2.2
通讯作者：
Kato, Hiroyuki
中科院分区：
文献类型：
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作者：
Nakamura, Yukio;Uchiyama, Shigeharu;Kato, Hiroyuki
骨质疏松症的特征是骨量、强度和微结构的全身性损害，导致脆性骨折风险增加。双膦酸类药物是治疗骨质疏松症的一线药物。维生素D被认为是治疗骨质疏松症所必需的。然而，BP对血清25-羟基维生素D-3(25(OH)D-3)水平的长期影响尚不清楚。因此，在这项回顾性研究中，我们收集了41名绝经后日本妇女骨质疏松症的临床数据，这些妇女接受BP治疗超过3年，没有补充维生素D。分别于治疗前和治疗3年后测定腰椎和股骨颈骨密度(BMD)和血清骨形成标志物-骨特异性碱性磷酸酶(BAP)，抗酒石酸酸性磷酸酶(TRACP)-5b作为骨吸收标志物。同时测定血清25(OH)D-3、1，25(OH)(2)D-3和甲状旁腺激素(PTH)水平。值得注意的是，在治疗过程中没有发生骨折。与基础值相比，25(OH)D-3水平显著升高(P=0.006)，从21.6 ng/m L升至26.4 ng/m L(P=0.05)。1，25(OH)2D3和总甲状旁腺素水平分别由62.6降至57.8 pg/mL和27.3降至25.1 pg/mL。骨形成和骨吸收标记物均受到显著抑制(P<；0.01)。治疗3年后，腰椎骨密度(增加7.3%)和股骨颈骨密度(增加4.1%)均有显著改善(P<；0.0001)。因此，即使没有补充维生素D，经过3年的BP治疗后，血清25(OH)D-3水平也显著升高。这些结果表明，在骨质疏松症的长期BP治疗中，可能不需要补充维生素D。
Osteoporosis is characterized by the systemic impairment of bone mass, strength, and microarchitecture, leading to an increased risk of fragility fracture. Bisphosphonates (BPs) are the first-line drugs for osteoporosis. Vitamin D is considered to be essential for osteoporotic treatment. However, long-term effects of BPs on the serum levels of 25-hydroxyvitamin D-3 (25(OH)D-3) are unknown. Accordingly, in this retrospective study, we collected clinical data of 41 post-menopausal Japanese women with osteoporosis treated with BP for over 3 years, without vitamin D supplementation. We measured lumbar and femoral neck bone mineral density (BMD) and serum levels of bone specific alkaline phosphatase (BAP) as a bone formation marker, and tartrate-resistant acid phosphatase (TRACP)-5b as a bone resorption marker, before and after the 3-year treatment. Serum 25(OH)D-3, 1,25(OH)(2)D-3, and whole parathyroid hormone (PTH) were also measured. Notably, no fracture occurred during the treatment. Compared with baseline values, 25(OH)D-3 levels were significantly increased from 21.6 to 26.4 ng/mL (P = 0.006), despite no vitamin D supplementation. 1,25(OH)2D3 and whole PTH levels tended to be decreased from 62.6 to 57.8 pg/mL and 27.3 to 25.1 pg/mL, respectively. Both bone formation and resorption markers were significantly suppressed (P < 0.01). Both lumbar BMD (7.3% increase) and femoral neck BMD (4.1% increase) were significantly improved (P < 0.0001) after 3 years of the treatment. Thus, even without vitamin D supplementation, serum 25(OH)D-3 levels were significantly increased after 3-year BP therapy. These results suggest that vitamin D supplementation might not be required in the long-term BP therapy for osteoporosis.