Ohishi Tsuyoshi, Matsuyama Yukihiro
Department of Orthopaedic Surgery, Enshu Hospital, Hamamatsu, Shizuoka, Japan.
Department of Orthopaedic Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan.
Ther Clin Risk Manag. 2018 Apr 17;14:729-739. doi: 10.2147/TCRM.S149236. eCollection 2018.
Minodronate is a third-generation bisphosphonate that was developed and approved for clinical use in osteoporosis therapy in Japan. The mechanism of action for suppressing bone resorption is the inhibition of farnesyl pyrophosphate synthase, a key enzyme in the mevalonic acid metabolic pathway of osteoclasts, to induce apoptosis of the cells. Minodronate is the strongest inhibitor of bone resorption among the currently available oral bisphosphonates. Large randomized, placebo-controlled, double-blind clinical trials have revealed an increase in bone mineral density of both the lumbar spine and femoral neck over 3 years of daily minodronate therapy and risk reduction in vertebral fractures over 2 years of therapy. The increase in bone mass and the prevention of vertebral fractures are similar to those with alendronate or risedronate. The incidence of adverse events, especially gastrointestinal disturbance, is the same as or less than that with weekly or daily alendronate or risedronate. The unique mechanism of action of minodronate via the inhibition of the P2X(2/3) receptor compared with other bisphosphonates may be an advantage in reducing low back pain in patients with osteoporosis. The monthly regimen of minodronate, introduced in 2011, is expected to have better patient adherence and longer persistence. In experimental animal models, minodronate preserved, or even ameliorated, bone microarchitectures, including microcracks and perforation of the trabeculae in the short term. The lowest incidence of bisphosphonate-related osteonecrosis of the jaw among all bisphosphonates and the lack of atypical femoral fractures attributed to its use to date, however, are partly because only a smaller population used minodronate than those using other bisphosphonates. To date, minodronate is available only in Japan. Hip fracture risk reduction has not been verified yet. More clinical studies on minodronate and its use in osteoporosis treatment, with a large number of subjects, should be conducted to verify hip fracture risk reduction and long-term results.
米诺膦酸是一种第三代双膦酸盐,在日本被研发并批准用于骨质疏松症治疗的临床应用。其抑制骨吸收的作用机制是抑制法尼基焦磷酸合酶,这是破骨细胞甲羟戊酸代谢途径中的关键酶,从而诱导细胞凋亡。米诺膦酸是目前可用的口服双膦酸盐中最强的骨吸收抑制剂。大型随机、安慰剂对照、双盲临床试验表明,每日服用米诺膦酸治疗3年可使腰椎和股骨颈的骨密度增加,治疗2年可降低椎体骨折风险。骨量增加和椎体骨折预防效果与阿仑膦酸钠或利塞膦酸钠相似。不良事件的发生率,尤其是胃肠道不适,与每周或每日服用阿仑膦酸钠或利塞膦酸钠相同或更低。与其他双膦酸盐相比,米诺膦酸通过抑制P2X(2/3)受体的独特作用机制可能在减轻骨质疏松症患者的腰痛方面具有优势。2011年引入的米诺膦酸每月给药方案预计具有更好的患者依从性和更长的持续时间。在实验动物模型中,米诺膦酸在短期内可保留甚至改善骨微结构,包括小梁微裂纹和穿孔。然而,在所有双膦酸盐中,米诺膦酸相关颌骨坏死的发生率最低,且迄今为止未发现因使用米诺膦酸导致的非典型股骨骨折,部分原因是使用米诺膦酸的人群比使用其他双膦酸盐的人群少。迄今为止,米诺膦酸仅在日本有售。尚未证实其可降低髋部骨折风险。应开展更多关于米诺膦酸及其在骨质疏松症治疗中应用的临床研究,纳入大量受试者,以验证其降低髋部骨折风险的效果和长期疗效。