Abstract:Monthly minodronate treatment increased BMDs in newly treated patients over 27 months. Serum Pen increased with M-MIN therapy, possibly indicating prolonged bone turnover. The initial 9-month changes in serum P1NP predicted the 27-month changes in hip BMDs when M-MIN replaced alendronate or risedronate.
“…Our study showed that estimated glomerular filtration rates (e-GFRs) were significantly decreased during the 27-month period of monthly minodronate therapy in female patients with osteoporosis. 38 However, the rate of decrease was almost the same as was found in the placebo group in the Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) Recurrent Fracture Trial, wherein zoledronate was administered intravenously once a year for 3 years after hip fracture. 46 It could indicate that the decrease in e-GFR observed during monthly minodronate therapy in our study was probably due to aging.…”
Section: Safetymentioning
confidence: 71%
“… 37 According to our study, a significant increase in the lumbar spine BMD at 27 months of monthly minodronate therapy, compared with the baseline value in the switch group, in 47 female patients with osteoporosis was observed. 38 Because of the stronger efficacy for the inhibition of bone resorption of minodronate than that of alendronate or risedronate, more BMD gain is expected when alendronate or risedronate is replaced by minodronate. However, when enough remodeling space in the bone is not available for minodronate to exert its action because of prior bisphosphonate therapy, the BMD may not increase.…”
Section: Other Clinical Studies On Minodronatementioning
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.
“…Our study showed that estimated glomerular filtration rates (e-GFRs) were significantly decreased during the 27-month period of monthly minodronate therapy in female patients with osteoporosis. 38 However, the rate of decrease was almost the same as was found in the placebo group in the Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) Recurrent Fracture Trial, wherein zoledronate was administered intravenously once a year for 3 years after hip fracture. 46 It could indicate that the decrease in e-GFR observed during monthly minodronate therapy in our study was probably due to aging.…”
Section: Safetymentioning
confidence: 71%
“… 37 According to our study, a significant increase in the lumbar spine BMD at 27 months of monthly minodronate therapy, compared with the baseline value in the switch group, in 47 female patients with osteoporosis was observed. 38 Because of the stronger efficacy for the inhibition of bone resorption of minodronate than that of alendronate or risedronate, more BMD gain is expected when alendronate or risedronate is replaced by minodronate. However, when enough remodeling space in the bone is not available for minodronate to exert its action because of prior bisphosphonate therapy, the BMD may not increase.…”
Section: Other Clinical Studies On Minodronatementioning
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.
“… 2008 ; Ohishi et al. 2017 ). In this current study, 7 weeks AU treatment significantly increased the serum concentrations of P1NP in OP mice relative to control mice, which preliminarily proves that AU slowed the development of OP by increasing bone formation.…”
“…If a metal implant was inserted on the left side, the BMD of the right hip was measured. The coefficient of variation (CV) for lumbar, femoral neck, and total hip BMD were described in our previous paper [ 16 ]. Serum type 1 procollagen N-terminal propeptide (S–P1NP), urinary N-terminal type I collagen telopeptide (U-NTX), serum total homocysteine (S-Hcy), and cystatin C levels were measured along with routine laboratory examinations.…”
Section: Methodsmentioning
confidence: 99%
“…P-values < 0.05 were defined as statistically significant. The a priori required sample size was calculated using the G∗Power 3.1.9.3 statistical power analysis software program by comparing our previous data on changes in eGFRcr in women with osteoporosis during 27-month minodronate therapy [ 16 ] with annual health check-up data of healthy individuals attending our hospital. The mean changes in eGFRcr during minodronate therapy in 99 postmenopausal women aged 43–93 years (average, 74.5 years) for 27 months was −8.5% with a standard deviation of 11.0%.…”
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