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      Clinical effect of Zoledronic Acid in the treatment of Senile Osteoporosis

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          Abstract

          Objective:

          To investigate the clinical efficacy of zoledronic acid in the treatment of senile osteoporosis.

          Methods:

          One hundred and six cases of senile osteoporosis who visited to our hospital from August 2017 to December 2018 for treatment were selected and randomly divided into a control group and an observation group. The control group was treated with conventional therapy, while the observation group was treated with zoledronic acid in addition to the treatment of the control group. Bone mineral density, pain degree, therapeutic effect and adverse reactions of the two groups were compared.

          Results:

          The total effective rate of the observation group was 96.67%, higher than 80.00% of the control group (P<0.05); the bone mineral density of lumbar vertebrae, femoral neck and Ward’ area in the two groups increased after 6 months of treatment, and the bone mineral density of the observation group increased more than that of the control group (P<0.05); the pain degree of the observation group was lower than that of the control group after 6 months of treatment, and the difference was significant (P<0.05). There was no significant difference in the occurrence of adverse reactions between the two groups (P>0.05).

          Conclusion:

          Zoledronic acid is helpful to alleviate clinical symptoms, reduce the degree of bone pain, and promote the increase of bone mass, and has high safety in the treatment of senile osteoporosis, which is worth promotion.

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          Most cited references20

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          Zoledronic acid and survival in patients with metastatic bone disease from lung cancer and elevated markers of osteoclast activity.

          Bone metastases from non-small cell lung cancer (NSCLC) are associated with skeletal-related events (SREs) and elevated levels of N-telopeptide of type I collagen (NTX) in some patients. Zoledronic acid (ZOL) reduces SRE risk and NTX levels. To assess effects of baseline variables, including NTX levels (normal = NTX or = 64 nmol/mmol creatinine), on treatment effects in NSCLC patients, a retrospective analysis was performed in NSCLC patients with bone metastases (N = 382) treated with ZOL or placebo every 3 weeks in a 21-month randomized clinical trial in patients with NSCLC or other solid tumors. Cox proportional hazards models assessed relative risks (RRs) of SREs, bone lesion progression, and death. Multivariate models analyzed covariate effects on survival. For both placebo- and ZOL-treated patients, high baseline NTX correlated with increased SRE risk (p = 0.068 and 0.012, respectively). Although high versus normal baseline NTX correlated with more than twofold increased risks of bone lesion progression and death in the placebo group (p = 0.039 and 0.001, respectively), correlations were weaker in the ZOL group (RR = 1.38; p = 0.0186 and RR = 1.27; p = 0.142, respectively), suggesting an interaction effect of ZOL and baseline NTX. Among patients with high baseline NTX, ZOL significantly reduced the RR of death by 35% versus placebo (p = 0.024). Per multivariate analysis, ZOL treatment (p = 0.005), higher lymphocyte count (p = 0.011), performance status 0 to 1 (p = 0.012), and absence of narcotic use (p = 0.016) correlated with improved survival. This retrospective analysis revealed statistically significant correlations between ZOL and increased survival versus placebo in NSCLC patients and high baseline NTX levels.
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            Effects of yearly zoledronic acid 5 mg on bone turnover markers and relation of PINP with fracture reduction in postmenopausal women with osteoporosis.

            In patients with osteoporosis treated with antiresorptive agents, reduction in bone turnover explains much of the observed fracture risk reduction. Lower levels of bone turnover markers (BTMs) appear to be associated with a lower risk of fracture in bisphosphonate-treated patients. BTMs were measured in a subset of subjects in the HORIZON Pivotal Fracture Trial. Annual infusions of zoledronic acid 5 mg significantly reduced BTMs: median decrease of 50% for beta-C-terminal telopeptides of type 1 collagen (beta-CTX), 30% for bone alkaline phosphatase (ALP), and 56% for procollagen type 1 amino-terminal propeptide (PINP). The mean level of BTMs decreased in treated patients but remained within the premenopausal range before the next injection. The percentage of zoledronic acid-treated patients with values below the premenopausal reference range at all time points was 1.7%, 17.8%, and 19% for bone ALP, CTX, and PINP, respectively. The third injection of zoledronic acid resulted in 60% reduction of beta-CTX within 9-11 days, followed by a gradual increase, indicating the persistence of osteoclastic bone resorption. The association between changes in BTMs and fracture incidence was assessed in 1132 patients who had PINP measurements at baseline and 1 yr. There was no association between low PINP levels at 1 yr and increased fracture incidence. In summary, (1) annual injections of zoledronic acid reduced BTMs in the premenopausal range, with a significant response persisting after the third infusion; and (2) low levels of PINP were not associated with increased fracture risk.
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              Phenotypic research on senile osteoporosis caused by SIRT6 deficiency

              Osteoporosis is a serious public bone metabolic disease. However, the mechanisms underlying bone loss combined with ageing, which is known as senile osteoporosis, remains unknown. Here we show the detailed phenotype of this disease caused by SIRT6 knock out (KO) in mice. To the best of our knowledge, this is the first study to reveal that SIRT6 is expressed in both bone marrow stroma cells and bone-related cells in both mouse and human models, which suggests that SIRT6 is an important regulator in bone metabolism. SIRT6-KO mice exhibit a significant decrease in body weight and remarkable dwarfism. The skeleton of the SIRT6-KO mouse is deficient in cartilage and mineralized bone tissue. Moreover, the osteocalcin concentration in blood is lower, which suggests that bone mass is markedly lost. Besides, the tartrate-resistant acid phosphatase 5b (TRAP5b) concentration is much higher, which suggests that bone resorption is overactive. Both trabecular and cortical bones exhibit severe osteopenia, and the bone mineral density is decreased. Moreover, double-labelling analysis shows that bone formation is much slower. To determine whether SIRT6 directly regulates bone metabolism, we cultured primary bone marrow stromal cells for osteogenesis and osteoclastogenesis separately to avoid indirect interference in vivo responses such as inflammation. Taken together, these results show that SIRT6 can directly regulate osteoblast proliferation and differentiation, resulting in attenuation in mineralization. Furthermore, SIRT6 can directly regulate osteoclast differentiation and results in a higher number of small osteoclasts, which may be related to overactive bone resorption.
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                Author and article information

                Journal
                Pak J Med Sci
                Pak J Med Sci
                Pakistan Journal of Medical Sciences
                Professional Medical Publications (Pakistan )
                1682-024X
                1681-715X
                Nov-Dec 2020
                : 36
                : 7
                : 1703-1707
                Affiliations
                [1 ]Li Kong, Pharmacy Intravenous Admixture Services, Binzhou People’s Hospital, Shandong 256610, P. R. China
                [2 ]Kai Zuo, Department of Infectious Diseases, Binzhou People’s Hospital, Shandong 256610, P. R. China
                [3 ]Long Ma, Department of Emergency Station, Binzhou People’s Hospital, Shandong 256610, P. R. China
                Author notes
                Correspondence: Li Kong, Pharmacy Intravenous Admixture Services, Binzhou People’s Hospital, Shandong, 256610, P. R. China. E-mail: kongliso@ 123456163.com
                Article
                PJMS-36-1703
                10.12669/pjms.36.7.1964
                7674899
                ef2d2484-8ef2-40f6-8fd0-3f359bcf1046
                Copyright: © Pakistan Journal of Medical Sciences

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 15 November 2019
                : 25 July 2020
                : 12 August 2020
                Categories
                Original Article

                zoledronic acid,senile osteoporosis,clinical observation

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