Early clinical effects, safety, and appropriate selection of bone markers in romosozumab treatment for osteoporosis patients: a 6-month study

Tominaga, Ayako; Wada, Keiji; Kato, Yoshiharu; Nishi, H.; Terayama, Yasushi; Okazaki, Ken

doi:10.1007/s00198-020-05639-y

Cited by 18 publications

(11 citation statements)

References 35 publications

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“…Besides, there were a few reports about the treatment of osteoporosis by romosozumab by comparing prior treatment of osteoporosis [ 5 , 6 ]; our study indicated that switch therapy after romosozumab was similar to the primary treatment of romosozumab. In regard to this point, Tominaga also suggested that the change of increase in BMD were naïve>teriparatide> bisphosphonate>denosumab in 6 months [ 6 ]. Moreover, Ebina also suggested that naïve, teriparatide, bisphosphonates and denosumab had higher increase of BMD in turn [ 5 ].…”

Section: Discussionmentioning

confidence: 57%

The Effects of Switch Therapy in Osteoporosis Treatment after Romosozumab after Comparing with Prior Treatment

Horikawa,

Kasukawa,

Hongo

et al. 2024

Journal of Osteoporosis

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Rationale. Although romosozumab is one of the most effective treatments for osteoporosis by increasing bone mineral density in the lumbar spine and femur and recommended for denosumab as switch therapy, these effects regarding its prior treatment have not yet been evaluated clearly. This study focused on the effects of switch therapy from romosozumab to denosumab in regard to prior treatment of osteoporosis including bone mineral density and bone turnover marker and other related factors. Patient Concerns. 15 osteoporotic patients were assigned to the naïve group, 15 were assigned to the teriparatide group, and 10 were assigned to the bisphosphonate group. Interventions. Patients who were treated as outpatients for osteoporosis with romosozumab for 1 year and switched to denosumab between 2020 and 2022 at our hospital were examined. Our hospital registry included 40 osteoporotic patients who were over 65 years of age with bone mineral density (bone mineral density): T score <−2.5 standard deviations (SDs) and fracture assessment tool (FRAX) score >20%. Outcomes. The naïve group had the highest increase in LS BMD among these three groups during switch therapy from romosozumab to denosumab, while there were no significant differences about adverse drug events and serum Ca concentration among them. There was no incidence of fracture. Conclusion. These findings indicate that the effects of osteoporotic treatment of switch therapy from romosozumab to denosumab were likely to affect prior treatment of osteoporosis.

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Section: Discussionmentioning

confidence: 57%

The Effects of Switch Therapy in Osteoporosis Treatment after Romosozumab after Comparing with Prior Treatment

Horikawa,

Kasukawa,

Hongo

et al. 2024

Journal of Osteoporosis

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“…Amylin can repress the activity of osteoclasts, decline the bone absorption of basal and parathyroid hormone, stimulate the generation of cAMP via combining with the calcitonin receptor on osteoclasts, and constrain the mutual fusion of osteoclast precursor cells for the formation of mature multinuclear giant cells. Therefore, osteocyte is suppressed to influence bone metabolism [19] . Our study showed APN of 5.15 μg/mL or less and amylin of 15.38 pmol/L or less in patients were risk factors impacting the aggravation of pathological condition of POP, elaborating that the declined serum APN and amylin in patients might aggravate the severity of the pathological condition of POP.…”

Section: Discussionmentioning

confidence: 99%

The assessment value of pathological condition of serum adiponectin and amylin in primary osteoporosis and its correlation analysis with bone metabolism indexes

Wang¹,

Bai²,

Miu³

et al. 2023

J Med Biochemistry

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Objective: To explore the assessment value of pathological condition of serum adiponectin (APN) and Amylin in primary osteoporosis (POP) and their correlation with bone metabolism indexes. Methods: From January 2019 to June 2021, selection of 79 cases of POP patients was as the research objects. Test of the bone density of the patients was conducted, and clinical grading of POP was via T value (normal, mild, moderate, severe). Analysis of the assessment value of pathological condition of serum APN and Amylin for POP and their association with bone metabolism indexes in patients was performed. Results: APN and Amylin in patients were declined with POP’s aggravation. Patients with APN of 5.15 μg/mL or less and Amylin of 15.38 pmol/L or less were risk factors influencing the aggravation of pathological condition of POP (P < 0.05); The area under the curve (AUC) of combined detection of APN and Amylin to assess the severity of POP was elevated vs. alone test of Amylin (P < 0.05); 25-hydroxyvitamin D (25-(OH) D) and total type 1 procollagen amino-terminal propeptide (t-PINP) in patients were descended with the aggravation of pathological condition of osteoporosis (P < 0.05), while no distinct differences were presented in the three groups of type I collagen hydroxyl terminal peptide β degradation product (β-CTX) and N-terminal osteocalcin (N-MID) (P > 0.05); APN, Amylin, 25-(OH)D, β-CTX and t-PINP were negatively linked with POP clinical grade (P < 0.05); APN and Amylin were associated with 25-(OH) D, β-CTX, t-PINP (P < 0.05), and APN and Amylin were not linked with N-MID (P > 0.05). Conclusions: Serum APN and Amylin are provided with evaluation value for the severity of POP, and are associated with the bone metabolism in patients.

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“…3 Recently, some targeted drugs for osteoporosis have been approved for clinical use and exhibit excellent curative effects. [4][5][6] As a predominant source of osteoblasts, it is crucial to maintain osteogenic differentiation and proliferation of bone marrow mesenchymal stem cells (BMMSCs) to preserve bone homeostasis. 7 Furthermore, several studies have revealed that BMMSC-mediated osteogenic differentiation and proliferation can be downregulated or impaired by multiple factors in the bone marrow (BM), which is markedly associated with osteoporosis.…”

Section: Introductionmentioning

confidence: 99%

“…Current strategies for osteoporotic prevention and treatment focus on promoting bone regeneration, suppressing bone resorption, or a combination of both 3 . Recently, some targeted drugs for osteoporosis have been approved for clinical use and exhibit excellent curative effects 4–6 …”

Section: Introductionmentioning

confidence: 99%

Platelet factor 4 induces bone loss by inhibiting the integrin α5‐FAK‐ERK pathway

Zhang

et al. 2023

Anim Models and Exp Med

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BackgroundThe effect of platelet factor 4 (PF4) on bone marrow mesenchymal stem cells (BMMSCs) and osteoporosis is poorly understood. Therefore, this study aimed to evaluate the effects of PF4‐triggered bone destruction in mice and determine the underlying mechanism.MethodsFirst, in vitro cell proliferation and cell cycle of BMMSCs were assessed using a CCK8 assay and flow cytometry, respectively. Osteogenic differentiation was confirmed using staining and quantification of alkaline phosphatase and Alizarin Red S. Next, an osteoporotic mouse model was established by performing bilateral ovariectomy (OVX). Furthermore, the PF4 concentrations were obtained using enzyme‐linked immunosorbent assay. The bone microarchitecture of the femur was evaluated using microCT and histological analyses. Finally, the key regulators of osteogenesis and pathways were investigated using quantitative real‐time polymerase chain reaction and Western blotting.ResultsHuman PF4 widely and moderately decreased the cell proliferation and osteogenic differentiation ability of BMMSCs. Furthermore, the levels of PF4 in the serum and bone marrow were generally increased, whereas bone microarchitecture deteriorated due to OVX. Moreover, in vivo mouse PF4 supplementation triggered bone deterioration of the femur. In addition, several key regulators of osteogenesis were downregulated, and the integrin α5‐focal adhesion kinase‐extracellular signal‐regulated kinase (ITGA5‐FAK‐ERK) pathway was inhibited due to PF4 supplementation.ConclusionsPF4 may be attributed to OVX‐induced bone loss triggered by the suppression of bone formation in vivo and alleviate BMMSC osteogenic differentiation by inhibiting the ITGA5‐FAK‐ERK pathway.

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Early clinical effects, safety, and appropriate selection of bone markers in romosozumab treatment for osteoporosis patients: a 6-month study

Cited by 18 publications

References 35 publications

The Effects of Switch Therapy in Osteoporosis Treatment after Romosozumab after Comparing with Prior Treatment

The Effects of Switch Therapy in Osteoporosis Treatment after Romosozumab after Comparing with Prior Treatment

The assessment value of pathological condition of serum adiponectin and amylin in primary osteoporosis and its correlation analysis with bone metabolism indexes

Platelet factor 4 induces bone loss by inhibiting the integrin α5‐FAK‐ERK pathway

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