Mechanism of Bazedoxifene/conjugated estrogens drugs therapy and its Clinical effect on osteoporosis

Main Article Content

Jiancheng Xu
Jing Ji
Zhan Wang
Tao Xu

Keywords

Estrogen; Bazedoxifene; Osteoporosis; Clinical effect

Abstract

Objective: To observe the clinical effects and explore the mechanism of Bazedoxifene/conjugated estrogens upon bone targeting in the treatment of postmenopausal osteoporosis. Methods:The study group was inclusive of 211 postmenopausal osteoporotic patients who were under treatment with Bazedoxifene/conjugated estrogens drugs in the study hospital during the period January and December 2018. The control group contained 56 patients and were treated only with calcium. The researchers analyzed the risks involved in the adverse events such as bone mineral density, osteoprotegerin (OPG) and insulin-like growth factor (IGF) and fracture prior to and after the treatment. Results:The study results inferred that the clinical treatment effective rate was 88.39% in Study group whereas it was 23.21% in the control group and were statistically significant (P<0.05). Prior to treatment, the researchers identified no significant difference in mean lumbar positive position (L2-4) and right femoral neck bone density IL-1β in between the groups (P>0.05). However, after the treatment, the study group data showed high mean lumbar positive position (L2-4) and heavy right femoral neck bone density in comparison with the control group (P<0.05). When compared to the control group (P<0.05), the Study group experienced less number of adverse events after 12 months of treatment. Conclusion:Bazedoxifene/conjugated estrogen is proved in the current study as an efficient drug to treat postmenopausal osteoporosis. It has the ability to arrest the rapid loss of bone mass, enhance the bone density, mitigate fracture risks and effectively reduce the symptoms of menopause.

Abstract 481 | PDF Downloads 211

References

[1] Coughlan T,Dockery F.Osteoporosis and fracture risk in older people[J]. Clinical medicine (London, England),2014,142:187-191.
[2] Xiang D,He J,Jiang T. The correlation between estrogen receptor gene polymorphism and osteoporosis in Han Chinese women[J]. European review for medical and pharmacological sciences,2018,22(23):8084-8090.
[3] Figliomeni A,Signorini V,Mazzantini M.One year in review 2018: progress in osteoporosis treatment[J].Clinical and experimental rheumatology,2018,366:948-958.
[4] Chen L R,Ko N Y,Chen K H. Medical Treatment for Osteoporosis: From Molecular to Clinical Opinions[J]. International journal of molecular sciences,2019,20(9):E2213.
[5] Schnitzer T J. Estrogen therapy in postmenopausal women[J]. Current rheumatology reports,2003,51:43-44.
[6] Xing Q,Tang P,Gao Y,et al. Proteomic analysis of estrogen mediated Signal Transduction in Osteoclasts Formation[J].Biomed Res Int,2015,2015: 596789.
[7] Hofbauer L C,Khosla S,Dunstan C R,et al. Estrogen stimulates gene expression and protein production of osteoprotegerin in human osteoblastic cells[J]. Endocrinology,1999,1409:4367-4370.
[8] Mano H,Hakeda Y,Kumegawa M.Estrogen directly down-regulates the bone-resorbing activity of mature osteoclasts through nuclear estrogen receptor alpha[J]. Cytotechnology,2001,351:17-23.
[9] Orimo H,Hayashi Y,Fukunaga M,et al. Diagnostic criteria for primary osteoporosis: year 2000 revision[J]. Journal of bone and mineral metabolism,2001,196:331-337.
[10] Li Z,Yuan G,Lin X,et al. Dehydrocostus lactone (DHC) suppresses estrogen deficiency-induced osteoporosis[J].Biochemical pharmacology,2019,163:279-289.
[11] Duursma S A,Raymakers J A,Boereboom F T,et al. Estrogen and bone metabolism[J].Obstetrical & gynecological survey,1992,471:38-44.
[12] Mesalić L,Tupković E,Kendić S,et al.Correlation between hormonal and lipid status in women in menopause[J].Bosnian Journal of Basic Medical Sciences,2008,8(2):188-92.
[13] Levin V A,Jiang X,Kagan R.Estrogen therapy for osteoporosis in the modern era[J].Osteoporosis international,2018,295:1049-1055.
[14] Hofbauer L C,Heufelder A E. Osteoprotegerin:a novel local player in bone metabolism[J].European journal of endocrinology,1997,1374:345-346.
[15] Yasuda H,Shima N,Nakagaw a N,et al.Ost eoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibit ory f actor and is iden tical to T RANCE/RANKL[J].Proc Natl Acad Sci USA,1998,95:3597-3602.
[16] Lacey D L,Timms E,Tan H L,et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation[J]. Cell,1998,932:165-176.
[17] Ferretti C,Vozzi G,Falconi M,et al. Role of IGF1 and IGF1/VEGF on human mesenchymal stromal cells in bone healing: two sources and two fates[J]. Tissue engineering.Part A,2014,2017(18):2473-2482.
[18] Jehle P M,Schulten K,Schulz W,et al. Serum levels of insulin-like growth factor (IGF)-I and IGF binding protein (IGFBP)-1 to -6 and their relationship to bone metabolism in osteoporosis patients[J]. European journal of internal medicine,2003,141:32-38.
[19] Sang C,Zhang Y,Chen F,et al.Tumor necrosis factor alpha suppresses osteogenic differentiation of MSCs by inhibiting semaphorin 3B via Wnt/β-catenin signaling in estrogen-deficiency induced osteoporosis[J].Bone,2016,84:78-87.
[20] Sun M,Yang J,Wang J,et al. TNF-α is upregulated in T2DM patients with fracture and promotes the apoptosis of osteoblast cells in vitro in the presence of high glucose[J].Cytokine,2016,80:35-42.