Optimization of the secondary prevention for bone fractures in osteoporosis in menopausal women and the role of comorbid metabolic syndrome
Background. Osteoporosis is characterized by the fragi-lity of the skeleton and the susceptibility to fractures due to a decrease in bone mass and deterioration in bone microarchitecture. In menopausal women, bone fragility is more pronounced, and osteoporotic fractures are three times more frequent. The presence and severity of the comorbid metabolic syndrome worsens the course of osteoporosis in menopausal women, which requires an improvement of therapeutic measures in such patients. The purpose was to increase the effectiveness of treatment for osteoporosis in menopausal women with metabolic syndrome and the quality of secondary prevention of bone fractures in them. Materials and methods. Twenty eight menopausal women with osteoporosis aged 37 to 72 years (average 50 years) were monitored for two years. In all cases, physio-logical menopause occurred. Bone mineral density was evaluated by the T-index of osteodensitograms, X-ray indices of Barnett-Nordin, Rokhlin and wedge shape. In the blood serum, parameters were studied that reflected the state of bone metabolism and metabolic syndrome. Results. In menopausal women suffering from osteoporosis, fractures of the femur, spine, wrist bones and second metatarsal were diagnosed in 39 % of cases. They were directly related to the age of the patients, bone density, the presence and severity of the course of comorbid metabolic syndrome, and constituents of the latter (type IV hyperlipidemia and type II diabetes melitus), the presence of diabetic neuropathy, as well as baseline blood concentrations of Mg, Mn, Pb and Se. An optimal secondary prevention of bone fractures in menopausal women with comorbid osteoporosis and metabolic syndrome was developed based on individual approaches to the long-term administration of Ca, Se, Zn, bisphosphonates, strontium ranelate, fibrates and drugs that block uric acid production, taking into account the nature and severity of metabolic syndrome. Conclusions. Proposed medical technique for the treatment of osteoporosis in menopausal women with metabolic syndrome has reduced the number of bone fractures by 10 times, as well as the blood activity of alkaline phosphatase and bone density.
Full Text:PDF (Русский)
Sugimoto T., Sato M., Dehle F.C., Brnabic A.J., Weston A., Burge R. Lifestyle-related metabolic disorders, osteoporosis, and fracture risk in Asia: A systematic review. Value Health Reg. Issues. 2016. 9 (1). 49-56. doi: 10.1016/j.vhri.2015.09.005.
Wong S.K., Chin K.Y., Suhaimi F.H., Ahmad F., Ima-Nirwana S. The relationship between metabolic syndrome and osteoporosis: a review. Nutrients. 2016. 8 (6). 347. doi: 10.3390/nu8060347.
Nayak N.K., Khedkar C.C., Khedkar G.D., Khedkar C.D. Osteoporosis. Encyclopedia of food and health. Oxford: Academic Press, 2016. 181-5.
Kaufman J.M., Goemaere S. Osteoporosis in men. Best Pract. Res. Clin. Endocrinol. Metab. 2008. 22 (5). 787-812.
Horikawa K., Kasai Y., Yamakawa T., Sudo A. Prevalence of osteoarthritis, osteoporotic vertebral fractures, and spondylolisthesis among the elderly in a Japanese village. J. Orthop. Surg. 2016. 14 (1). 9-12.
Li R.C., Zhang L., Luo H., Lei Y., Zeng L., Zhu J. et al. Subclinical hypothyroidism and anxiety may contribute to metabolic syndrome in Sichuan of China: a hospital-based population study. Sci Rep. 2020. 10 (1). 2261. doi: 10.1038/s41598-020-58973-w.
Seo Y.G., Song H.J., Song Y.R. Fat-to-muscle ratio as a predictor of insulin resistance and metabolic syndrome in Korean adults. J. Cachexia Sarcopenia Muscle. 2020. 7 (2). 12548. doi: 10.1002/jcsm.12548.
Kayal R.A., Tsatsas D., Bauer M.A., Allen B., Al-Sebaei M.O., Kakar S. et al. Diminished bone formation during diabetic fracture healing is related to the premature resorption of cartilage associated with increased osteoclast acti-vity. J. Bone Miner. Res. 2007. 22 (2). 560-8. doi: 10.1359/jbmr.070115.
Yamagishi S., Nakamura K., Inoue H. Possible participation of advanced glycation end products in the pathogenesis of osteoporosis in diabetic patients. Med. Hypotheses. 2005. 65. 1013-5. doi: 10.1016/j.mehy.2015.07.017.
Vollenweider P., Randin D., Tappy L., Jequier E., Nicod P., Scherrer U. Impaired insulin-induced sympathetic neural activation and vasodilation in skeletal muscle in obese humans. J. Clin. Invest. 2014. 93. 2365-71.
Brown J.P., Morin S., Leslie W. Bisphosphonates for treatment of osteoporosis. Expected benefits, potential harms, and drug holidays. Canad. Fam. Physic. 2014. 60 (1). 324-33. doi: 10.1210/endo.141.3.7366.
Compston J., Cooper A., Cooper C. UK clinical guideline for the prevention and treatment of osteoporosis. Arch. Osteoporos. 2017. 12 (1). 43-9.
Copyright (c) 2020 TRAUMA
This work is licensed under a Creative Commons Attribution 4.0 International License.
© Publishing House Zaslavsky, 1997-2020