PubMed · 9254801
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S Wynchank, P D Saltman. 1997. Trace elements and osteoporosis.. https://pubmed.ncbi.nlm.nih.gov/9254801/
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BACKGROUND: In a great many of observational studies, whether there is a relevance of resistin levels on bone mineral density (BMD) and fracture occurrence has been inconsistently reported, and the causality is unclear. METHODS: We aim to assess the resistin levels on BMD and fracture occurrence within a Mendelian randomization (MR) analysis. Exposure and outcome data were derived from the Integrative Epidemiology Unit (IEU) Open genome wide association studies (GWAS) database. Screening of instrumental variables (IVs) was performed subject to conditions of relevance, exclusivity, and independence. Inverse variance weighting (IVW) was our primary method for MR analysis based on harmonized data. Weighted median and MR-Egger were chosen to evaluate the robustness of the results of IVW. Simultaneously, heterogeneity and horizontal pleiotropy were also assessed and the direction of potential causality was detected by MR Steiger. Multivariable MR (MVMR) analysis was used to identify whether confounding factors affected the reliability of the results. RESULTS: After Bonferroni correction, the results showed a suggestively positive causality between resistin levels and total body BMD (TB-BMD) in European populations over the age of 60 [β(95%CI): 0.093(0.021, 0.165), P = 0.011]. The weighted median [β(95%CI): 0.111(0.067, 0.213), P = 0.035] and MR-Egger [β(95%CI): 0.162(0.025, 0.2983), P = 0.040] results demonstrate the robustness of the IVW results. No presence of pleiotropy or heterogeneity was detected between them. MR Steiger supports the causal inference result and MVMR suggests its direct effect. CONCLUSIONS: In European population older than 60 years, genetically predicted higher levels of resistin were associated with higher TB-BMD. A significant causality between resistin levels on BMD at different sites, fracture in certain parts of the body, and BMD in four different age groups between 0-60 years of age was not found in our study.
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Chronic glucocorticoid treatment is the most frequent cause of secondary osteoporosis. The direct inhibitory effect of glucocorticoids on osteoblasts results in decreased bone formation. Increased osteoclastic bone resorption due to low concentrations of gonadal steroid hormones and glucocorticoid-induced direct suppression of intestinal calcium absorption also contribute to the decrease of bone mass in these patients. Bone loss is rapid, particularly in the first months of glucocorticoid therapy. Bone mineral density of the lumbar spine and proximal femur should be measured in patients who are starting chronic therapy with glucocorticoids. Although glucocorticoid-induced osteoporosis is a severe and nowadays partially preventable disorder, osteoporosis prophylaxis is only rarely prescribed to these patients. Recent randomized, controlled trials proved the therapeutic effects of hormone replacement therapy, as well as of bisphosphonates and active vitamin D analogs in primary and secondary prevention of glucocorticoid-induced osteoporosis.