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PURPOSE: Osteoporotic fracture is the main complication of osteoporosis. The current management is to discharge patients as early as possible so they can get back to their daily activities. Once discharged, there are three main issues relating to morbidity, mortality, and risk of a subsequent fracture that need to be addressed and discussed. Therefore, the aim of this systematic review was to summarize and evaluate the evidence from published literature, to determine the outcome of osteoporotic fracture patients after their hospital discharge. METHODS: The MEDLINE and Cumulative Index to Nursing and Allied Health Literature (CINAHL) databases were searched, using the terms "osteoporosis", "fracture", "osteoporotic fracture", "hip fracture", and "vertebral fracture". We included only human studies published in English between 2004 and 2014. The reference lists of included studies were thoroughly reviewed in search for other relevant studies. RESULTS: A total of 18 studies met the selection criteria. Most were observational and cohort studies. Out of all the studies, five studies looked into the morbidity, six studies looked into the risk of subsequent fractures, and seven studies looked into mortality. Vertebral fracture caused the greatest health burden, but hip fracture patients were the main users of informal care after hospital discharge. There was an increased risk of a subsequent fracture after a primary fracture compared with the control group, a cohort comparison, or the general population. Osteoporotic fractures, especially hip fractures, are associated with higher mortality rate despite the advances in the management of osteoporotic fracture cases. CONCLUSION: There is strong evidence to show that after hospital discharge, osteoporotic fracture patients are faced with higher morbidity, subsequent fractures, and mortality.
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INTRODUCTION: Vitamin E is beneficial in restoring bone histomorphometric parameters in nicotine-treated rats. This study determined the effectiveness of 3 forms of vitamin E in restoring bone metabolism in nicotine-treated rats. MATERIAL AND METHODS: Thirty-five male Sprague-Dawley rats were divided into 5 groups: (1) control (C), (2) nicotine cessation (NC), (3) α-tocopherol (ATF), (4) tocotrienol-enhanced fraction (TEF) and (5) γ-tocotrienol (GTT). Treatment was carried out for 4 months. The control group was administered normal saline and olive oil throughout the treatment period while treatment for groups 2-5 was performed in 2 phases. In the first phase, the groups received nicotine 7 mg/kg intraperitoneally for 2 months. The following 2 months, group 2 received normal saline and olive oil while groups 3-5 received ATF, TEF or GTT, 60 mg/kg orally. Pre-treatment and post-treatment serum was collected for bone biochemical marker measurement using the ELISA method. RESULTS: Nicotine increased serum bone-resorbing cytokines (interleukin-1 and interleukin-6) and the bone resorption marker pyridinoline (PYD) while reducing the bone formation marker osteocalcin after 2 months of nicotine treatment. The parameters failed to improve after nicotine was stopped for 2 months. Supplementation with the 3 forms of vitamin E improved the parameters, i.e. reduced the cytokines and pyridinoline as well as increased the osteocalcin. In addition, the TEF and GTT groups had a higher level of osteocalcin than the control group. CONCLUSIONS: Nicotine impaired bone metabolism and cessation of nicotine treatment did not reverse the effects. Vitamin E, especially the tocotrienols, restored bone metabolism that was impaired due to nicotine.
