老年骨质疏松性骨折患者的危险因素与护理干预措施

目的 探讨老年骨质疏松性骨折发生的危险因素,旨在为指导老年骨质疏松性骨折的防治提供参考依据.方法 选择2008年8月至2011年8月在我院住院治疗的239例老年骨质疏松症患者为研究对象,根据老年骨质疏松症患者是否出现骨折分为老年骨质疏松性骨折组和老年骨质疏松症无骨折组,收集符合条件的患者的临床资料,采用多因素Logistic回归分析找出骨质疏松性骨折的危险因素.结果 多因素Logistic回归分析结果表明:骨密度是老年骨质疏松症患者发生骨折的保护因素,而年龄、低钙饮食、跌倒、脆性骨折史及骨折家族史是老年骨质疏松症患者发生骨折的危险因素.结论 老年骨质疏松症患者发生骨折受多种因素影响,可从饮食、体育锻炼及药物等多方面进行干预.     

老年患者骨质疏松性骨折的影响因素与护理干预

目的 探讨引起老年患者骨质疏松性骨折发生的诸多危险因素,为老年患者骨质疏松性骨折的临床防治提供重要参考依据。方法 选择2010年12月至2013年12月在我院门诊随访和住院治疗的240例老年骨质疏松症患者为研究对象,根据老年骨质疏松症患者有/无骨折分为骨折组和非骨折组,采用多因素Logistic回归分析老年患者骨质疏松性骨折的危险因素。结果 骨密度值是防止老年患者骨质疏松症骨折发生的重要因素,而高龄、长期低钙饮食、意外跌倒、脆性骨折史、骨折家族史是老年患者骨质疏松症骨折发生的重要危险因素。结论 老年患者骨质疏松症骨折的发生受诸多因素共同影响,改变饮食结构、积极体育锻炼、相关药物治疗等方法可防止其骨折的发生。     

老年女性原发性骨质疏松症患者发生骨折的相关影响因素

目的探讨老年女性原发性骨质疏松症(POP)患者发生骨折的相关影响因素并提出预防对策。方法对635例老年女性POP患者进行骨密度检测和影像学检查,将其分为骨折组和无骨折组;比较两组患者的各因素分布差异性,采用逐步Logistic回归法筛选老年女性POP患者发生骨折的高危因素。结果 635例老年女性POP患者骨折发生率为28.66%(182/635),Logistic回归结果显示影响老年女性POP患者发生骨折的危险因素包括高龄(OR=3.607)、缺乏阳光照射(OR=3.235)、缺乏运动(OR=2.883)、骨质丢失过多(OR=1.696)、无规律补钙(OR=4.821)、近1个月跌倒(OR=4.402),而腰椎骨密度(OR=0.546)则为保护因素。结论老年女性POP患者具有较高的脆性骨折发生率,且影响其发生骨折的高危因素较多,应结合其特点及高危因素对高危人群进行针对性管理和干预,降低骨折发生率,改善老年女性患者的预后。     

老年骨质疏松性骨折的影响因素及社区康复效果

目的探讨老年骨质疏松性骨折的影响因素及社区康复治疗对患者的治疗效果。方法选取2015年1月—2017年1月同济大学附属杨浦医院收治的老年骨质疏松症患者300例,根据患者是否出现骨折分为对照组(n=150,非骨折组)和观察组(n=150,骨折组),对比分析老年骨质疏松性骨折的影响因素,同时给予社区康复治疗,探讨社区康复治疗效果。结果经骨折的影响因素分析结果显示,年龄、TC、LDL、总髋部BMD水平及阳光照射情况均为老年骨质疏松患者骨折发生的影响因素(P0.05);经logistic回归分析显示,女性、年龄较大、缺乏阳光照射和总髋部BMD水平低均为老年骨质疏松患者发生骨折的独立危险因素(P0.05);老年骨质疏松性骨折患者经社区康复治疗其前屈后伸痛、翻身痛、负重痛及总髋部BMD水平均有所改善(P0.05)。结论女性、年龄较大、缺乏阳光照射及总髋部BMD水平低均为老年骨质疏松患者发生骨折的独立危险因素,临床医生应根据患者的实际情况有针对性地实施社区康复。     

老年骨质疏松性骨折的危险因素与护理干预

目的:分析老年骨质疏松性骨折的危险因素与护理干预方法.方海选择我院2014年12月-2016年12月收治的97例老年骨质疏松性骨折患者,将所有随机分为两组.对照组(n=49)采用常规护理方法进行干预,治疗组(n=48)在对照组的基础进行综合护理干预,分析两组患者出现老年骨质疏松性骨折的危险因素,并对比两组患者的骨折发生率.结果:影响患者出现骨质疏松性骨折的主要危险因素有骨折家族史、骨折史、跌例以及饮食缺钙等.通过对两组患者进行护理干预对比分析发现,治疗组患者出现骨质疏松性骨折的概率要小于对照组(P＜0.05).结论:老年发生骨质巯松性骨折与多种因素有关,护理人员必须要针对患者的实际情况进行综合护理,以此避免发生骨质疏松性骨折的情况,提高老年患者的身体和生活质量.     

健康教育在老年骨质疏松性髋部骨折护理中的应用

目的探讨老年骨质疏松性髋部骨折的危险因素,并提出相应的健康教育,以提高其生活质量。方法对92例老年骨质疏松性髋部骨折患者进行问卷调查,分析骨折的诱发因素、以往含钙相关饮食、运动锻炼等情况,并提出健康教育。结果老年人对骨质疏松症相关知识及预防方法缺乏认识,营养摄入减少是主要诱因,跌倒是导致其髋部骨折的主要危险因素。结论骨质疏松性老年患者受轻微外力作用即可发生骨折,护理人员应针对其危险因素,采取有效的健康教育干预措施,降低老年骨质疏松性髋部骨折发生率。     

老年女性骨质疏松性股骨颈骨折患者雌激素、骨密度状况检测及其危险因素分析

目的分析老年女性骨质疏松性股骨颈骨折患者的雌激素、骨密度状况及危险因素,为预防股骨颈骨折提供依据。方法选取2016年9月-2018年9月在温州市中心医院进行诊治的60例老年女性骨质疏松性股骨颈骨折患者为观察组;选取同期在该院进行诊治的60例女性骨质疏松无股骨颈骨折患者为对照组。测量并记录所有患者的雌激素水平和骨密度,通过问卷调查的方法,记录每位研究对象的一般资料、生育和月经情况、既往病史和生活习惯等方面的相关内容,并采用Logistic回归分析法对影响股骨颈骨折的因素进行分析。结果两组患者的年龄、吸烟、饮酒率比较差异无统计学意义(P>0. 05);观察组患者的BMI、骨密度、雌激素水平、绝经年龄和体育锻炼率明显低于对照组(P<0. 05),初潮年龄、怀孕次数、生产次数、母乳喂养时间、高血压、糖尿病者明显高于对照组(P<0. 05)。Logistic回归分析显示,BMI、初潮年龄、绝经年龄、怀孕次数、生产次数和母乳喂养时间是老年女性骨质疏松性股骨颈骨折的独立危险因素。患者的初潮年龄、怀孕次数、生产次数、母乳喂养时间及雌激素水平与骨质疏松性股骨颈骨折呈正相关(P<0. 05),BMI和绝经年龄与其呈负相关(P<0. 05)。结论老年骨质疏松性股骨颈骨折女性患者的骨密度较小,雌激素水平较低。此外,BMI低、初潮时间晚、绝经时间早、怀孕和生产次数多及母乳喂养时间长是老年女性发生骨质疏松性股骨颈骨折的危险因素。     

类风湿性关节炎患者并发骨质疏松的危险因素

目的 分析类风湿性关节炎（RA）患者并发骨质疏松的危险因素。方法 选取2020年1月至2021年12月于医院就诊的86例RA患者作为研究对象。患者均进行骨密度检测，根据是否并发骨质疏分为发生组和未发生组。比较两组一般资料，并分析RA患者并发骨质疏松的危险因素。结果 86例RA患者中31例并发骨质疏松，55例未发生骨质疏松。两组年龄、摄入钙剂情况、糖皮质激素使用情况及25羟基维生素D[25(OH)D]水平比较，差异有统计学意义（P<0.05）；经Logistic回归分析结果显示，年龄大、未摄入钙剂、使用糖皮质激素是RA患者并发骨质疏松症的危险因素（OR>1,P<0.05）;25(OH)D水平是RA患者并发骨质疏松的保护因素（OR <1,P <0.05）。结论 RA患者并发骨质疏松率较高，可能受患者年龄大、未摄入钙剂、使用糖皮质激素及25(OH)D水平的影响。     

绝经后骨质疏松患者发生骨折的相关因素分析

目的分析女性绝经后骨质疏松患者发生骨折的影响因素。方法以2015—2016年6月期间就诊于绍兴第二医院的110例绝经后骨质疏松患者为研究对象,按是否发生骨折分为对照组72例和观察组38例,收集并比较两组患者临床资料,采用Logistic回归模型分析绝经后骨质疏松患者骨折的影响因素。结果对照组腰椎骨密度、I型前胶原氮端肽、25-(OH)D、骨保护素水平均高于观察组(P0.05);对照组I型前胶原羧基端肽及细胞核因子κB受体活化因子配体(RANKL)水平均低于观察组(P0.05);两组患者年龄、体质指数、血清钙及血清磷水平比较,差异均无统计学意义(P0.05)。Logistic回归结果显示,血清骨保护素水平高是绝经后骨质疏松患者发生骨折的保护因素(OR=0.035,95%CI:0.001~0.932),年龄大、血清RANKL水平高是危险因素(OR年龄=2.555,95%CI:1.384~4.719;ORRANKL=3.916,95%CI:1.029~14.905)。结论血清骨保护素水平高是绝经后骨质疏松患者发生骨折的保护因素,年龄大、血清RANKL水平高是危险因素。     

上海市枫林社区老年人骨质疏松性骨折的相关因素分析

目的了解老年骨质疏松性骨折的相关因素。方法对在上海市枫林街道社区卫生服务中心就诊的骨质疏松症无骨折患者118例及骨质疏松性骨折患者82例进行问卷调查。结果老年骨质疏松性骨折与年龄、性别、体重、职业、膳食结构、运动方式、骨质疏松性骨折史及骨折家族史等有关。结论提倡正确锻炼方式,均衡饮食,避免低体重对降低骨质疏松性骨折发生率有重要意义。     

Risk factors for osteoporosis: A review

Skeletal fragility and falls are the 2 most potent factors leading to osteoporotic fractures. The aim of this article is to review factors associated with women's risk of developing skeletal fragility and subsequent osteoporosis. Many factors have been implicated, but the evidence for some is unsubstantial. Low premenopausal bone mineral density (BMD), a decrease in BMD, and an increase in bone fragility -- which occur as a result of both aging and the menopause -- are major determinants of subsequent risk for osteoporotic fracture. In addition, low body mass index (BMI), low calcium intake, low physical activity, and smoking can affect BMD. The relative importance of the effects these physical and lifestyle factors have on BMD in midlife women is not fully established. The impact of gynecologic history (parity, lactation, oral contraceptive use, age of menarche) on BMD is uncertain.     

珠海地区575名女性骨密度测定及骨质疏松症危险因素初析

目的了解珠海地区女性骨密度和骨量分布情况以及影响骨质疏松症(OP)的危险因素。方法采用双能X线骨密度仪对珠海地区的575例女性进行骨密度检测,并对个人疾病史、生活习性及月经史进行调查,根据OP发生与否,进行单因素和多因素分析。结果女性骨密度和骨量呈现年龄分布趋势;单因素分析结果显示年龄、绝经年限、体重指数(BMI)、糖尿病、骨折以及慢性病对OP存在影响;多因素分析结果显示年龄和慢性病是OP发病的危险因素,而BMI是OP的保护因素。结论女性骨密度随年龄的增长、绝经年限的增加而逐步下降,而保持一定体型及体重,有利于骨密度的维持及提高;及时发现、治疗糖尿病、慢性病(如甲亢、风湿)等,对防治骨质疏松有积极作用。     

Who is at risk of osteoporosis?

This contribution assesses who is at risk of osteoporosis, by delineating the key risk factors involved in the condition. Osteoporosis represents a major public health problem through its association with fragility fractures, primarily of the hip, spine and distal forearm. Some risk factors for fragility fracture act through bone mineral density (BMD), for example female gender, asian or Caucasian race, premature menopause, primary or secondary amenorrhoea, primary and secondary hypogonadism in men, prolongued immobilisation, low dietary calcium intake, vitamin D deficiency. However, a number of others contribute significantly to fracture risk over and above their association with BMD (age, high bone turnover, poor visual acuity, neuromuscular disorders, previous fragility fracture, glucocorticoid therapy, family history of hip fracture, low body weight, cigarette smoking, excess alcohol consumption).     

Vitamin D and bone health in postmenopausal women

Osteoporosis, a disease of increased skeletal fragility, is becoming increasingly common as the U.S. population ages. Adequate vitamin D and calcium intake is the cornerstone of osteoporosis prevention and treatment. Age-related changes in vitamin D and calcium metabolism increase the risk of vitamin D insufficiency and secondary hyperparathyroidism. Although longitudinal data have suggested a role of vitamin D intake in modulating bone loss in perimenopausal women, studies of vitamin D and calcium supplementation have failed to support a significant effect of vitamin D and calcium during early menopause. There is a clearer benefit in vitamin D and calcium supplementation in older postmenopausal women. Vitamin D intake between 500 and 800 IU daily, with or without calcium supplementation, has been shown to increase bone mineral density (BMD) in women with a mean age of approximately 63 years. In women older than 65, there is even more benefit with vitamin D intakes of between 800 and 900 IU daily and 1200-1300 mg of calcium daily, with increased bone density, decreased bone turnover, and decreased nonvertebral fractures. The decreases in nonvertebral fractures may also be influenced by vitamin D-mediated decreases in body sway and fall risk. There are insufficient available data supporting a benefit from vitamin D supplementation alone, without calcium, to prevent osteoporotic fracture in postmenopausal women.     

CBO guideline 'Osteoporosis' (second revision

Risk factors for osteoporotic fractures that can be used for case-finding according to the recent guidelines from the Dutch Institute for Health Care Improvement (CBO) include: a vertebral fracture, a fracture past the age of 50, a positive family history, low body weight, severe immobility and the use of corticosteroids. Measurement of bone mineral density (BMD) is only recommended for case-finding and not for population screening. Measurement of the BMD is advised in women > or = 50 years of age with a fracture, women with a vertebral fracture regardless of age, women > or = 60 years of age with three of the following risk factors, and women > or = 70 years of age with two of the following risk factors: positive family history, low body weight and severe immobility. Persons with less than 1000-1200 mg calcium in their daily food who are using corticosteroids, persons with osteoporotic fractures and persons who are being treated with drugs for osteoporosis are eligible for calcium supplementation. Vitamin D supplementation is recommended for persons who do not come outdoors. For the drug treatment of osteoporosis in the first years after menopause, oestrogens, tibolone and raloxifene may be used. It is recommended that postmenopausal women with one or more osteoporotic vertebral fractures or an increased risk and a T-score below -2.5 be treated with a bisphosphonate. Patients who are expected to be treated with > or = 15 mg prednisolone equivalent per day for more than 3 months and postmenopausal women and older men (> or = 70) who will be treated with > or = 7.5 mg prednisolone equivalent per day should be started on a bisphosphonate as soon as possible. Other patients who will be treated with > or = 7.5 mg prednisolone equivalent per day should take a bisphosphonate if their Z-score is below -1 or their T-score is below -2.5.     

Factores de riesgo de fracturas por fragilidad en una cohorte de mujeres españolas

Introduction

Fragility fractures are an important public health issue. The aim of this study was to analyze the association of the main osteoporotic risk factors related to fragility fracture in a cohort of women with an indication of bone densitometry (BD).

Methods

A retrospective cohort was followed-up until a fragile fracture occurred, in a population of women aged 40 to 90 years with a first visit for BD between January 1992 and February 2008. We calculated the incidence rate of fracture per 1000 women-years of follow-up, and the hazard ratio (HR) of fragile fracture using a Cox regression model.

Results

A total of 49,735 women were studied. The average age of participants was 57.8 years (SD: 8.5). Of these, 3631 women (7.1%) reported a new fragility fracture in post-baseline visits. Risk factors with higher adjusted HR were age ≥ 75 years compared with age < 55 years (HR: 3.8; 95% CI: 3.3-4.4) and having a BC result evaluated as osteoporosis compared to normal (HR: 2.0; 95% CI: 1.8-2.2). A personal history of humerus, hip or vertebral fractures had an adjusted HR of 1.2 (95% CI: 1.1-1.3).

Conclusions

The main risk factors for fragility fracture were advanced age, BD result and a personal history of fracture, although 74% of fractures were detected with a bone mineral density classified as normal or osteopenia. Other relevant factors were rheumatoid arthritis or having received prolonged corticosteroid therapy.     

Genetics of osteoporosis

Osteoporosis is a common disease with a strong genetic component characterised by reduced bone mass and an increased risk of fragility fractures. Twin and family studies have shown that genetic factors contribute to osteoporosis by influencing bone mineral density (BMD), and other phenotypes that are associated with fracture risk, although the heritability of fracture itself is modest. Linkage studies have identified several quantitative trait loci that regulate BMD but most causal genes remain to be identified. In contrast, linkage studies in monogenic bone diseases have been successful in gene identification, and polymorphisms in many of these genes have been found to contribute to the regulation of bone mass in the normal population. Population-based studies have identified polymorphisms in several candidate genes that have been associated with bone mass or osteoporotic fracture, although individually these polymorphisms only account for a small amount of the genetic contribution to BMD regulation. Environmental factors such as diet and physical activity are also important determinants of BMD, and in some cases specific nutrients have been found to interact with genetic polymorphisms to regulate BMD. From a clinical standpoint, advances in knowledge about the genetic basis of osteoporosis are likely to be important in increasing the understanding of the pathophysiology of the disease; providing new genetic markers with which to assess fracture risk and in identifying genes and pathways that form molecular targets for the design of the next generation of drug treatments.     

Management of Postmenopausal Osteoporosis

Postmenopausal osteoporosis is a very common disease, and approximately half of all women aged >50 years will experience an osteoporotic fracture during the remainder of their lifetime. The predominant cause of postmenopausal osteoporosis is the decline in estrogen levels, which causes an increase in bone turnover, and results in a loss of bone mass throughout the entire skeleton. Fragility fractures, either vertebral or nonvertebral, have a considerable adverse effect on quality of life in women with osteoporosis and place a significant burden on society in terms of healthcare costs.Management of postmenopausal osteoporosis includes alteration of modifiable risk factors (e.g. lifestyle and propensity to fall), ensuring adequate calcium and vitamin D intake, and pharmacological treatment to decrease fracture risk by slowing or preventing bone loss and preserving bone strength. Raloxifene (Evista®), a selective estrogen receptor modulator that partially mimics the effects of estrogen on bone and lipid metabolism and acts as an antiestrogen in the breast and endometrium, is indicated for the prevention and treatment of postmenopausal osteoporosis. Raloxifene increases bone mineral density at vertebral and nonvertebral sites, and decreases the risk of vertebral fracture to a similar extent to the bisphosphonates alendronate and risedronate. However, effects on nonvertebral fracture risk, including the risk of hip fracture, have not been observed.Raloxifene appears to reduce breast cancer risk (in women at average risk) and cardiovascular risk (in women at increased risk) without stimulating the endometrium, and does not cause vaginal bleeding or breast pain. However, the drug causes hot flashes in some women, and increases the risk of venous thromboembolic events by about the same amount as hormone replacement therapy (HRT).In economic models, raloxifene is cost effective compared with no treatment, HRT, calcitonin, or alendronate for the prevention or treatment of postmenopausal osteoporosis.In conclusion, raloxifene is a valuable and cost-effective therapy for preventing the progression of osteoporosis and for reducing vertebral fracture risk in osteoporotic postmenopausal women. The tendency for raloxifene to cause hot flashes, and its apparent lack of effect on hip fracture risk, may preclude its use in women with vasomotor symptoms and in patients at high risk for hip fracture. Results from large ongoing trials are needed to confirm the effects of raloxifene on breast cancer and cardiovascular disease. However, the effects of raloxifene on breast cancer and cardiovascular risk without stimulating the endometrium make the drug an attractive therapy for the prevention and treatment of postmenopausal osteoporosis.     

Glucocorticoid induced risk of fractures

In recent years studies have emphasized the importance of glucocorticoid-induced osteoporosis as the second most common form of osteoporosis after postmenopausal osteoporosis. Several studies have underlined that glucocorticoids are responsible for decreasing bone mineral density and increasing bone fragility, resulting in a large increase in fracture risk. This review wants to provide a background regarding the fracture risk of patients exposed to glucocorticoid treatment, considering the fracture risk as the most appropriate parameter to valuate glucocorticoid-induced osteoporosis. In fact, glucocorticoid treatment induces bone loss and increases fracture risk above all affecting trabecular bone, probably through an alteration in bone turnover and microarchitectural changes responsible for an early increased fracture risk which is primary influenced by dose and duration of treatment, body mass index, age and female gender.