Stellenwert von nativem und biologisch aktivem Vitamin D bei der Prävention und Therapie der Osteoporose

Vitamin D metabolism has an important role in the pathogenesis of osteoporosis. Vitamin D deficiency is very common in elderly people in central Europe. This leads to secondary hyperparathyroidism and to increased bone resorption, resulting in osteoporosis. Combined with the elevated risk of falling that results from vitamin D deficiency, this increases the frequency of bone fractures. Severe vitamin D deficiency also causes impaired bone mineralization (osteomalacia). Controlled intervention trials with native vitamin D (and calcium) yielded no consistent results in terms of the prevention of extravertebral fractures. It appears likely that treatment with plain vitamin D is effective only in populations with vitamin D deficiency. Treatment with active vitamin D (1-alpha-hydroxylated metabolites such as alfacalcidol) has to be considered a pharmacological intervention that exerts pleiotropic effects on the gut (calcium absorption), bone (stimulation of formation), muscle (decreasing of the risk of falling), and immune system. Target groups are patients with disturbed vitamin D metabolism (renal insufficiency, glucocorticoid therapy, inflammatory disease such as rheumatoid arthritis). Alfacalcidol can prevent glucocorticoid-induced bone loss (high-grade evidence). In comparative studies alfacalcidol was superior to plain vitamin D.     

Superiority of alfacalcidol over plain vitamin D in the treatment of glucocorticoid-induced osteoporosis

Supplementation therapy with plain vitamin D plus calcium is in general regarded as effective prevention or first-step treatment of glucocorticoid-induced osteoporosis (GIOP). The aim of our study was to compare the therapeutic efficacy of the D-hormone analog alfacalcidol with plain vitamin D in patients with established GIOP with or without vertebral fractures. Patients on long-term glucocorticoid (GC) therapy were included as matched pairs to receive randomly either 1 microg alfacalcidol plus 500 mg calcium per day (group A, n=103) or 1000 IU vitamin D3 plus 500 mg calcium (group B, n=101). The two groups were well matched in terms of mean age, sex ratio, mean height and weight, daily dosage, and duration of GC therapy, and the percentages of the three underlying diseases included chronic obstructive pulmonary disease, rheumatoid arthritis, and polymyalgia rheumatica. The baseline mean bone mineral density (BMD) values at the lumbar spine for the two groups were -3.26 (alfacalcidol) and -3.25 (vitamin D(3)) and, at the femoral neck, -2.81 and -2.84, respectively (T scores). Rates of prevalent vertebral and nonvertebral fractures did not differ between groups. During the 3-year study, we observed a median percentage increase of BMD at the lumbar spine of 2.4% in group A and a loss of 0.8% in group B ( P<0.0001). There also was a larger median increase at the femoral neck in group A (1.2%) than in group B (0.8%) ( P<0.006). The 3-year rates of patients with at least one new vertebral fracture were 9.7% among those assigned to the alfacalcidol group and 24.8% in the vitamin D group (risk reduction 0.61, 95% CI 0.24-0.81, P=0.005). The 3-year rates of patients with at least one new nonvertebral fracture were 15% in the alfacalcidol group and 25% in the vitamin D group (risk reduction 0.41, 95% CI 0.06-0.68, P=0.081). The 3-year rates of patients with at least one new fracture of any kind were 19.4% among those treated with alfacalcidol and 40.65% with vitamin D (risk reduction 0.52, 95% CI 0.25-0.71, P=0.001). In accordance with the observed fracture rates, the alfacalcidol group showed a substantially larger decrease in back pain than the plain vitamin D group ( P<0.0001). Generally, side effects in both groups were mild, and only three patients in the alfacalcidol group and two in the vitamin D group had moderate hypercalcemia. We conclude that alfacalcidol plus calcium is highly superior to plain vitamin D3 plus calcium in the treatment of established GIOP.     

The effect of vitamin D on bone and osteoporosis

The main effect of the active vitamin D metabolite 1,25(OH)2D is to stimulate the absorption of calcium from the gut. The consequences of vitamin D deficiency are secondary hyperparathyroidism and bone loss, leading to osteoporosis and fractures, mineralization defects, which may lead to osteomalacia in the long term, and muscle weakness, causing falls and fractures. Vitamin D status is related to bone mineral density and bone turnover. Vitamin D supplementation may decrease bone turnover and increase bone mineral density. Several randomized placebo-controlled trials with vitamin D and calcium showed a significant decrease in fracture incidence. However, very high doses of vitamin D once per year may have adverse effects. When patients with osteoporosis are treated with a bisphosphonate, they should receive a vitamin D and calcium supplement unless the patient is vitamin D replete. These subjects are discussed in detail in this review. Finally, the knowledge gaps and research agenda are discussed.     

Vitamin D deficiency and osteoporosis

Osteoporosis is a disease of disequilibrium between bone formation and bone loss, and vitamin D is one of the key hormones in the regulation of bone metabolism, the major role of which is to provide the proper micro‐environment for bone mineralization. Vitamin D deficiency which has been defined by most experts as circulating 25‐hydroxyvitamin D levels of less than 20 ng/mL (50 nmol/L) is widespread all over the world. As shown by the results of recent studies, vitamin D deficiency could increase the risk of low bone mineral density or osteoporosis, muscle disorders, falls, and as a matter of course, fractures due to both osteoporosis and falls. Long‐term supplementation of vitamin D and calcium are good prevention measures for osteoporosis, falls and fractures. At the same time, they are essential components of osteoporosis management. Many studies show that sufficient vitamin D intake could increase bone mass, and decrease the risk of falls and fractures.     

Therapie der Glucocorticoid-induzierten Osteoporose mit Alfacalcidol/Kalzium und Vitamin D/Kalzium

Calcium/vitamin D supplementation is generally used as a first step treatment of glucocorticoid-induced osteoporosis (GIOP). The aim of this trial was to compare the efficacy of the D-hormone alfacalcidol with plain vitamin D in patients with established GIOP with or without vertebral fractures. Patients on long-term glucocorticoid-therapy were treated either with 1 microgram alfacalcidol plus 5000 mg calcium (group A: n = 43) or with 1000 IU vitamin D plus 500 mg calcium (group B: n = 42). The two groups were not different in respect to initial characteristics such as age, sex distribution, concomittant diseases, bone mineral density (mean T-score values at lumbar spine and femoral neck: -3.29 and -3.25 resp.), and in the number of prevalent vertebral and non-vertebral fractures. During the 3 years of treatment we found a significant increase in lumbar spine density in group A (+2.0%, p < 0.0001), while no significant changes could be documented in group B at both measuring sites. After 3 years 12 new vertebral fractures had occurred in 10 patients of group A and 21 in 17 patients in group B (ns). Correspondingly we registered a significant decrease of back pain only in group A (p < 0.0001). We conclude that alfacalcidol treatment in superior to plain vitamin D in GIOP.     

Vitamin D and the elderly

This review summarizes current knowledge on vitamin D status in the elderly with special attention to definition and prevalence of vitamin D insufficiency and deficiency, relationships between vitamin D status and various diseases common in the elderly, and the effects of intervention with vitamin D or vitamin D and calcium. Individual vitamin D status is usually estimated by measuring plasma 25-hydroxyvitamin D (25OHD) levels. However, reference values from normal populations are not applicable for the definition of vitamin D insufficiency or deficiency. Instead vitamin D insufficiency is defined as the lowest threshold value for plasma 25OHD (around 50 nmol/l) that prevents secondary hyperparathyroidism, increased bone turnover, bone mineral loss, or seasonal variations in plasma PTH. Vitamin D deficiency is defined as values below 25 nmol/l. Using these definitions vitamin D deficiency is common among community-dwelling elderly in the developed countries at higher latitudes and very common among institutionalized elderly, geriatric patients and patients with hip fractures. Vitamin D deficiency is an established risk factor for osteoporosis, falls and fractures. Clinical trials have demonstrated that 800 IU (20 microg) per day of vitamin D in combination with 1200 mg calcium effectively reduces the risk of falls and fractures in institutionalized patients. Furthermore, 400 IU (10 microg) per day in combination with 1000 mg calcium or 100 000 IU orally every fourth month without calcium reduces fracture risk in individuals over 65 years of age living at home. Yearly injections of vitamin D seem to have no effect on fracture risk probably because of reduced bioavailability. Simulation studies suggest that fortification of food cannot provide sufficient vitamin D to the elderly without exceeding present conventional safety levels for children. A combination of fortification and individual supplementation is proposed. It is argued that all official programmes should be evaluated scientifically. Epidemiological studies suggest that vitamin D insufficiency is related to a number of other disorders frequently observed among the elderly, such as breast, prostate and colon cancers, type 2 diabetes, and cardiovascular disorders including hypertension. However, apart from hypertension, causality has not been established through randomized intervention studies. It seems that 800 IU (20 microg) vitamin D per day in combination with calcium reduces systolic blood pressure in elderly women.     

Vitamin D and fractures: a systematic review

Vitamin D deficiency is a relevant problem particularly in south Europe and in over 65 year old subjects, that is often underestimated. Vitamin D deficiency represents a real medical emergency also for its role in the patho-physiology of muscular-skeletal diseases. Chronic vitamin D deficiency leads to severe bone and muscular outcomes including: osteoporosis, osteomalacia and proximal limb myopathy. These increase the risk of falling and fractures. The efficacy of vitamin D treatment in decreasing the fracture risk has been reporting in several studies. The negative results of some recent studies questioned the clinical vitamin D efficacy. However these studies have a number of methodological problems and even the interpretation of the results is questionable. In this paper we review all these aspects. This analysis permits to confirm that vitamin D treatment can be extremely cost-effective when given to people at high risk of deficiency. An acceptable compliance is obviously of critical importance.     

Potential of alfacalcidol for reducing increased risk of falls and fractures

There are no general accepted strategies for combined drug treatments in osteoporosis, while in other important chronic diseases combinations of different medications are used as a rule to improve therapeutic results and reduce the risk of adverse events. It is suggested that the success of combined treatments is related to the different modes of action of the respective single therapies. On the other hand it was shown that a strong antiresorptive bisphosphonate is able to blunt at least in part the effects of anabolic parathyroid hormone peptides Calcitriol, the active vitamin D-hormone and its prodrug alfacalcidol lead to pleiotropic effects on bone remodelling (antiresorptive, anabolic and enhancing mineralization) and in addition to effects on other important target tissues (e.g. gut, parathyroid glands, muscle). With active D-analogs significant improvements in the therapeutic outcome of osteoporosis can be achieved by the resulting improvements of bone quality, calcium absorption and risk reduction of falling. The same beneficial effects cannot be achieved with plain vitamin D due to feedback controlled, limited renal activation or insufficient conversion in the elderly with impairment of renal function. Accordingly alfacalcidol, approved as a treatment for different forms of osteoporosis, is besides adoption as a mono-therapy an interesting candidate for combined therapies. There are interesting preclinical trials and clinical pilote studies in the literature proving that a parallel therapy with selectively anti-osteoclastic bisphophonates and pleiotropically acting D-analogs is able to optimize therapeutic results in osteoporosis. In the AAC-Trial (Alfacalcidol-Alendronate-Combined) we studied 90 patients with established osteoporosis (57 women, 33 men) over two years after alternate allocation to three treatment arms (alfacalcidol plus calcium, alendronate plus plain vitamin D and Ca, and alendronate plus alfacalcidol and Ca). During the 2-year-study we observed the significantly highest lumbar spine and hip BMD increases in the combined treatment group (p < 0.001). The number of patients with new vertebral and non-vertebral fractures after 2 years was 9 with alfacalcidol alone, 10 with alfacalcidol and plain vitamin D and 2 in the group receiving alendronate plus alfacalidol (p < 0.02). Furthermore there was a lower rate of falls and an earlier reduction in back pain in the patients treated with the active combination. This trial confirms the demonstrated highly significant advantages of this combined treatment regimen used in the pilote studies. Especially in patients with severe osteoporosis this interesting combination of two substances with complete different mechanisms of action should be taken into consideration.     

Diabetes and the vitamin D connection

Vitamin D deficiency, which is common in children and adults, causes rickets, osteomalacia, and osteoporosis. Most organs and immune cells have a vitamin D receptor, and some also have the capacity to metabolize 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. 1,25-Dihydroxyvitamin D is a potent immunomodulator that also enhances the production and secretion of several hormones, including insulin. Vitamin D deficiency has been associated with increased risk of type 1 diabetes. Glycemic control and insulin resistance are improved when vitamin D deficiency is corrected and calcium supplementation is adequate. 25-Hydroxyvitamin D (measure of vitamin D status) of less than 20 ng/mL is vitamin D deficiency and 21 to 29 ng/mL is insufficiency. Children and adults need at least 1000 IU of vitamin D per day to prevent deficiency when there is inadequate sun exposure.     

Advantages of active vitamin D metabolites in the treatment of osteoporosis as compared with calciferol

Vitamin D is one of the most important regulating agents in the development of bone mass. Therefore administration of calciferol along with calcium in patients with nutritional vitamin D deficiency leads to improvement of bone density. In patients with osteoporosis who do not respond to vitamin D, insensitivity of osseous tissue to the active metabolite of vitamin D--1,25(OH)2 D3--is involved or inadequate synthesis of active metabolites in the liver or kidneys. Administration of 1alpha-OH vitamin D3 and in particular 1,25(OH) 2D3 improves the general calcium balance in the organism and increases by direct osteoforming action the value of bone mass and improves its quality. Administration of active vitamin D metabolites is unequivocally better in treatment of involutional osteoporosis, either along with calcium or in combination with some antiresorption substance, in osteoporosis associated with chronic inflammatory diseases, after organ transplantation or glukcocorticoid treatment. Even patients with postmenopausal osteoporosis respond better to 1,25(OH)2D3.     

维生素D内分泌系统与骨质疏松

钙代谢紊乱是引起骨质疏松的直接原因。钙调激素、钙转运蛋白、维生素D代谢酶等所构成的维生素D内分泌系统,在体内的主要作用是调控钙代谢,维持钙平衡。在增龄、性激素水平下降、营养缺乏、药物、制动等各种诱因所致骨质疏松症中,维生素D内分泌系统发生着适应性及病理性变化,并介导骨质疏松的发生、发展。从细胞、分子水平对维生素D内分泌系统的研究,可进一步阐明骨质疏松发生的分子机制,为防治骨质疏松提供新的思路。     

维生素D缺乏与骨质疏松

维生素D对骨骼最主要的作用之一是为骨质矿化提供合适的微环境。尽管部分食物中强化维生素D,或额外补充维生素D,但人群中维生素D缺乏仍很普遍。维生素D缺乏可导致甲状旁腺功能亢进、骨转换增加和骨丢失,引起骨折风险增加。维生素D和钙剂补充是防治骨质疏松症的基本措施。研究表明补充足量维生素D能增加骨量、肌肉容量,和肌肉协调功能,有助于预防骨质疏松及其骨折。     

适量补充钙和维生素D是防治骨质疏松症的基础措施——评新英格兰医学杂志Jackson等"补充钙和维生素D与骨折危险"一文

对2006年2月16日新英格兰医学杂志(NEJM)发表的“补充钙和维生素D与骨折危险”一文进行评述。这是一项大样本的随机、对照临床试验,评价绝经后妇女长期补充钙和维生素D对预防骨质疏松性骨折的效果。结果显示,在健康的绝经后妇女中补充钙和维生素D后髋部骨密度少量增加,但未能显著减少髋部骨折的发生,而肾结石的危险增加。由于该研究在研究设计、人群的选择、依从性等方面存在明显的局限与缺陷,影响了研究结果的真实性、科学性和推广价值。本文的结论是:该研究没有提供充分可靠的证据否定补充钙和维生素D对防治骨质疏松的益处。基于以往的众多研究证据,继续推荐以钙和维生素D的适量补充作为防治骨质疏松的基础措施。     

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维生素D缺乏所致的儿童佝偻病和成年后骨软化会促发并加重年老后发生的骨量减少或骨质疏松。因此,充足的维生素D是保证有效预防和治疗骨质疏松的基础。反映体内维生素D水平的最佳指标是血清25-羟维生素D[25(OH)D],其水平与骨密度、骨折风险和跌倒风险呈负相关。最优化的25(OH)D范围为30~50μg/L,20~<30μg/L为不足,低于20μg/L为缺乏。推荐老年人每天补充800~1000 U普通维生素D,骨质疏松患者、肥胖、缺乏日照和吸收不良的人可酌情增加至2000 U。     

维生素D缺乏与高血压相关研究进展

维生素D是一种脂溶性维生素,目前已知其在调节骨骼代谢、钙盐平衡方面起着重要的作用。近年来,虽然许多研究者发现高血压患者中维生素D缺乏的发生率很高,维生素D缺乏可能导致高血压的发生、发展,但是补充维生素D与高血压的研究结果不一致。因此文章就维生素D缺乏与高血压的相关研究进展作一综述。     

Meta-analyses of therapies for postmenopausal osteoporosis. VIII: Meta-analysis of the efficacy of vitamin D treatment in preventing osteoporosis in postmenopausal women

OBJECTIVE: To review the effect of vitamin D on bone density and fractures in postmenopausal women. DATA SOURCE: We searched MEDLINE and EMBASE from 1966 to 1999 and examined citations of relevant articles and proceedings of international meetings. We contacted osteoporosis investigators and primary authors to identify additional studies and to obtain unpublished data. STUDY SELECTION: We included 25 trials that randomized women to standard or hydroxylated vitamin D with or without calcium supplementation or a control and measured bone density or fracture incidence for at least 1 yr. DATA EXTRACTION: For each trial, three independent reviewers assessed the methodological quality and abstracted data. DATA SYNTHESIS: Vitamin D reduced the incidence of vertebral fractures [relative risk (RR) 0.63, 95% confidence interval (CI) 0.45-0.88, P < 0.01) and showed a trend toward reduced incidence of nonvertebral fractures (RR 0.77, 95% CI 0.57-1.04, P = 0.09). Most patients in the trials that evaluated vertebral fractures received hydroxylated vitamin D, and most patients in the trials that evaluated nonvertebral fractures received standard vitamin D. Hydroxylated vitamin D had a consistently larger impact on bone density than did standard vitamin D. For instance, total body differences in percentage change between hydroxylated vitamin D and control were 2.06 (0.72, 3.40) and 0.40 (-0.25, 1.06) for standard vitamin D. At the lumbar spine and forearm sites, hydroxylated vitamin D doses above 50 microg yield larger effects than lower doses. Vitamin D resulted in an increased risk of discontinuing medication in comparison to control as a result of either symptomatic adverse effects or abnormal laboratory results (RR 1.37, 95% CI 1.01-1.88), an effect that was similar in trials of standard and hydroxylated vitamin D. CONCLUSIONS: Vitamin D decreases vertebral fractures and may decrease nonvertebral fractures. The available data are uninformative regarding the relative effects of standard and hydroxylated vitamin D.     

REVIEW ARTICLE: Reducing fracture risk with calcium and vitamin D

Studies of vitamin D and calcium for fracture prevention have produced inconsistent results, as a result of different vitamin D status and calcium intake at baseline, different doses and poor to adequate compliance. This study tries to define the types of patients, both at risk of osteoporosis and with established disease, who may benefit from calcium and vitamin D supplementation. The importance of adequate compliance in these individuals is also discussed. Calcium and vitamin D therapy has been recommended for older persons, either frail and institutionalized or independent, with key risk factors including decreased bone mineral density (BMD), osteoporotic fractures, increased bone remodelling as a result of secondary hyperparathyroidism and increased propensity to falls. In addition, treatment of osteoporosis with a bisphosphonate was less effective in patients with vitamin D deficiency. Calcium and vitamin D supplementation is a key component of prevention and treatment of osteoporosis unless calcium intake and vitamin D status are optimal. For primary disease prevention, supplementation should be targeted to those with dietary insufficiencies. Several serum 25‐hydroxyvitamin D (25(OH)D) cut‐offs have been proposed to define vitamin D insufficiency (as opposed to adequate vitamin D status), ranging from 30 to 100 nmol/l. Based on the relationship between serum 25(OH)D, BMD, bone turnover, lower extremity function and falls, we suggest that 50 nmol/l is the appropriate serum 25(OH)D threshold to define vitamin D insufficiency. Supplementation should therefore generally aim to increase 25(OH)D levels within the 50–75 nmol/l range. This level can be achieved with a dose of 800 IU/day vitamin D, the dose that was used in succesfull fracture prevention studies to date; a randomized clinical trial assessing whether higher vitamin D doses achieve a greater reduction of fracture incidence would be of considerable interest. As calcium balance is not only affected by vitamin D status but also by calcium intake, recommendations for adequate calcium intake should also be met. The findings of community‐based clinical trials with vitamin D and calcium supplementation in which compliance was moderate or less have often been negative, whereas studies in institutionalized patients in whom medication administration was supervised ensuring adequate compliance demonstrated significant benefits.     

Vitamin D: More than just affecting calcium and bone

Vitamin D is a fat-soluble steroid that is essential for maintaining normal calcium metabolism. In vitamin D deficiency, calcium absorption is insufficient and cannot satisfy the body's needs. Consequently, parathyroid hormone production increases and calcium is mobilized from bones and reabsorbed in the kidneys to maintain normal serum calcium levels--a condition defined as secondary hyperparathyroidism. Most organs, including the gut, brain, heart, pancreas, skin, kidneys, and immune system have receptors for 1,25 (OH)vitamin D. Furthermore, all of these organs have the capacity to synthesize 1,25 (OH)vitamin D from vitamin D. Extensive research suggests that vitamin D deficiency is common and represents a global health problem. Clinical consequences related to low vitamin D levels include not only osteomalacia, osteoporosis, and rickets, but also neuro-muscular dysfunction and fractures. Falls related to neuromuscular dysfunction lead to 40% of all nursing home admissions and are the largest single cause of injury-related deaths in elderly people. About one-third of all persons 65 and older fall at least once a year, resulting in more than 1.5 million emergency room treatments and more than 300,000 hospitalizations. Falls cause more than 11,000 deaths per year, most of them in elderly patients (> or = 75 years) who suffer hip fractures. It is well established that vitamin D deficiency not only has serious consequences for bone health, but also for other organ systems. Previous studies have shown that vitamin D supplementation reduces the number of fractures and directly improves neuromuscular function, thus helping to prevent falls and subsequent fractures. In addition, vitamin D appears to have other important functions as a regulator of cell differentiation and cell growth.     

Managing osteoporosis in ulcerative colitis: Something new?

The authors revise the latest evidence in the literature regarding managing of osteoporosis in ulcerative colitis(UC), paying particular attention to the latest tendency of the research concerning the management of bone damage in the patient affected by UC. It is wise to assess vitamin D status in ulcerative colitis patients to recognize who is predisposed to low levels of vitamin D, whose deficiency has to be treated with oral or parenteral vitamin D supplementation. An adequate dietary calcium intake or supplementation and physical activity, if possible, should be guaranteed. Osteoporotic risk factors, such as smoking and excessive alcohol intake, must be avoided. Steroid has to be prescribed at the lowest possible dosage and for the shortest possible time. Moreover, conditions favoring falling have to been minimized, like carpets, low illumination, sedatives assumption, vitamin D deficiency. It is advisable to assess the fracture risk in all UC patient by the fracture assessment risk tool(FRAX tool), that calculates the ten years risk of fracture for the population aged from 40 to 90 years in many countries of the world. A high risk value could indicate the necessity of treatment, whereas a low risk value suggests a followup only. An intermediate risk supports the decision to prescribe bone mineral density(BMD) assessment and a subsequent patient revaluation for treatment. Dual energy X-ray absorptiometry bone densitometry can be used not only for BMD measurement, but also to collect data about bone quality by the means of trabecular bone score and hip structural analysis assessment. These two indices could represent a method of interesting perspectives in evaluating bone status in patients affected by diseases like UC, which may present an impairment of bone quality as well as of bone quantity. In literature there is no strong evidence for instituting pharmacological therapy of bone impairment in UC patients for clinical indications other than those that are also applied to the patients with osteoporosis. Therefore, a reasonable advice is to consider pharmacological treatment for osteoporosis in those UC patients who already present fragility fractures, which bring a high risk of subsequent fractures. Therapy has also to be considered in patients with a high risk of fracture even if it did not yet happen, and particularly when they had long periods of corticosteroid therapy or cumulative high dosages. In patients without fragility fractures or steroid treatment, a medical decision about treatment could be guided by the FRAX tool to determine the intervention threshold. Among drugs for osteoporosis treatment, the bisphosphonates are the most studied ones, with the best and longest evidence of efficacy and safety. Despite this, several questions are still open, such as the duration of treatment, the necessity to discontinue it, the indication of therapy in young patients, particularly in those without previous fractures. Further, it has to be mentioned that a longterm bisphosphonates use in primary osteoporosis has been associated with an increased incidence of dramatic side-effects, even if uncommon, like osteonecrosis of the jaw and atypical sub-trochanteric anddiaphyseal femoral fractures.UC is a long-lasting disease and the majority of patients is relatively young.In this scenario primary prevention of fragility fracture is the best cost-effective strategy.Vitamin D supplementation,adequate calcium intake,suitable physical activity(when possible),removing of risk factors for osteoporosis like smoking,and avoiding falling are the best medical acts.     

Secondary hyperparathyroidism in patients from Western Australia with hip fracture: relationship to type of hip fracture, renal function, and vitamin D deficiency

OBJECTIVES: To determine the frequency of vitamin D deficiency and secondary hyperparathyroidism in Australian hip fracture patients living in the community. PATIENTS: A total of 283 consecutive patients with hip fracture admitted over a 15-month period to a university teaching hospital in Western Australia. Included were residents of hostels for the elderly, and excluded were nursing home residents and those with malignant fractures. METHOD: Data collected included biochemistry (25 hydroxyvitamin D, parathyroid hormone and creatinine levels), measurements of function and disability (Barthel Index, Frenchay Activity Index), sunshine exposure, and basic demographics. RESULTS: Vitamin D deficiency occurred in 31.7% and secondary hyperparathyroidism occurred in 17.7% of cases. The major determinants of vitamin D deficiency were outdoor sunshine exposure, ambient daily sunshine, and disability (low Frenchay Activity Index or ADL difficulty). Secondary hyperparathyroidism was related to older age, renal dysfunction, and vitamin D deficiency. Secondary hyperparathyroidism was associated with an excess of trochanteric over subcapital hip fractures. CONCLUSIONS: Secondary hyperparathyroidism appears to be a heterogeneous condition, caused in approximately equal proportions by vitamin D deficiency and renal dysfunction, that may confer increased cortical bone fragility and trochanteric fractures. Renal dysfunction in old age may be an important additional determinant of senile osteoporosis, which has implications for preventive therapy. Vitamin D deficiency occurs in disabled and, presumably, housebound older people despite near optimal climatic conditions.