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<pubDate>Thu, 21 Aug 2008 05:29:39 BST</pubDate>


	<title>CiteULike: omalbam's osteoporosis</title>
	<description>CiteULike: omalbam's osteoporosis</description>


	<link>http://www.citeulike.org/user/omalbam/tag/osteoporosis</link>
	<dc:publisher>CiteULike.org</dc:publisher>
	<dc:language>en-gb</dc:language>
	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2297945"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2285068"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2277521"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2277500"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2216540"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2209624"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2209615"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2208587"/>

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<item rdf:about="http://www.citeulike.org/user/omalbam/article/2297945">
    <title>Osteoporosis and male age-related hypogonadism: role of sex steroids on bone (patho)physiology.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2297945</link>
    <description>&lt;i&gt;Eur J Endocrinol, Vol. 154, No. 2. (February 2006), pp. 175-185.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Male age-related bone loss is caused, at least in part, by hypogonadism that occurs with advancing age. The study of the effects of sex steroids on bone physiology in men has recently highlighted the central role of estrogens on bone pathophysiology. This review focuses on particular aspects of bone physiology and pathophysiology in aging men, noting both the similarities to and the differences from female counterparts. In particular, the role of sex steroids on bone sexual dimorphism in health and disease has been analyzed.</description>
    <dc:title>Osteoporosis and male age-related hypogonadism: role of sex steroids on bone (patho)physiology.</dc:title>

    <dc:creator>V Rochira</dc:creator>
    <dc:creator>A Balestrieri</dc:creator>
    <dc:creator>B Madeo</dc:creator>
    <dc:creator>L Zirilli</dc:creator>
    <dc:creator>AR Granata</dc:creator>
    <dc:creator>C Carani</dc:creator>
    <dc:identifier>doi:10.1530/eje.1.02088</dc:identifier>
    <dc:source>Eur J Endocrinol, Vol. 154, No. 2. (February 2006), pp. 175-185.</dc:source>
    <dc:date>2008-01-28T14:32:31-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Eur J Endocrinol</prism:publicationName>
    <prism:issn>0804-4643</prism:issn>
    <prism:volume>154</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>175</prism:startingPage>
    <prism:endingPage>185</prism:endingPage>
    <prism:category>androgen</prism:category>
    <prism:category>igf</prism:category>
    <prism:category>malegonadal</prism:category>
    <prism:category>osteoporosis</prism:category>
    <prism:category>physiology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2285068">
    <title>The role of IGF-I and IGFBP-1 status and secondary hyperparathyroidism in relation to osteoporosis in elderly Swedish women</title>
    <link>http://www.citeulike.org/user/omalbam/article/2285068</link>
    <description>&lt;i&gt;Osteoporosis International, Vol. 19, No. 2. (4 February 2008), pp. 201-209.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Abstract Summary&#160;&#160;IGFBP-1 showed a strong inverse relation to the BMD values. The IGF-I values had a significant positive relation to the BMD values at all sites with the exception of the lumbar spine. The use of loop diuretics was a more important cause of secondary hyperparathyroidism than vitamin D status. Introduction&#160;&#160;Our aim was to investigate among elderly women the relationship to osteoporosis of calcium-regulating hormones and insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-1 (IGFBP-1). Methods&#160;&#160;A population-based cross-sectional study of 350 elderly women (mean age 73&#160;years). Measurements of bone mineral density (BMD) of the left hip, lumbar spine and heel and risk markers for osteoporosis were studied. Results&#160;&#160;The BMD values showed significant inverse relationship with the values of IGFBP-1 at all sites of measurement and significant positive relationship with the values of IGF-I at all sites with the exception of the lumbar spine. There was no significant association between the values of BMD and the values of 25-hydroxy vitamin D (25(OH)D). The use of loop diuretics was strongly and significantly associated with elevated levels of PTH &#62;65&#160;pg/ml (OR 4.4, P &#60; 0.001). Conclusions&#160;&#160;The anabolic growth factor IGF-I and its modulating binding protein IGFBP-1 showed a stronger association with the BMD values than the calcium regulating hormones 25(OH)D and PTH. In this study the use of loop diuretics was a more important cause of secondary hyperparathyroidism than vitamin D status.</description>
    <dc:title>The role of IGF-I and IGFBP-1 status and secondary hyperparathyroidism in relation to osteoporosis in elderly Swedish women</dc:title>

    <dc:creator>H Salminen</dc:creator>
    <dc:creator>M Sääf</dc:creator>
    <dc:creator>H Ringertz</dc:creator>
    <dc:creator>L Strender</dc:creator>
    <dc:identifier>doi:10.1007/s00198-007-0463-4</dc:identifier>
    <dc:source>Osteoporosis International, Vol. 19, No. 2. (4 February 2008), pp. 201-209.</dc:source>
    <dc:date>2008-01-24T15:31:24-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Osteoporosis International</prism:publicationName>
    <prism:volume>19</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>201</prism:startingPage>
    <prism:endingPage>209</prism:endingPage>
    <prism:category>aging</prism:category>
    <prism:category>bone</prism:category>
    <prism:category>growth-factors</prism:category>
    <prism:category>osteoporosis</prism:category>
    <prism:category>physiology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2277521">
    <title>Underdeveloped trabecular bone microarchitecture is detected in children with cerebral palsy using high-resolution magnetic resonance imaging</title>
    <link>http://www.citeulike.org/user/omalbam/article/2277521</link>
    <description>&lt;i&gt;Osteoporosis International, Vol. 19, No. 2. (4 February 2008), pp. 169-176.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Abstract Summary&#160;&#160;Using high resolution magnetic resonance imaging, we detected severely underdeveloped trabecular bone microarchitecture in the distal femur of children with cerebral palsy who can not ambulate independently vs. typically developing controls. Furthermore, very good short-term reliability of trabecular bone microarchitecture measurements was observed in both groups of children. Introduction&#160;&#160;Severe forms of cerebral palsy (CP) are associated with very low areal bone mineral density and a very high incidence of fracture in the distal femur; however, the state of trabecular bone microarchitecture has not been evaluated. Furthermore, the short-term reliability of trabecular bone microarchitecture assessment in children using high-resolution magnetic resonance imaging (MRI) has not been determined. Methods&#160;&#160;Apparent bone volume to total volume (appBV/TV), trabecular number, (appTb.N), trabecular thickness (appTb.Th) and trabecular separation (appTb.Sp) were determined in the distal femur of non-ambulatory children with CP and typically developing children using MRI. Results&#160;&#160;Children with CP had a 30% lower appBV/TV, a 21% lower appTb.N, a 12% lower appTb.Th and a 48% higher appTb.Sp in the distal femur than controls (n = 10/group; P &#60; 0.001). The short-term reliability of the trabecular bone microarchitecture measures was very good, with coefficients of variation ranging from 2.0 to 3.0% in children with CP (n = 6) and 1.8 to 3.5% in control children (n = 6). Conclusions&#160;&#160;Underdeveloped trabecular bone microarchitecture can be detected in the distal femur of children with CP who can not ambulate independently using high-resolution MRI. Furthermore, MRI can be used to assess trabecular bone microarchitecture in children with a high degree of reliability.</description>
    <dc:title>Underdeveloped trabecular bone microarchitecture is detected in children with cerebral palsy using high-resolution magnetic resonance imaging</dc:title>

    <dc:creator>C Modlesky</dc:creator>
    <dc:creator>P Subramanian</dc:creator>
    <dc:creator>F Miller</dc:creator>
    <dc:identifier>doi:10.1007/s00198-007-0433-x</dc:identifier>
    <dc:source>Osteoporosis International, Vol. 19, No. 2. (4 February 2008), pp. 169-176.</dc:source>
    <dc:date>2008-01-22T20:45:18-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Osteoporosis International</prism:publicationName>
    <prism:volume>19</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>169</prism:startingPage>
    <prism:endingPage>176</prism:endingPage>
    <prism:category>bone</prism:category>
    <prism:category>diagnosis</prism:category>
    <prism:category>osteoporosis</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2277500">
    <title>Skeletal consequences of thiazolidinedione therapy</title>
    <link>http://www.citeulike.org/user/omalbam/article/2277500</link>
    <description>&lt;i&gt;Osteoporosis International, Vol. 19, No. 2. (4 February 2008), pp. 129-137.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Abstract&#160;&#160;Thiazolidinediones (TZDs) are agonists of the peroxisome proliferator-activated receptor gamma (PPARγ) nuclear transcription factor. Two members of this drug class, rosiglitazone and pioglitazone, are commonly used in the management of type II diabetes mellitus, and play emerging roles in the treatment of other clinical conditions characterized by insulin resistance. Over the past decade, a consistent body of in vitro and animal studies has demonstrated that PPARγ signaling regulates the fate of pluripotent mesenchymal cells, favoring adipogenesis over osteoblastogenesis. Treatment of rodents with TZDs decreases bone formation and bone mass. Until recently, there were no bone-related data available from studies of TZDs in humans. In the past year, however, several clinical studies have reported adverse skeletal actions of TZDs in humans. Collectively, these investigations have demonstrated that the TZDs currently in clinical use decrease bone formation and accelerate bone loss in healthy and insulin-resistant individuals, and increase the risk of fractures in the appendicular skeleton in women with type II diabetes mellitus. These observations should prompt clinicians to evaluate fracture risk in patients for whom TZD therapy is being considered, and initiate skeletal protection in at-risk individuals.</description>
    <dc:title>Skeletal consequences of thiazolidinedione therapy</dc:title>

    <dc:creator>A Grey</dc:creator>
    <dc:identifier>doi:10.1007/s00198-007-0477-y</dc:identifier>
    <dc:source>Osteoporosis International, Vol. 19, No. 2. (4 February 2008), pp. 129-137.</dc:source>
    <dc:date>2008-01-22T20:41:12-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Osteoporosis International</prism:publicationName>
    <prism:volume>19</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>129</prism:startingPage>
    <prism:endingPage>137</prism:endingPage>
    <prism:category>diabetes</prism:category>
    <prism:category>osteoporosis</prism:category>
    <prism:category>review</prism:category>
    <prism:category>sideffects</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2216540">
    <title>Approach to the Prostate Cancer Patient with Bone Disease</title>
    <link>http://www.citeulike.org/user/omalbam/article/2216540</link>
    <description>&lt;i&gt;J Clin Endocrinol Metab, Vol. 93, No. 1. (1 January 2008), pp. 2-7.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Prostate cancer is the most common visceral malignancy in men. Androgen deprivation therapy (ADT) is commonly used in patients with nonmetastatic prostate cancer and is associated with significant bone loss and fractures. The greatest bone loss occurs during initiation of ADT. Men should have assessment of skeletal integrity with bone mineral density examination by dual x-ray absorptiometry of the hip and spine. Men with fragility fractures or osteoporosis by bone density should be considered for bisphosphonate therapy. Men with low bone mass may need antiresorptive therapy, depending on other risk factors. Men with a normal bone mineral density should be followed up closely with bone densitometry while on ADT. All men should receive preventive measures with calcium (1200 mg daily in divided doses), vitamin D (8001000 IU/d), and weight-bearing exercise. Men should be evaluated for additional secondary causes of bone loss including vitamin D insufficiency. Guidelines are needed for androgen-induced bone loss screening and treatment. 10.1210/jc.2007-1402</description>
    <dc:title>Approach to the Prostate Cancer Patient with Bone Disease</dc:title>

    <dc:creator>Susan Greenspan</dc:creator>
    <dc:identifier>doi:10.1210/jc.2007-1402</dc:identifier>
    <dc:source>J Clin Endocrinol Metab, Vol. 93, No. 1. (1 January 2008), pp. 2-7.</dc:source>
    <dc:date>2008-01-10T22:51:41-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J Clin Endocrinol Metab</prism:publicationName>
    <prism:volume>93</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>2</prism:startingPage>
    <prism:endingPage>7</prism:endingPage>
    <prism:category>cancer</prism:category>
    <prism:category>osteoporosis</prism:category>
    <prism:category>sideffects</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2209624">
    <title>Zoledronic acid and clinical fractures and mortality after hip fracture.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2209624</link>
    <description>&lt;i&gt;N Engl J Med, Vol. 357, No. 18. (1 November 2007), pp. 1799-1809.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Mortality is increased after a hip fracture, and strategies that improve outcomes are needed. METHODS: In this randomized, double-blind, placebo-controlled trial, 1065 patients were assigned to receive yearly intravenous zoledronic acid (at a dose of 5 mg), and 1062 patients were assigned to receive placebo. The infusions were first administered within 90 days after surgical repair of a hip fracture. All patients (mean age, 74.5 years) received supplemental vitamin D and calcium. The median follow-up was 1.9 years. The primary end point was a new clinical fracture. RESULTS: The rates of any new clinical fracture were 8.6% in the zoledronic acid group and 13.9% in the placebo group, a 35% risk reduction with zoledronic acid (P=0.001); the respective rates of a new clinical vertebral fracture were 1.7% and 3.8% (P=0.02), and the respective rates of new nonvertebral fractures were 7.6% and 10.7% (P=0.03). In the safety analysis, 101 of 1054 patients in the zoledronic acid group (9.6%) and 141 of 1057 patients in the placebo group (13.3%) died, a reduction of 28% in deaths from any cause in the zoledronic acid group (P=0.01). The most frequent adverse events in patients receiving zoledronic acid were pyrexia, myalgia, and bone and musculoskeletal pain. No cases of osteonecrosis of the jaw were reported, and no adverse effects on the healing of fractures were noted. The rates of renal and cardiovascular adverse events, including atrial fibrillation and stroke, were similar in the two groups. CONCLUSIONS: An annual infusion of zoledronic acid within 90 days after repair of a low-trauma hip fracture was associated with a reduction in the rate of new clinical fractures and with improved survival. (ClinicalTrials.gov number, NCT00046254 [ClinicalTrials.gov].).</description>
    <dc:title>Zoledronic acid and clinical fractures and mortality after hip fracture.</dc:title>

    <dc:creator>KW Lyles</dc:creator>
    <dc:creator>CS Colón-Emeric</dc:creator>
    <dc:creator>JS Magaziner</dc:creator>
    <dc:creator>JD Adachi</dc:creator>
    <dc:creator>CF Pieper</dc:creator>
    <dc:creator>C Mautalen</dc:creator>
    <dc:creator>L Hyldstrup</dc:creator>
    <dc:creator>C Recknor</dc:creator>
    <dc:creator>L Nordsletten</dc:creator>
    <dc:creator>KA Moore</dc:creator>
    <dc:creator>C Lavecchia</dc:creator>
    <dc:creator>J Zhang</dc:creator>
    <dc:creator>P Mesenbrink</dc:creator>
    <dc:creator>PK Hodgson</dc:creator>
    <dc:creator>K Abrams</dc:creator>
    <dc:creator>JJ Orloff</dc:creator>
    <dc:creator>Z Horowitz</dc:creator>
    <dc:creator>EF Eriksen</dc:creator>
    <dc:creator>S Boonen</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1056/NEJMoa074941</dc:identifier>
    <dc:source>N Engl J Med, Vol. 357, No. 18. (1 November 2007), pp. 1799-1809.</dc:source>
    <dc:date>2008-01-09T04:24:55-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>N Engl J Med</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>357</prism:volume>
    <prism:number>18</prism:number>
    <prism:startingPage>1799</prism:startingPage>
    <prism:endingPage>1809</prism:endingPage>
    <prism:category>fractures</prism:category>
    <prism:category>mortality</prism:category>
    <prism:category>osteoporosis</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2209615">
    <title>Teriparatide or alendronate in glucocorticoid-induced osteoporosis.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2209615</link>
    <description>&lt;i&gt;N Engl J Med, Vol. 357, No. 20. (15 November 2007), pp. 2028-2039.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Bisphosphonate therapy is the current standard of care for the prevention and treatment of glucocorticoid-induced osteoporosis. Studies of anabolic therapy in patients who are receiving long-term glucocorticoids and are at high risk for fracture are lacking. METHODS: In an 18-month randomized, double-blind, controlled trial, we compared teriparatide with alendronate in 428 women and men with osteoporosis (ages, 22 to 89 years) who had received glucocorticoids for at least 3 months (prednisone equivalent, 5 mg daily or more). A total of 214 patients received 20 microg of teriparatide once daily, and 214 received 10 mg of alendronate once daily. The primary outcome was the change in bone mineral density at the lumbar spine. Secondary outcomes included changes in bone mineral density at the total hip and in markers of bone turnover, the time to changes in bone mineral density, the incidence of fractures, and safety. RESULTS: At the last measurement, the mean (+/-SE) bone mineral density at the lumbar spine had increased more in the teriparatide group than in the alendronate group (7.2+/-0.7% vs. 3.4+/-0.7%, P&#60;0.001). A significant difference between the groups was reached by 6 months (P&#60;0.001). At 12 months, bone mineral density at the total hip had increased more in the teriparatide group. Fewer new vertebral fractures occurred in the teriparatide group than in the alendronate group (0.6% vs. 6.1%, P=0.004); the incidence of nonvertebral fractures was similar in the two groups (5.6% vs. 3.7%, P=0.36). Significantly more patients in the teriparatide group had at least one elevated measure of serum calcium. CONCLUSIONS: Among patients with osteoporosis who were at high risk for fracture, bone mineral density increased more in patients receiving teriparatide than in those receiving alendronate. (ClinicalTrials.gov number, NCT00051558 [ClinicalTrials.gov].).</description>
    <dc:title>Teriparatide or alendronate in glucocorticoid-induced osteoporosis.</dc:title>

    <dc:creator>KG Saag</dc:creator>
    <dc:creator>E Shane</dc:creator>
    <dc:creator>S Boonen</dc:creator>
    <dc:creator>F Marín</dc:creator>
    <dc:creator>DW Donley</dc:creator>
    <dc:creator>KA Taylor</dc:creator>
    <dc:creator>GP Dalsky</dc:creator>
    <dc:creator>R Marcus</dc:creator>
    <dc:identifier>doi:10.1056/NEJMoa071408</dc:identifier>
    <dc:source>N Engl J Med, Vol. 357, No. 20. (15 November 2007), pp. 2028-2039.</dc:source>
    <dc:date>2008-01-09T04:16:26-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>N Engl J Med</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>357</prism:volume>
    <prism:number>20</prism:number>
    <prism:startingPage>2028</prism:startingPage>
    <prism:endingPage>2039</prism:endingPage>
    <prism:category>glucocorticoids</prism:category>
    <prism:category>osteoporosis</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2208587">
    <title>Ten-year GH replacement increases bone mineral density in hypopituitary patients with adult onset GH deficiency.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2208587</link>
    <description>&lt;i&gt;Eur J Endocrinol, Vol. 156, No. 1. (January 2007), pp. 55-64.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;There are few studies that have determined the effects of long-term GH replacement on bone mineral density (BMD) in GH-deficient (GHD) adults. In this study, the effects of 10 years of GH replacement on BMD were assessed in 87 GHD adults using dual energy X-ray absorptiometry (DEXA). The results show that GH replacement induced a sustained increase in BMD at all the skeletal sites measured. INTRODUCTION: Little is known of the effect of more than 5 years of GH replacement therapy on bone metabolism in GHD adults. PATIENTS AND METHODS: In this prospective, open-label, single-center study, which included 87 consecutive adults (52 men and 35 women; mean age of 44.1 (range 22-74) years) with adulthood onset GHD, the effect of 10 years of GH replacement on BMD was determined. RESULTS: The mean initial dose of GH was 0.98 mg/day. The dose was gradually lowered and after 10 years the mean dose was 0.47 mg/day. The mean insulin-like growth factor-I (IGF-I) SDS increased from 1.81 at baseline to 1.29 at study end. The GH replacement induced a sustained increase in total, lumbar (L2-L4) and femur neck BMD, and bone mineral content (BMC) as measured by DEXA. The treatment response in IGF-I SDS was more marked in men, whereas women had a more marked increase in the total body BMC and the total body z-score. There was a tendency for women on estrogen treatment to have a larger increase in bone mass and density compared with women without estrogen replacement. CONCLUSIONS: Ten years of GH replacement in hypopituitary adults induced a sustained, and in some variables even a progressive, increase in bone mass and bone density. The study results also suggest that adequate estrogen replacement is needed in order to have an optimal response in BMD in GHD women.</description>
    <dc:title>Ten-year GH replacement increases bone mineral density in hypopituitary patients with adult onset GH deficiency.</dc:title>

    <dc:creator>G Götherström</dc:creator>
    <dc:creator>BA Bengtsson</dc:creator>
    <dc:creator>I Bosaeus</dc:creator>
    <dc:creator>G Johannsson</dc:creator>
    <dc:creator>J Svensson</dc:creator>
    <dc:identifier>doi:10.1530/eje.1.02317</dc:identifier>
    <dc:source>Eur J Endocrinol, Vol. 156, No. 1. (January 2007), pp. 55-64.</dc:source>
    <dc:date>2008-01-08T19:02:04-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Eur J Endocrinol</prism:publicationName>
    <prism:issn>0804-4643</prism:issn>
    <prism:volume>156</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>55</prism:startingPage>
    <prism:endingPage>64</prism:endingPage>
    <prism:category>osteoporosis</prism:category>
    <prism:category>r-gh</prism:category>
    <prism:category>therapy</prism:category>
</item>



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