长期糖皮质激素治疗系统性红斑狼疮对骨量变化的研究
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摘要
目的：研究长期服用糖皮质激素治疗系统性红斑狼疮(SLE)患者的骨量变化,适时干预骨质疏松的发生。
方法：对20例SLE女性患者进行1年的治疗及前后对照,糖皮质激素(泼尼松)起始剂量为1mg(kg.d),6-8周后逐渐减量,每2周5mg递减至维持量(10mg以下),服用糖皮质激素前及之后3个月、6个月、12个月应用双能X线骨密度仪检测股骨近端、腰椎2-4骨密度(BMD),并与20例同年龄组健康女性比较,组间比较采用配对t检验,SLE组内比较采用自身对照t检验。P<0.05为差异有统计学意义。
结果：SLE组服用激素后的腰椎及股骨近端BMD明显低于正常对照组,腰椎BMD(1.112±0.131 vs1.225±0.134,t=2.62,P<0.01),股骨近端(0.816±0.125vs0.915±0.128,t=2.58,P<0.01)；服用激素6个月后的腰椎BMD值明显低于3个月后的腰椎BMD值(1.001-±0.132vs1.112-+0.131,t=2.65,P<0.01),与12个月后的腰椎BMD比较差异无显著性(1.001+0.132vs0.998+0.130,t=1.32,P>0.05)；服用激素3个月、6个月、12个月后的股骨近端BMD值之间比较差异无显著性(0.816+0.125vs0.810+0.123vs0.806+0.123,t≤1.56,P>0.05)。(2)在腰椎位点,SLE组服用激素3个月、6个月、12个月后骨量减少的发生率分别为10%、25%、30%；在股骨近端则均为10%,12个月后在腰椎位点和股骨近端各有10%患者出现骨质疏松。
结论：(1)长期服用糖皮质激素治疗的SLE患者较同年龄组健康女性易发生骨量减少及骨质疏松(2)不同的部位骨量丢失度不同(3)糖皮质激素治疗对患者不同部位的骨量影响亦有差别。
Objective A study to observe the alternations of bone mass in women with systemic lupus erythematosus (Systemic Lupus Erythematosus, SLE) after long-term treatment with glucocorticoids so that intervening the occurence of osteoporosis timely. Methods 20 Patients with SLE were treated and followed up for 1 year. The initial dose of glucocorticoids(prednisone) was 1mg (kg.d). The daily dose was diminished gradually after 6-8 weeks on the basis of 5mg per 2 weeks until the maintenance dose(below 10mg). Proximal femur and lumbar spine dual-energy X-ray absorptiometry results were evaluated in SLE patients before taking glucocorticoids and after oral glucocorticoids treatment for 3 months,6 months and 12months,and 20 age-matched healthy women were compared with SLE patients. The data between two groups were compared with paired t test. The data in SLE group were compared with self-comparison t test. There were statistical difference when P<0.05. Results BMD of lumar spine and proximal femur were lower in SLE patients after oral glucocorticoids treatment than matched normal controls(P<0.01).Lu mbar spine BMD (1.112±0.131 vsl.225±0.134,t=2.62,P<0.01), proximal femur BMD (0.816±0.125vs0.915±0.128,t=2.58,P<0.01). lumbar spine in SLE patients after taking glucocorticoids for 6 months were less than 3 months. BMD (1.001±0.132vs1.112±0.131,1=2.65, P<0.01).There were no difference in BMD of Lumbar spine after taking glucocorticoids for 6 months and 12 months. BMD (1.001±0.132vs1.112±0.131, t=2.65, P<0.01).There were no difference in BMD of proximal femur in SLE patients with oral glucocorticoids for 3 months and 6 months and 12 months, proximal femur BMD (0.816±0.125vs0.810±0.123vs0.806±0.123, t≤1.56, P>0.05). The occurrence rate of osteopenia were 10%,25%,30% after taking glucocorticoids for 3 months,6 months and 12 months at the lumbar spine, and the occurrence rate of osteopenia were all 10% at the proximal femur. The occurrence rate of osteoporosis were all 10% at the proximal femur and the lumbar spine 12 months later. Conclusion BMD in SLE patients treated with long-term glucocorticoids was significantly less than normal controls. The speed of bone loss was also different because of different part in human body. The influence of glucocorticoids on bone mass was different based on different part in human body.
方法：对20例SLE女性患者进行1年的治疗及前后对照,糖皮质激素(泼尼松)起始剂量为1mg(kg.d),6-8周后逐渐减量,每2周5mg递减至维持量(10mg以下),服用糖皮质激素前及之后3个月、6个月、12个月应用双能X线骨密度仪检测股骨近端、腰椎2-4骨密度(BMD),并与20例同年龄组健康女性比较,组间比较采用配对t检验,SLE组内比较采用自身对照t检验。P<0.05为差异有统计学意义。
结果：SLE组服用激素后的腰椎及股骨近端BMD明显低于正常对照组,腰椎BMD(1.112±0.131 vs1.225±0.134,t=2.62,P<0.01),股骨近端(0.816±0.125vs0.915±0.128,t=2.58,P<0.01)；服用激素6个月后的腰椎BMD值明显低于3个月后的腰椎BMD值(1.001-±0.132vs1.112-+0.131,t=2.65,P<0.01),与12个月后的腰椎BMD比较差异无显著性(1.001+0.132vs0.998+0.130,t=1.32,P>0.05)；服用激素3个月、6个月、12个月后的股骨近端BMD值之间比较差异无显著性(0.816+0.125vs0.810+0.123vs0.806+0.123,t≤1.56,P>0.05)。(2)在腰椎位点,SLE组服用激素3个月、6个月、12个月后骨量减少的发生率分别为10%、25%、30%；在股骨近端则均为10%,12个月后在腰椎位点和股骨近端各有10%患者出现骨质疏松。
结论：(1)长期服用糖皮质激素治疗的SLE患者较同年龄组健康女性易发生骨量减少及骨质疏松(2)不同的部位骨量丢失度不同(3)糖皮质激素治疗对患者不同部位的骨量影响亦有差别。
Objective A study to observe the alternations of bone mass in women with systemic lupus erythematosus (Systemic Lupus Erythematosus, SLE) after long-term treatment with glucocorticoids so that intervening the occurence of osteoporosis timely. Methods 20 Patients with SLE were treated and followed up for 1 year. The initial dose of glucocorticoids(prednisone) was 1mg (kg.d). The daily dose was diminished gradually after 6-8 weeks on the basis of 5mg per 2 weeks until the maintenance dose(below 10mg). Proximal femur and lumbar spine dual-energy X-ray absorptiometry results were evaluated in SLE patients before taking glucocorticoids and after oral glucocorticoids treatment for 3 months,6 months and 12months,and 20 age-matched healthy women were compared with SLE patients. The data between two groups were compared with paired t test. The data in SLE group were compared with self-comparison t test. There were statistical difference when P<0.05. Results BMD of lumar spine and proximal femur were lower in SLE patients after oral glucocorticoids treatment than matched normal controls(P<0.01).Lu mbar spine BMD (1.112±0.131 vsl.225±0.134,t=2.62,P<0.01), proximal femur BMD (0.816±0.125vs0.915±0.128,t=2.58,P<0.01). lumbar spine in SLE patients after taking glucocorticoids for 6 months were less than 3 months. BMD (1.001±0.132vs1.112±0.131,1=2.65, P<0.01).There were no difference in BMD of Lumbar spine after taking glucocorticoids for 6 months and 12 months. BMD (1.001±0.132vs1.112±0.131, t=2.65, P<0.01).There were no difference in BMD of proximal femur in SLE patients with oral glucocorticoids for 3 months and 6 months and 12 months, proximal femur BMD (0.816±0.125vs0.810±0.123vs0.806±0.123, t≤1.56, P>0.05). The occurrence rate of osteopenia were 10%,25%,30% after taking glucocorticoids for 3 months,6 months and 12 months at the lumbar spine, and the occurrence rate of osteopenia were all 10% at the proximal femur. The occurrence rate of osteoporosis were all 10% at the proximal femur and the lumbar spine 12 months later. Conclusion BMD in SLE patients treated with long-term glucocorticoids was significantly less than normal controls. The speed of bone loss was also different because of different part in human body. The influence of glucocorticoids on bone mass was different based on different part in human body.
引文
1陈灏珠主编.内科学.北京：人民卫生出版社,1995.811-817.
2 Lakshminarayanan S, walsh S, Mohanraj M, et al. Factors associated with low bone mineral density in female patients with systemic lupus erythem-atosus[J]. J Rheumatol,2001,28:102-108.
3 R. Eastell, D.M.Reid, J. Compston, etc. A UK Consensus Group on manageme nt of glucocorticoidinduced osteoporosis:an update. Journal of Internal Medicine,1998,244:271-292.
4 Cunnane G, Lane NE, Steroid-induced osteoporosis in systemic lupus eryt-hematosus [J]. Rheum Dis Clin North Am,2000,26:311-329.
5梁九根蒋宁一徐志英,等.长期强的松治疗对绝经前SLE患者骨密度的影响.中国骨质疏松杂志,2006,12：57-61.
6 Mario Garcia-carrasco MD PhD, Claudia Mendoza-Pinto MD, etc. Osteoporosis in Patients with Systemic Lupus Erythematosus. IMAJ,2009,11:486-491.
7 E. K. LI. Loss of bone mineral density in chinese pre-menopausal women with systemic lupus erythematosus treated with corticosteroids. British Journ-al of Rheumatology,1998,37:405-410.
8 Matsuyama T, Ishii S, Tokita A, et al. Vitamin D receptor genotypes and bonemineral density. Lancet,1995,345(8):1238-1239.
9 Dawson-Hughes B, Harris SS, Finneran S. Calcium absorption On high and low calcium intakes in relation to vitamin D receptor genotype. J cl in Endoc-rinol Metab,1995,8o(2o):3657-3661.
lOKenneth G, Saag. MD. MSc. Glucocorticoid-induced osteoporosis. Endocrinol Metab Clin N Am,2003,32:135-157.
11 Van Staa TP, Lenfkens HG, Cooper C, et al. The epidemiology of corticoste-roid-induced osteoporosis:8meta-analysis.Osteoporos Int,2002,13:777-787
12Gherardo Mazziotti Alberto Angeli, etc. Glucocorticoid-induced osteoporosi-s. Trends in Endocrinology and Metabolism,2006,17(4):144-149.
13Canalis, E,et al. (2004) Perspectives on glucocorticoid-induced osteoporo-sis. Bone 34,593-598.
140hnaka, K. et al. (2005) Glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts. Biochem. Biophys. Res. Commun,329:177-181.
15 Pons F, Pefis P, Guan abens N, et al. The efect of systemic lupus erythe-matosus an d long-term steroid therapy on bo ne mass in premenopausal women. Br J Rheumatol.1995,34(8):742-746.
16王巧宏,吴华香,薛静.绝经前女性系统性红斑狼疮患者骨密度和骨代谢指标测定.中国骨质疏松杂志,2008,14(1)：41-43.
17 Mok CC, Mak A, Ma KM. Bone mineral density in postmenopausal Chinese pati-ents with systemic lupus erythematosus. Lupus,2005,14:106-12.
18 E. Canalis. G, Mazziotti.A. Glucocorticoid-induced osteoporosis:patho-physiology and therapy. Osteoporos Int,2007,18:1319-1328.
19 Tomlinson JW, Walker EA,Bujalska IJ, et al.11betahydroxysteroid de-hydrogenase type 1:a tissue-specific regulator of glucocorticoid r-esponse. Endocr Rev,2004,25:31-66.
20 Cooper MS, Bujalska I, Rabbitt E, et al. Modulation of 11-ahydroxy s-teroid dehydrogenase isozymes by proinflammatory cytokines in osteo-blasts:an autocrine switch from glucocorticoid In activation to ac-tivation. J Bone Miner Res,2001,16:1037-1044.
21 Williams LJ, Lyons V, MacLeod I, et al. C/EBP regulates hepatic trans-cription of llbeta-hydroxysteroid dehydrogenase type 1. A novel mech-anism for cross-talk between the C/EBP and glucocorticoid signaling pathways. J Biol Chem,2000,275:30232-30239.
22 Cooper MS, Rabbitt EH, Goddard PE, et al. Osteoblastic 11 a-hydroxy steroid dehydrogenase type 1 activity increases with age and glucoc-orticoid exposure. J Bone Miner Res,2002,17:979-986.
23 Kanis Ji, Gluer CC. An update on the diagnosis and assessment Of osteo-porosis with densitometry. Osteoporosis bat,2000,11:192-202.
24 E. Canalis. G, Mazziotti.A. Glucocorticoid-induced ostooporosis:patho-physiology and therapy. Osteoporos Int,2007,18:1319-1328.
25 Kamen DL,Alele JD. Skeletal manifestations of systemic autoimmune diseases. Current Opinion in Endocrinology, Diabetes and Obesity 2010,17 :540-545.
26 Angeli A, Guglielmi G, Dovio A, et al. High prevalence of asymptomati-c vertebral fractures in postmenopausal women receiving chronic gluco corticoid therapy:a cross-sectional outpatient study. Bone 20-06,39: 253-259.
[1]American College of Rheumatoiogy Ad Hoc Committee on Glucocoritcoid Induced Osteoporesis. Recommendations for the prevention an d treatment of glucocorticoid——induced osteoporosis:2001 update[J]. Arthritis Rheum,2001,44(7):1496-1503.
[2]Devogelaer JP, Goemaere S, Boonen S, et al. Evidence. based guidelines for the prevention and treatment of glucocorticoid induced osteoporosis: a consensus document of the belgian bone club. Osteoporos lnt,2006, 17(1):8-19.
[3]Cunnane G, Lane NE, Steroid-induced osteoporosis in systemic lupus erythematosus [J]. Rheum Dis Clin North Am,2000,26:311-329.
[4]Delany AM, Durant D, Canalis E. Glucocorticoid suppression of insulin-like growth factor I transcription in osteoblasts. Mol Endocrinol, 2001,15:1781-1789.
[5]Kbosla S, Dunstan CR. The roles of osteoprotegenn and osteoprotegerin ligand in the paracrine regulation of bone resorption. J Bone Miner Res, 2000.15(1):2-12.
[6]Hofbauer LC, Coil F, Riggs BL, et al. Stimulation of osteoprotegerin ligand and inhibition of osteoprotein prod uction by glucocorticoids in human osteoblastic lineage cells:potential paracrine mechanisms of glucoc-orticoid-induced osteoporosis [J]. Endocrinology,1999,140:4382-4389.
[7]Canalis E Glueocorticoid-induced Osteoporosis [J] Curr Opin Endocrinol Diab,2000.7:320-324.
[8]Dovio A, Sartori ML, Masera RG, et al. Inhibitory effect of physiological concentrations of cortisol but notestradiol on interleukin(IL-6) produ-ction by human osteoblast—like cell lines with different constitutive IL-6 expression[J]. Cytokine,2001,15(1):47.
[9]Koedam J A, Hoogerbrngge C M, Van S C Diferential regulation of IGF--binding proteitn in rabbit costal chondro—cytes by IGF-I and dexa-methazone [J] Endocrinol,2000.165:557-567.
[10]Se. saki N, Kusano E, Ando Y, et al. Changes in osteoprotegerin and markers of bone metabolism during glucocorticoid treatment in patients with chronic glomerulonephritis[J].2002,30:853-858.
[11]Homik J, Suare_z—AlmazorME, SheaB, et al. Calcium and vitamin D for corticosteroid—induced osteoporosis. Cochrane Database Syst Rev, 2000.2:CI)000952.
[12]American College of Rheumatology Ad Hoc committee. Glucocorticoid-Induced Osteoporosis. Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis[J]. Arthritis Rheum,2001,44: 1496.
[13]Adachi J D, Roux C, Pitt PI, et al. A pooled data analysis on the use of intermittent cyclical etidronate therapy for the prevention and treatment of corticosteroid induced bone loss. J Rheumatol,2000:27: 2424.
[14]Bousten Y, Jamart J, Esselinckx W, et al. Primary prevention of glucocorticoid-induced osteoporosis with intravenous pamidronate and calcium:a prospective controlled 1-year study comparing a single infusion, an infusion given once every 3 months, and calcium alone [J]. J Bone Miner Res,2001,
[15]Cranney A, Welch V, Adachi JD, et al. Calcitonin for the treatment and prevention of corticodteroid-induced osteoporosis [J]. Cochrane Database Syst Rev,2000,2:1983.
[16]Lane NE, Lukert B. The science and therapy of glucocorticoid induced bone loss[J]. Endocrinol Metab Clin North Am,1998,27(2):465.
[17]Hodsman All, Bauer DC, Dempster DW, et al. Parathyroid hormone and teriparatide for the treatment of osteoporosis:a review of the evidence and suggested guidelines for its use. Endoer Rev,2005,26:688-703.
[18]RehmanQ, Lang TF, Amaud CD。et,al. Daily treatment with parathyroid hormone is associated with an increase in vertebral cross-sectional area in postmenopausal women with glucocor-ticoid induced osteoporosis. Osteo-poros Int,2003,14:77-81.
[19]Van't HOf RJ, Ralston SH. Nitric oxide and bone. Immunology,,2001, 103:255-61.
[20]Wimalawansa S, Chapa T, et al. Frequency-dependent effect Of nitric oxide donor nitroglycerin on bone. J Bone Miner Res,2000,15:1119-1125
[21]lwamoto J, Takeda T, Sato Y. Effects Of vitamin K2 on osteoporosis, Curr Pharm Des,2004,10:2557.2576.
[22]Humphrey EL, Williams JH, Davie MW, et al. Effects of dissociated glucocorticoids on OPG and RANKL in osteoblastic cells. Bone,2006,5: 652.661.
2 Lakshminarayanan S, walsh S, Mohanraj M, et al. Factors associated with low bone mineral density in female patients with systemic lupus erythem-atosus[J]. J Rheumatol,2001,28:102-108.
3 R. Eastell, D.M.Reid, J. Compston, etc. A UK Consensus Group on manageme nt of glucocorticoidinduced osteoporosis:an update. Journal of Internal Medicine,1998,244:271-292.
4 Cunnane G, Lane NE, Steroid-induced osteoporosis in systemic lupus eryt-hematosus [J]. Rheum Dis Clin North Am,2000,26:311-329.
5梁九根蒋宁一徐志英,等.长期强的松治疗对绝经前SLE患者骨密度的影响.中国骨质疏松杂志,2006,12：57-61.
6 Mario Garcia-carrasco MD PhD, Claudia Mendoza-Pinto MD, etc. Osteoporosis in Patients with Systemic Lupus Erythematosus. IMAJ,2009,11:486-491.
7 E. K. LI. Loss of bone mineral density in chinese pre-menopausal women with systemic lupus erythematosus treated with corticosteroids. British Journ-al of Rheumatology,1998,37:405-410.
8 Matsuyama T, Ishii S, Tokita A, et al. Vitamin D receptor genotypes and bonemineral density. Lancet,1995,345(8):1238-1239.
9 Dawson-Hughes B, Harris SS, Finneran S. Calcium absorption On high and low calcium intakes in relation to vitamin D receptor genotype. J cl in Endoc-rinol Metab,1995,8o(2o):3657-3661.
lOKenneth G, Saag. MD. MSc. Glucocorticoid-induced osteoporosis. Endocrinol Metab Clin N Am,2003,32:135-157.
11 Van Staa TP, Lenfkens HG, Cooper C, et al. The epidemiology of corticoste-roid-induced osteoporosis:8meta-analysis.Osteoporos Int,2002,13:777-787
12Gherardo Mazziotti Alberto Angeli, etc. Glucocorticoid-induced osteoporosi-s. Trends in Endocrinology and Metabolism,2006,17(4):144-149.
13Canalis, E,et al. (2004) Perspectives on glucocorticoid-induced osteoporo-sis. Bone 34,593-598.
140hnaka, K. et al. (2005) Glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts. Biochem. Biophys. Res. Commun,329:177-181.
15 Pons F, Pefis P, Guan abens N, et al. The efect of systemic lupus erythe-matosus an d long-term steroid therapy on bo ne mass in premenopausal women. Br J Rheumatol.1995,34(8):742-746.
16王巧宏,吴华香,薛静.绝经前女性系统性红斑狼疮患者骨密度和骨代谢指标测定.中国骨质疏松杂志,2008,14(1)：41-43.
17 Mok CC, Mak A, Ma KM. Bone mineral density in postmenopausal Chinese pati-ents with systemic lupus erythematosus. Lupus,2005,14:106-12.
18 E. Canalis. G, Mazziotti.A. Glucocorticoid-induced osteoporosis:patho-physiology and therapy. Osteoporos Int,2007,18:1319-1328.
19 Tomlinson JW, Walker EA,Bujalska IJ, et al.11betahydroxysteroid de-hydrogenase type 1:a tissue-specific regulator of glucocorticoid r-esponse. Endocr Rev,2004,25:31-66.
20 Cooper MS, Bujalska I, Rabbitt E, et al. Modulation of 11-ahydroxy s-teroid dehydrogenase isozymes by proinflammatory cytokines in osteo-blasts:an autocrine switch from glucocorticoid In activation to ac-tivation. J Bone Miner Res,2001,16:1037-1044.
21 Williams LJ, Lyons V, MacLeod I, et al. C/EBP regulates hepatic trans-cription of llbeta-hydroxysteroid dehydrogenase type 1. A novel mech-anism for cross-talk between the C/EBP and glucocorticoid signaling pathways. J Biol Chem,2000,275:30232-30239.
22 Cooper MS, Rabbitt EH, Goddard PE, et al. Osteoblastic 11 a-hydroxy steroid dehydrogenase type 1 activity increases with age and glucoc-orticoid exposure. J Bone Miner Res,2002,17:979-986.
23 Kanis Ji, Gluer CC. An update on the diagnosis and assessment Of osteo-porosis with densitometry. Osteoporosis bat,2000,11:192-202.
24 E. Canalis. G, Mazziotti.A. Glucocorticoid-induced ostooporosis:patho-physiology and therapy. Osteoporos Int,2007,18:1319-1328.
25 Kamen DL,Alele JD. Skeletal manifestations of systemic autoimmune diseases. Current Opinion in Endocrinology, Diabetes and Obesity 2010,17 :540-545.
26 Angeli A, Guglielmi G, Dovio A, et al. High prevalence of asymptomati-c vertebral fractures in postmenopausal women receiving chronic gluco corticoid therapy:a cross-sectional outpatient study. Bone 20-06,39: 253-259.
[1]American College of Rheumatoiogy Ad Hoc Committee on Glucocoritcoid Induced Osteoporesis. Recommendations for the prevention an d treatment of glucocorticoid——induced osteoporosis:2001 update[J]. Arthritis Rheum,2001,44(7):1496-1503.
[2]Devogelaer JP, Goemaere S, Boonen S, et al. Evidence. based guidelines for the prevention and treatment of glucocorticoid induced osteoporosis: a consensus document of the belgian bone club. Osteoporos lnt,2006, 17(1):8-19.
[3]Cunnane G, Lane NE, Steroid-induced osteoporosis in systemic lupus erythematosus [J]. Rheum Dis Clin North Am,2000,26:311-329.
[4]Delany AM, Durant D, Canalis E. Glucocorticoid suppression of insulin-like growth factor I transcription in osteoblasts. Mol Endocrinol, 2001,15:1781-1789.
[5]Kbosla S, Dunstan CR. The roles of osteoprotegenn and osteoprotegerin ligand in the paracrine regulation of bone resorption. J Bone Miner Res, 2000.15(1):2-12.
[6]Hofbauer LC, Coil F, Riggs BL, et al. Stimulation of osteoprotegerin ligand and inhibition of osteoprotein prod uction by glucocorticoids in human osteoblastic lineage cells:potential paracrine mechanisms of glucoc-orticoid-induced osteoporosis [J]. Endocrinology,1999,140:4382-4389.
[7]Canalis E Glueocorticoid-induced Osteoporosis [J] Curr Opin Endocrinol Diab,2000.7:320-324.
[8]Dovio A, Sartori ML, Masera RG, et al. Inhibitory effect of physiological concentrations of cortisol but notestradiol on interleukin(IL-6) produ-ction by human osteoblast—like cell lines with different constitutive IL-6 expression[J]. Cytokine,2001,15(1):47.
[9]Koedam J A, Hoogerbrngge C M, Van S C Diferential regulation of IGF--binding proteitn in rabbit costal chondro—cytes by IGF-I and dexa-methazone [J] Endocrinol,2000.165:557-567.
[10]Se. saki N, Kusano E, Ando Y, et al. Changes in osteoprotegerin and markers of bone metabolism during glucocorticoid treatment in patients with chronic glomerulonephritis[J].2002,30:853-858.
[11]Homik J, Suare_z—AlmazorME, SheaB, et al. Calcium and vitamin D for corticosteroid—induced osteoporosis. Cochrane Database Syst Rev, 2000.2:CI)000952.
[12]American College of Rheumatology Ad Hoc committee. Glucocorticoid-Induced Osteoporosis. Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis[J]. Arthritis Rheum,2001,44: 1496.
[13]Adachi J D, Roux C, Pitt PI, et al. A pooled data analysis on the use of intermittent cyclical etidronate therapy for the prevention and treatment of corticosteroid induced bone loss. J Rheumatol,2000:27: 2424.
[14]Bousten Y, Jamart J, Esselinckx W, et al. Primary prevention of glucocorticoid-induced osteoporosis with intravenous pamidronate and calcium:a prospective controlled 1-year study comparing a single infusion, an infusion given once every 3 months, and calcium alone [J]. J Bone Miner Res,2001,
[15]Cranney A, Welch V, Adachi JD, et al. Calcitonin for the treatment and prevention of corticodteroid-induced osteoporosis [J]. Cochrane Database Syst Rev,2000,2:1983.
[16]Lane NE, Lukert B. The science and therapy of glucocorticoid induced bone loss[J]. Endocrinol Metab Clin North Am,1998,27(2):465.
[17]Hodsman All, Bauer DC, Dempster DW, et al. Parathyroid hormone and teriparatide for the treatment of osteoporosis:a review of the evidence and suggested guidelines for its use. Endoer Rev,2005,26:688-703.
[18]RehmanQ, Lang TF, Amaud CD。et,al. Daily treatment with parathyroid hormone is associated with an increase in vertebral cross-sectional area in postmenopausal women with glucocor-ticoid induced osteoporosis. Osteo-poros Int,2003,14:77-81.
[19]Van't HOf RJ, Ralston SH. Nitric oxide and bone. Immunology,,2001, 103:255-61.
[20]Wimalawansa S, Chapa T, et al. Frequency-dependent effect Of nitric oxide donor nitroglycerin on bone. J Bone Miner Res,2000,15:1119-1125
[21]lwamoto J, Takeda T, Sato Y. Effects Of vitamin K2 on osteoporosis, Curr Pharm Des,2004,10:2557.2576.
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