缓释左旋-18甲基炔诺酮皮埋避孕剂对骨密度和骨代谢的影响

对采用 Norplant R埋植剂和仿制 Norplant的国产埋植剂 型避孕的育龄妇女骨密度和骨代谢改变进行了 1年的随机前瞻性临床观察。 6 1例正常妇女被分为两组 :Norplant埋植剂组 30例 ,国产埋植剂组 31例。两组于埋植前和埋植后第 12个月时采用双能 X线骨密度测定仪 (DEXA)分别测定了腰椎 L2 ～ L4、股骨近端骨密度和骨矿含量。两组妇女埋植后第 12个月时腰椎 L2 ～ L4骨密度和骨矿含量均较埋植前明显增加 (P<0 .0 1) ,Norplant组骨密度平均增加2 .40 % ,骨矿含量平均增加 3.34 % ,国产埋植剂组分别增加 2 .75 %和 4.47% ;从年龄分析 ,以 2 5～ 2 9岁组腰椎 L2 ～ L4骨密度埋植后增加最为显著 ,Norplant组 P<0 .0 5 ,国产埋植剂组 P<0 .0 1。国产埋植剂组妇女埋植后第 12个月时股骨大粗隆骨密度和骨矿含量较埋植前明显增加 (P<0 .0 1) ;国产埋植剂组妇女空腹尿羟脯氨酸 /肌酐比值埋植后第 12个月时较埋植前明显下降 (P<0 .0 1) ;对使用妇女腰椎、股骨骨密度和骨代谢生化指标的影响 ,在两种埋植剂之间埋植前后比较均无显著差别 (P>0 .0 5 )。左旋 - 18甲基炔诺酮皮埋避孕剂对绝经妇女的骨骼是非有害的 ,对年轻妇女骨峰值的获得无明显影响。     

女性不同绝经年龄骨密度和骨强度256例分析

目的　研究绝经年龄对女性骨密度和骨强度的影响 ,为骨质疏松症 (OP)的预防提供科学依据。方法　采用双能X线骨密度仪和骨超声仪 ,测量 2 5 6例绝经年限 10～ 2 5年的健康女性志愿者骨密度 (BMD)和胫骨超声传导速度 (SOS) ,按绝经年龄不同分为Ⅰ组 (绝经年龄 <4 5岁 )、Ⅱ组 (绝经年龄 4 5～ 5 1岁 )、Ⅲ组 (绝经年龄>5 1岁 )进行分析。结果　三组除腰椎正、侧位 ,髋部wards区 ,尺骨和桡骨超远端外 ,其他部位BMD均与绝经年龄呈正相关 (r =0 10 7～ 0 2 11,P <0 0 5或P <0 0 1) ;Ⅱ、Ⅲ组髋部股骨颈、髋部总体、尺骨和桡骨远端 1/ 3段、尺骨和桡骨总体BMD均高于Ⅰ组对应部位 (P <0 0 5或P <0 0 1) ,且OP的患病率均低于Ⅰ组 (P <0 0 5或P <0 0 1) ;Ⅱ、Ⅲ组之间各部位BMD以及OP的患病率差异无显著性意义 ;胫骨SOS值与绝经年龄无相关性 ,且Ⅰ、Ⅱ、Ⅲ组之间胫骨SOS值以及OP的患病率差异无显著性意义 (P >0 0 5 )。结论　绝经年龄早 (<4 5岁 )主要引起皮质骨BMD降低 (腰椎正位除外 ) ,对松质骨BMD影响小 ;正常和晚绝经年龄对BMD影响小 ;绝经年龄对骨强度影响小     

经皮用雌二醇凝胶预防绝经早期骨丢失的三年探索性观察

目的 探索经皮用雌二醇（E2）凝胶在中国妇女中预防绝经早期骨丢失的用法。方法 将60例身体健康、绝经1－5年的妇女,开放随机分为4组,每组15例,采用周期联合方法分别予含0．75或1．5mgE2的经皮17β-E2凝胶（E2凝胶）与100mg微粉化天然黄体酮（MP）或2mg醋甲羟孕酮（MPA）口服,每日睡前应用,每月连用25d,停药5d。用单光子吸收法测前臂皮质骨骨密度;定量CT法测腰椎松质骨骨密度;双能X线吸收法测腰椎与髋部骨密度。在治疗0、6、12、18、24与36个月时分别测量骨密度、骨代谢生化指标,行绝经症状评分。结果 59例（98％）完成1年;56例（93％）完成2年,51例（85％）完成3年。治疗6个月时,4个组症状缓解率平均约80％;2年时腰椎松质骨骨密度升高平均为4．3％－7．5％;3年时第2－4腰椎骨密度升高4．2％－6．2％;股骨颈骨密度升高1．6％－3．8％。与治疗前相比,差异均有显著性（P＜0．05）;4组间比较,骨密度的改善差异无显著性（P＞0．05）。阴道出血率1．5mgE2凝胶＋2mgMPA治疗者、0．75mgE2凝胶＋2mgMPA治疗者较高,其他两组较低。结论 每日0．75mg与1．5mgE2凝胶可有效缓解绝经相关症状,预防绝经早期骨丢失。雌孕激素补充治疗3年,可连续增加腰椎骨密度,增加并维持股骨上端骨密度。     

两种激素补充治疗方案联合钙剂对绝经后妇女骨密度的影响

目的　研究利维爱 1 2 5mg d和结合雌激素 (CEE) 0 6 2 5mg +安宫黄体酮 (MPA) 2mg联合钙剂对绝经后骨质疏松和低骨量妇女骨密度的影响。方法　绝经后妇女 30人 ,分为利维爱组和CEE组。利维爱组8例为骨质疏松 ,中位年龄 6 4岁 ,中位绝经年限 1 4年 ;9例为低骨量 ,中位年龄 5 2岁 ,中位绝经年限 3年 ,均给予利维爱 1 2 5mg d、Ca -D 6 0 0mg d口服。CEE组中位年龄为 5 1岁 ,中位绝经年限为 2 5年。治疗前及治疗 1年时用DEXA方法检查前臂远端骨密度各 1次 ,做为自身对照 ,对比骨密度变化情况同时每年通过阴道B超监测子宫内膜的厚度。结果　利维爱组骨质疏松患者 ,松质骨骨密度增长中位数为 +4 0 % ,密质骨为 +2 6 % ;低骨量者 ,用利维爱者分别为 0和 - 1 0 % ,用CEE者为 +0 3%和 - 0 7%。所有患者依从性好 ,无明显副作用发生。结论　利维爱 1 2 5mg d联合钙剂能够提高绝经后骨质疏松妇女的前臂骨密度     

小剂量结合型雌激素或合用醋酸甲羟孕酮对绝经早期妇女骨骼的影响

为探讨小剂量结合型雌激素 (CEEs)与合用醋酸甲羟孕酮 (MPA ) (CEEs- MPA )对绝经后妇女脊柱、髋骨骨密度(BMD)、总骨矿含量 (BMC)和骨转化指标的影响 ,美国于1995年 8月～ 2 0 0 0年 10月间进行了一项为期 2年的多中心随机、双盲、安慰剂对照试验。病例纳入标准 :14 0～ 6 5岁健康绝经妇女。 2绝经 1～ 4年。3血 FSH≥ 30 IU / L。4血 E2 ≤ 185 pmol/ L ,5子宫完整。6体重不超出正常范围 2 0 %。排除标准 :1合并影响骨代谢的疾病或可能影响 BMD测定的腰椎退行性变等。 2腰椎 BMD基线水平低于健康青年妇女均值的 3个标准差。 …     

妊娠期及哺乳期妇女跟骨骨密度的超声定量检测

为探讨妊娠期及哺乳期妇女骨密度的变化规律 ,我们采用MARCURY超声骨密度仪对孕 16～ 2 0周的孕妇 4 1例 (A组 ) ,孕 30～ 33周的孕妇 35例 (B组 )及产后 4 0～ 6 0d的哺乳期健康妇女 36例 (C组 )进行跟骨骨密度测定。结果显示 ,A组孕妇跟骨骨密度为 ( 0 5 3± 0 12 )g/cm2 ,B组孕妇跟骨骨密度为 ( 0 5 0± 0 0 8) g/cm2 ,C组妇女跟骨骨密度为( 0 4 6± 0 0 5 ) g/cm2 ,A、B两组比较 ,差异无显著性(P >0 0 5 ) ,C组与A、B两组明显降低 ,差异有显著性 (P<0 0 1)。超声传导速度 :A组为 ( 1837± 12 0 )m/s,B组为( 1835± 133…     

绝经后妇女雌激素受体基因多态性与骨和脂代谢的相关性研究

目的 :研究绝经后妇女雌激素受体 (ER)基因PvuII、XbaI限制性片段长度多态性与骨和脂代谢的关系。方法 :随机选取 5 7名已排除影响骨代谢、脂代谢疾病的绝经后妇女 ,采空腹血和晨尿 ,用PCR RFLP法对ER基因多态性进行分析 ;DEXA测定腰椎正侧位及股骨骨密度 ,同时检测血骨钙素、尿I型胶原N末端肽和血脂指标。结果 :xx组股骨干(SHAFT)骨密度明显低于Xx组 (P <0 .0 5 )。XbaI限制性片段长度多态性与股骨SHAFT骨密度相关 (r =0 .36 7,P =0 .0 39) ;XX组骨钙素高于xx(P =0 .0 4 1)和Xx(P =0 .0 11)组。apoA1含量和A1/B比值在xx、Xx、XX三组递增 ,各组间差异有显著性 (P <0 .0 5 )。Lp(a)与股骨骨密度 (除SHAFT外 )呈负相关。结论 :ER基因XbaI RFLP是影响绝经后妇女骨和脂代谢的重要因素 ;X基因型可维持股骨骨量 ,xx基因型与低apoA1含量和A1/B比值相关 ,Lp(a)也影响股骨骨密度     

小剂量雌激素对绝经后骨质疏松症的治疗

目的:探讨减半剂量雌激素联合孕激素和钙剂对绝经后骨质疏松症的防治作用。方法:138例绝经2年以上因骨痛就诊的妇女。①测定用药前血性激素,血、尿骨代谢生化,并与20例未绝经的正常妇女相比较;②绝经者随机分为3组(每组46例),A组给予倍美力0.625mg+安宫黄体酮2mg+钙尔奇D1g/d,B组给予倍美力0.3mg+安宫黄体酮2mg+钙尔奇D1g/d,C组给予安慰剂+钙尔奇D1g/d,均连续用药2年。在用药前、用药后6个月、12个月、24个月分别测定血骨钙素(BGP)、碱性磷酸酶(BAP)、I型羧基末端终肽(CICP)、比林二酚(Pyd)、尿钙(Ca)、肌酐(Cr)、IL-6;行双光子(DEXA)测定骨密度(BMD),并超声测定子宫内膜及钼靶摄片了解乳房情况。结果:①与未绝经组比,绝经后血清E2、BGP、BMD值下降(P<0.05),血FSH、LH,尿Pyd/Cr、Ca/Cr比值增高(P<0.05)。②3组对象用药后3个月,骨痛均有不同程度改善;A组和B组用药后1年骨密度有明显提高,而C组在1年后骨密度呈下降趋势。3组对象治疗过程中均未发现子宫内膜的异常增厚。用药6个月时骨代谢生化指标及血清IL-6水平就有显著下降。结论:绝经后妇女中,小剂量雌、孕激素加钙剂能防治骨质疏松症的发生。     

年龄、绝经年限与骨代谢指标相关性研究

目的 :探讨妇女不同年龄段、绝经年限、初潮年龄的骨代谢指标的变化。方法 :随机选择年龄 2 0～ 75岁的妇女 2 10例 ,测定血清钙 (Ca)、磷 (P)、碱性磷酸酶 (ALP)、性激素 ,尿钙 /肌酐 (Ca/Cr)值。结果 :骨代谢指标与年龄、绝经年限、初潮年龄均呈正相关 ,40岁以上的妇女的骨代谢指标明显高于 40岁以下的妇女 (P <0 0 5 ) ;初潮年龄在 18岁以上的妇女骨代谢指标明显增高 (P <0 0 5 ) ;绝经后E2 水平较绝经前降低 (P <0 0 5 ) ,但不同绝经年限间差异无显著性 (P >0 0 5 ) ;绝经后骨代谢指标较绝经前增高 (P <0 0 5 ) ,尤其在绝经后 10年以上增高更明显。结论 :妇女在围绝经早期出现骨转换率增高 ,可能与雌激素下降有关 ,因此对围绝经早期妇女 ,尤其是初潮年龄晚者 ,应进行骨代谢指标测定 ,筛查并及时预防骨质疏松症     

绝经后妇女宫颈病变的特点及其早期诊断

目的　探讨绝经后妇女宫颈病变的特点、筛查的必要性及早期诊断。方法　对北京大学第三医院自2 0 0 1年 1月至 2 0 0 4年 1月因宫颈涂片异常或临床检查可疑宫颈病变者 934例进行总结分析。根据绝经与否分为未绝经组和绝经组 ,对患者行宫颈涂片、阴道镜下宫颈多点活检。结果　未绝经组及绝经组宫颈异常涂片的检出率分别为 6 8 2 6 % (40 0 / 5 86 )及 85 31% (2 73/ 32 0 ) ,二组比较差异有显著性意义 (P <0 0 5 )。阴道镜下宫颈活检组织病理学诊断宫颈上皮内瘤变 (cervicalintraepithelialneoplasia ,CIN)分别为 2 4 34% (138/ 5 6 7)及 15 0 6 %(5 0 / 332 ) ,二组比较差异有显著性意义 (P <0 0 5 ) ;其中CINⅢ的检出率分别为 8 99% (5 1/ 5 6 7)及 8 73%(2 9/ 332 )。未绝经组与绝经组涂片及组织病理学提示人乳头瘤病毒 (humanpapillomavirus ,HPV)感染共 138例 ,其中高危型HPV阳性率分别为 6 2 2 2 % (5 6 / 90 )和 4 3 75 % (2 1/ 4 8) ,二组比较差异有显著性意义 (P <0 0 5 )。结论　为早期发现宫颈病变 ,阻遏疾病进展为宫颈癌 ,在绝经后妇女进行宫颈细胞学筛查是必要的。     

Safety and efficacy of drospirenone used in a continuous combination with 17beta-estradiol for prevention of postmenopausal osteoporosis.

OBJECTIVE: To evaluate the combination of 17beta-estradiol and continuous drospirenone for the prevention of postmenopausal osteoporosis. METHODS: A total of 180 (75%) healthy postmenopausal women aged 45-65 years completed a 2-year prospective study. Bone mineral density (BMD) at lumbar spine, hip and total body as well as endometrial thickness, markers of bone turnover and serum lipids were measured regularly. Treatment groups were given placebo or 1 mg 17beta-estradiol combined with 1, 2 or 3 mg drospirenone daily. RESULTS: BMD at the lumbar spine, hip and total body increased by 7, 4 and 3%, respectively, in all hormone groups versus placebo (all p < 0.001). Bone markers all decreased accordingly (serum osteocalcin 52%, serum bone specific alkaline phosphatase 36%, serum CrossLaps 67% and urinary CrossLaps 75% from baseline; all p < 0.001). Total cholesterol and low-density lipoprotein cholesterol decreased by 8% and 13%, respectively (both p < 0.001). High-density lipoprotein cholesterol and triglycerides remained unchanged. No significant dose-related effects were found. Endometrial thickness increased by 1.2 mm only in the 1-mg drospirenone group (p < 0.01 versus placebo). CONCLUSION: The combination of 17beta-estradiol and drospirenone has a positive effect on BMD and a potentially beneficial effect on lipids. Although endometrial thickness increased slightly, the safety of the endometrium was assured, as no cases of hyperplasia or cancer occurred.     

A randomized trial of oral contraceptive and hormone replacement therapy on bone mineral density and coronary heart disease risk factors in postmenopausal women

OBJECTIVE: To identify the effects of oral contraceptive (OC) and hormone replacement therapy (HRT) on bone mineral density and coronary heart disease risk factors in postmenopausal women. METHODS: Eighty healthy postmenopausal women were randomly assigned to a cyclic regimen of OC containing 30 microg of ethinyl estradiol and 150 microg of desogestrel or HRT containing 0.625 mg of conjugated equine estrogens 21 days per cycle and 5 mg of medrogestone 10 days per cycle for 12 months. Bone mineral density of lumbar spine and hip, biochemical markers of bone turnover, lipid-lipoprotein profiles, coagulation profiles, fasting plasma glucose, and blood pressure were evaluated. RESULTS: Both regimens caused significant increase in bone mineral density of lumbar spine, trochanter, intertrochanteric region, total hip, and Ward triangle. Only OC therapy was associated with a significant increase in femoral neck bone mineral density (mean score +/- standard error 2.5% +/- 0.7%, P < .01). Biochemical markers of bone turnover, total cholesterol, and low-density lipoprotein cholesterol decreased significantly in both groups. Posttreatment levels of those bone markers and lipid-lipoprotein were significantly lower after OC therapy than HRT. Fasting plasma glucose and systolic blood pressure decreased significantly in both groups; however, only the OC group showed a significant decrease in diastolic blood pressure. CONCLUSION: Both OC and HRT increased bone mineral density of lumbar spine and hip, but OC suppressed bone turnover more than HRT. Both methods favorably affected lipid-lipoprotein metabolism, fasting plasma glucose, and blood pressure during the 12 months of treatment.     

The impact of subcutaneous oestradiol implants on biochemical markers of bone turnover and bone mineral density in postmenopausal women

Objective To evaluate the anabolic effect of oestrogen on bone by comparing the response of markers of bone formation (and resorption) and bone mineral density (BMD) to subcutaneous oestradiol implants.
Design One year double-blind placebo controlled randomised study.
Setting Clinical research unit within a teaching hospital.
Population Twenty-one hysterectomised postmenopausal women were randomised to 25 mg oestradiol implants at baseline and at six months or to have a sham procedure at baseline and six months.
Methods BMD and quantitative ultrasound (QUS) were assessed at baseline and one year. Bone alkaline phosphatase (bone ALP), procollagen type I N-terminal propeptide (PINP), osteocalcin (OC), free deoxypyridinoline (iFDPD), N-telopeptide of type I collagen (NTX), serum oestradiol and intact parathyroid hormone (PTH) were measured at baseline, 4, 8, 12 and 24 weeks.
Main outcome measures Percentage change markers of bone turnover and PTH and change in oestradiol levels over first six months and percentage of changes in DXA and QUS over one year.
Results PINP, bone ALP and OC increased by 28%, 7% and 9%, respectively (   P < 0.01  ) during the first four weeks of treatment and then decreased significantly. Lumbar spine (LS) and total hip (TH) BMD increased by 5.4% and 6.0% (   P < 0.001  ), respectively, and femoral neck (FN) BMD by 3.7% (   P < 0.05  ) during the first year of treatment compared with control subjects. The peak serum oestradiol level was achieved four weeks after implant insertion. Mean PTH levels increased significantly in subjects receiving subcutaneous oestradiol.
Conclusion Subcutaneous oestrogen exerted an apparent anabolic effect on bone, which was initially reflected by an increase in bone formation markers and later by a large increase in BMD.     

Comparison of the effects of raloxifene and low-dose hormone replacement therapy on bone mineral density and bone turnover in the treatment of postmenopausal osteoporosis.

OBJECTIVE: The aim of the present study was to compare the effects of raloxifene and low-dose hormone replacement therapy (HRT) on bone mineral density (BMD) and bone turnover markers in the treatment of postmenopausal osteoporosis. METHODS: Forty-two postmenopausal osteoporotic women, who were randomized to receive raloxifene 60 mg or estradiol 1 mg/norethisterone acetate 0.5 mg daily for 1 year, were studied. All women received calcium 600 mg/day and vitamin D 400 IU/day. BMD and markers of bone turnover were measured at baseline and at 12 months. RESULTS: After 12 months of treatment, there were statistically significant increases in BMD in both groups at all sites (all p < 0.05). For the lumbar spine, the increase in BMD was 2.3% for raloxifene compared with 5.8% for low-dose HRT and corresponding values for total body BMD were 2.9% for raloxifene and 4.6% for low-dose HRT; the increases being significantly greater in the low-dose HRT group (p < 0.001 and p = 0.02, respectively). Although the increase in BMD at the hip was significant for both raloxifene (2.1%) and low-dose HRT (3.2%) compared with baseline, the difference between the two regimens did not reach statistical significance. The decrease in serum C-terminal telopeptide fragment of type I collagen and serum osteocalcin levels for the low-dose HRT group (-53% and -47%, respectively) was significantly greater than for the raloxifene group (-23% and -27%, respectively; both p < 0.01). CONCLUSIONS: In postmenopausal women with osteoporosis, low-dose HRT produced significantly greater increases in BMD of the lumbar spine and total body and greater decreases in bone turnover than raloxifene at 12 months.     

Comparison of changes in biochemical markers of bone turnover after 6 months of hormone replacement therapy with either transdermal 17 beta-estradiol or equine conjugated estrogen plus nomegestrol acetate

OBJECTIVE: To compare changes in biochemical markers of bone turnover in postmenopausal women who received sequential discontinuous hormone replacement therapy (HRT) with either transdermal 17 beta-estradiol gel (group 1) or oral equine sulfoconjugated estrogen (group 2), plus nomegestrol acetate. PATIENTS AND METHOD: Prospective, open, randomized, controlled trial, conducted on 3 parallel groups of 106 postmenopausal women. All treated groups received estrogen therapy for 25 consecutive days every month. The estrogen used was either 1.5 mg/day of transdermal 17 beta-estradiol gel (group 1) [N = 42, average age (AA) = 51.6 years, average duration of menopause (ADM = 21.5 months)], or 0.625 mg/day of oral equine sulfoconjugated estrogen (group 2) [N = 39, AA = 51.3 years, ADM = 16.8 months]. In all cases nomegestrol acetate 5 mg/day was added for 12 consecutive days every month. The control group comprised 25 patients, [AA = 53.4 years, ADM = 33.7 months]. Two bone resorption markers: urinary cross-linked N-telopeptide and C-telopeptide of type I collagen (U-NTX/Cr, U-CTX/Cr), and a bone formation marker: serum bone specific alkaline phosphatase activity were measured before and 6 months after treatment start. RESULTS: Significant decreases from baseline values were observed for the 3 biochemical markers in both treated groups compared with control (P < 0.001). There were no significant differences in changes between the 2 treated groups for the 3 biochemical markers. The mean percentage change in the 3 biochemical markers was: from -9.3 to -45.5% in group 1, from -20.5 to -39% in group 2, and from -3.3 to 2% in control group. In group 1, the mean percentage decreases in U-CTX reached optimal threshold of bone turnover change (-45%) which is considered by the International Osteoporosis Foundation as clinically relevant because it predicts an increase in BMD greater than 3% when treatment is maintained over a long term. DISCUSSION AND CONCLUSION: Both treated groups induced a significant comparable decrease of bone turnover markers after 6 months of intervention, compared with control. The group treated with cyclic administration of transdermal 17 beta-estradiol (1.5 mg/day) and nomegestrol acetate (5 mg/day) showed a bone resorption markers decrease corresponding to the threshold of clinical relevance described in the international literature and predictive of positive BMD response in long term.     

Two new combinations of estrogen and progestogen for prevention of postmenopausal bone loss: long-term effects on bone, calcium and lipid metabolism, climacteric symptoms, and bleeding.

Bone mass, calcium and lipid metabolism, climacteric symptoms, bleeding, blood pressure, and weight changes were studied in 62 healthy postmenopausal women at 3-month intervals throughout 2 years of treatment with continuous estradiol valerate (2 mg) plus cyproterone acetate (1 mg), sequential estradiol valerate (2 mg) plus levonorgestrel (75 micrograms), or placebo. During the 2 years of the study, bone mineral content of the distal and ultradistal regions of the forearm (measured by single-photon absorptiometry) remained unchanged in the hormone groups, whereas bone mineral content at these sites decreased by 5 and 6%, respectively, in the placebo group. Bone mineral density in the spine (measured by dual-photon absorptiometry and dual-energy x-ray absorptiometry) increased by 3-4% in the hormone groups and decreased by 2% in the placebo group. Biochemical estimates of bone turnover (serum alkaline phosphatase and fasting urinary calcium/creatinine) decreased significantly to premenopausal levels in the hormone groups, but remained unchanged in the placebo group. Serum concentrations of total and low-density lipoprotein cholesterol were significantly reduced by 5-10% (P less than .05-.01) in the estradiol + cyproterone acetate group and by 10-15% (P less than .001) in the estradiol valerate + levonorgestrel group. There were no significant changes in high-density lipoprotein cholesterol in the hormone groups. Virtually no changes were observed in the placebo group. Climacteric symptoms and hot flushes were significantly reduced in both hormone groups compared with the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of the effects of raloxifene and low-dose hormone replacement therapy on bone mineral density and bone turnover in the treatment of postmenopausal osteoporosis

Objective. The aim of the present study was to compare the effects of raloxifene and low-dose hormone replacement therapy (HRT) on bone mineral density (BMD) and bone turnover markers in the treatment of postmenopausal osteoporosis.

Methods. Forty-two postmenopausal osteoporotic women, who were randomized to receive raloxifene 60 mg or estradiol 1 mg/norethisterone acetate 0.5 mg daily for 1 year, were studied. All women received calcium 600 mg/day and vitamin D 400 IU/day. BMD and markers of bone turnover were measured at baseline and at 12 months.

Results. After 12 months of treatment, there were statistically significant increases in BMD in both groups at all sites (all p < 0.05). For the lumbar spine, the increase in BMD was 2.3% for raloxifene compared with 5.8% for low-dose HRT and corresponding values for total body BMD were 2.9% for raloxifene and 4.6% for low-dose HRT; the increases being significantly greater in the low-dose HRT group (p < 0.001 and p = 0.02, respectively). Although the increase in BMD at the hip was significant for both raloxifene (2.1%) and low-dose HRT (3.2%) compared with baseline, the difference between the two regimens did not reach statistical significance. The decrease in serum C-terminal telopeptide fragment of type I collagen and serum osteocalcin levels for the low-dose HRT group (?53% and ?47%, respectively) was significantly greater than for the raloxifene group (?23% and ?27%, respectively; both p < 0.01).

Conclusions. In postmenopausal women with osteoporosis, low-dose HRT produced significantly greater increases in BMD of the lumbar spine and total body and greater decreases in bone turnover than raloxifene at 12 months.     

Double-blind, placebo-controlled study of the effects of tibolone on bone mineral density in postmenopausal osteoporotic women with and without previous fractures.

A 2-year placebo-controlled, randomized, two-center prospective study was carried out to assess the effects of tibolone (Org OD14, Livial) on trabecular and cortical bone mass and bone biochemistry parameters in elderly postmenopausal women with and without previous fractures. In total, 107 subjects, 71 with fractures and 36 without fractures, were randomized to tibolone (n = 64) or placebo (n = 43). Their mean age was 63.1 years. Bone mineral density (BMD) (g/cm2) was assessed at baseline and every 6 months for 2 years by dual-energy X-ray absorptiometry (DXA). Mean baseline values were 0.79 and 0.80 for the lumbar spine in the tibolone and placebo groups, respectively, and for the femoral neck 0.64 in both groups. Serum and urinary bone biochemistry parameters were measured concurrently. An analysis of variance (ANOVA) model including center and group was applied. The completers' group was the primary subset for the analysis; the intention-to-treat (ITT) group was also analyzed. Results are expressed as the percentage change at 24 months and the annual rate of change percentage year. The tibolone group showed an overall mean increase (vs. placebo) in BMD at the lumbar spine of 7.2% (p < 0.001) and for the femoral neck 2.6% (p < 0.001). In subjects with previous fractures increases were 6.0% and 4.0% for the lumbar spine and femoral neck, while in those with no fractures, respective changes were 8.9% and 1.1%. Overall changes in the placebo group were 0.9% and -1.6% for the lumbar spine and femoral neck, respectively. A significant fall in bone biochemistry parameters showed that tibolone inhibits osteoclastic activity. In conclusion we have found that tibolone 2.5 mg induces significant increases of trabecular and cortical bone mass in elderly postmenopausal osteoporotic women with and without previous fractures.     

Risedronate prevents bone loss in early postmenopausal women: a prospective randomized, placebo-controlled trial.

OBJECTIVES: To assess the efficacy and tolerability of risedronate, a pyridinyl bisphosphonate, in preventing loss of bone mineral density (BMD) of the lumbar spine and proximal femur in early postmenopausal women. METHODS: A total of 383 patients were randomly assigned to receive risedronate 2.5 or 5 mg or placebo once daily for 24 months. All patients received 1 g elemental calcium daily. BMD was measured by dual X-ray absorptiometry at baseline and at 3, 6, 12, 18, and 24 months. RESULTS: Risedronate 5 mg significantly increased BMD at the lumbar spine and femoral neck and trochanter in early postmenopausal women. Significant results were observed as early as 3 months. In the control calcium-supplemented group, BMD decreased steadily at each site throughout the study. The mean percentage change from baseline in BMD in the risedronate 5 mg group was significantly different from that in the control group at each determination at each site. At 24 months, the differences were 4.5 +/- 0.45% at the lumbar spine, 3.3 +/- 0.49% at the femoral neck, and 4.3 +/- 0.67% at the femoral trochanter. Risedronate 2.5 mg maintained BMD at each site, although the effect was less pronounced than that of risedronate 5 mg. Risedronate was well tolerated and was not associated with an increased incidence of overall or upper gastrointestinal adverse events. CONCLUSIONS: Risedronate 5 mg prevents bone loss in early postmenopausal women, is well tolerated, and represents an effective choice to maintain bone mass and prevent osteoporosis.