阿仑膦酸钠与唑来膦酸治疗绝经后骨质疏松症疗效比较

目的回顾性分析口服阿仑膦酸钠以及静脉注射唑来膦酸治疗绝经后骨质疏松症的临床疗效。方法从2014年12月-2016年1月就诊的绝经后骨质疏松妇女中筛选出接受阿仑膦酸钠治疗至少1年和接受唑来膦酸治疗至少1年的妇女各80例作为研究对象,分别为口服阿仑膦酸钠组(70 mg/周)以及静脉注射唑来膦酸组(5 mg/年),所有患者均口服碳酸钙600 mg/d和维生素D 125 IU/d。采集所有患者基线及治疗12个月后腰椎L1-4、股骨颈和全髋部位的骨密度(bone mineral density,BMD),血清I型胶原羧基端肽交联(carboxy-telopeptide of type Ⅰ collagen,β-CTX)等资料,进行组间及药物治疗前后对照。结果阿仑膦酸钠组患者平均年龄(66.48±8.39)岁,唑来膦酸组患者平均年龄(65.11±7.69)岁。治疗12个月后,阿仑膦酸钠组腰椎BMD上升(5.46±4.42)%、股骨颈BMD上升(2.81±3.83)%,全髋BMD上升(2.72±2.76)%(均P0.001)。唑来膦酸组腰椎BMD上升(6.66±6.37)%、股骨颈BMD上升(1.97±3.13)%,全髋BMD上升(2.20±3.63)%(均P0.001)。分别比较两药物组腰椎、股骨颈、全髋BMD以及β-CTX变化率差异均无统计学意义(P值分别为0.216、0.132、0.312、0.066)。结论阿仑膦酸钠70 mg/周和唑来膦酸5 mg/年治疗1年均能够显著提高绝经后骨质疏松妇女的腰椎以及髋部BMD,两者疗效比较,差异无统计学意义(P0.05)。     

男性肝硬化患者并发骨质疏松及阿仑膦酸钠的近期疗效观察

目的观察男性肝硬化患者骨质疏松的发生率并评价阿仑膦酸钠的近期疗效。方法127例男性肝硬化患者接受骨密度检测，并对其中筛检出的骨质疏松患者进行阿仑膦酸钠治疗，疗程6个月，对比观察治疗前后骨密度的改变和骨转化指标。结果男性肝硬化患者的骨质疏松发生率为（57．48％），显著高于正常对照组（P〈0．01），且与肝功能分级相关；阿仑膦酸钠治疗6个月后，患者腰椎，股骨颈，Ward’s三角区骨密度值显著上升（P均〈0．05）。治疗后血清钙升高，血清磷、尿DPD／Cr值下降。结论男性肝硬化患者存在较高的骨质疏松的发生率，阿仑膦酸钠治疗男性肝硬化并发骨质疏松的近期疗效显著。     

阿仑膦酸钠治疗绝经后骨质疏松或骨量减少妇女1年间的β-CTX和骨密度的相关性研究

目的 通过观察阿仑膦酸钠治疗绝经后骨质疏松或骨量减少1年后骨密度和骨吸收指标(β-CTX)的变化,了解骨密度变化与骨吸收指标变化的关系.方法 入选了35例绝经后骨质疏松或骨量减少患者,给予阿仑膦酸钠70mg/w,碳酸钙600 mg/d和维生素D125 IU/d,治疗12m.在基线和治疗12m后进行DXA骨密度测定,在基线、治疗3 m和12 m后测定骨吸收指标β-CTX.结果 治疗1年后腰椎2～4、股骨颈和全髋骨密度均有上升,而所有受试者治疗3m后β-CTX均较基线下降(74.21±43.66)％.治疗3m后β-CTX的变化率和治疗12m后腰椎2～4和股骨颈骨密度绝对值呈相关(Betastd=-0.418,P=0.017; Betastd =-0.321,P=0.032).结论 治疗3m骨吸收指标β-CTX的变化率有望成为预示患者对阿仑膦酸钠反应的早期指标.     

骨转换指标对阿仑膦酸钠治疗的绝经后骨质疏松症患者骨密度变化的早期预测价值

目的了解绝经后骨质疏松症患者使用阿仑膦酸钠的治疗效果, 探讨骨转换指标(bone turnover markers, BTMs)对绝经后骨质疏松症患者骨密度变化的早期预测价值。方法本研究为回顾性研究, 选取2012年至2020年在上海市第六人民医院骨质疏松与骨病专科门诊就诊的409例绝经后骨质疏松症患者作为研究对象, 年龄为(64.86±7.21)岁。收集所有患者治疗前后的骨密度、血清Ⅰ型胶原交联羧基端肽β特殊序列(β-CTX)和骨钙素(osteocalcin)等临床资料。结果与治疗前相比, 阿仑膦酸钠治疗1年后患者腰椎1～4、股骨颈和全髋部骨密度分别上升4.84%、2.13%和2.89%(P<0.05)。治疗6个月和1年后, 患者β-CTX和骨钙素分别下降77.7%、42.3%和78.2%、49.5%(P<0.05)。线性回归分析结果显示, 阿仑膦酸钠治疗6个月时, β-CTX的变化率每下降10%, 治疗1年后, 腰椎1～4、股骨颈和全髋部骨密度的变化率分别上升0.417%、0.127%和0.213%;骨钙素的变化率每下降10%, 治疗1年后, 腰椎1～4、股骨颈和全髋部...     

阿仑膦酸钠联合骨松宝颗粒治疗老年女性骨质疏松的效果

目的 探讨倾向性评分匹配下阿仑膦酸钠联合骨松宝颗粒治疗老年女性骨质疏松(OP)的效果。方法 回顾性分析150例老年女性OP患者临床资料,其中85例采用阿仑膦酸钠治疗为对照组,65例接受阿仑膦酸钠联合骨松宝颗粒治疗为观察组,用倾向性评分匹配分析患者年龄、体重指数(BMI)、病程、合并糖尿病、合并高血压基线资料,采用近邻法进行1∶1匹配,经倾向性评分配比后,最终纳入观察组、对照组各30例。评估两组治疗6个月时的治疗效果,比较两组治疗前、治疗6个月时骨代谢指标[骨钙素(BGP)、Ⅰ型胶原β降解产物(β-CTX)]、骨密度T值(腰椎L1～4、股骨颈),统计两组治疗期间不良反应发生情况。结果 观察组治疗6个月时总体治疗效果优于对照组,且治疗总有效率高于对照组,差异有统计学意义(P<0.05);两组治疗6个月时BGP较治疗前升高,且观察组高于对照组,两组β-CTX水平均较治疗前降低,且观察组低于对照组,差异有统计学意义(P<0.05);两组治疗6个月时腰椎L1～4、股骨颈骨密度T值均较治疗前升高,且观察组高于对照组,差异有统计学意义(P<0.05);治疗期间,两组均无不良反应发生...     

早期PKP联合阿仑膦酸钠治疗高龄骨质疏松性椎体骨折的疗效

目的探讨早期经皮椎体后凸成形术(PKP)联合阿仑膦酸钠治疗高龄骨质疏松性椎体骨折患者的临床效果。方法 60例高龄骨质疏松性椎体骨折患者,依据治疗方案的不同分为对照组(接受早期PKP治疗,30例)与观察组(接受早期PKP+阿仑膦酸钠治疗,30例),比较两组围术期腰背痛情况、骨密度[腰椎(L)3～L4节段及股骨颈]与生活质量。结果术前与术后3个月,两组视觉模拟评分(VAS)对比差异无统计学意义(P0.05);术后14、28、42 d,观察组VAS显著低于对照组(P0.05)。术前,两组L3～L4节段及股骨颈骨密度对比差异无统计学意义(P0.05);术后3个月,观察组L3～L4节段及股骨颈骨密度明显高于对照组(P0.05)。术前,两组躯体健康总评(PCS)及精神健康总评(MCS)对比差异无统计学意义(P0.05);术后3个月,观察组PCS评分及MCS评分均明显高于对照组(P0.05)。结论高龄骨质疏松性椎体骨折患者通过早期PKP与阿仑膦酸钠联合治疗,可有效缓解腰背疼痛程度,调节骨密度,利于提高患者生活质量。     

阿仑膦酸钠治疗男性原发性骨质疏松症临床研究

目的 探讨骨吸收抑制剂阿仑膦酸钠对男性原发性骨质疏松症骨密度和骨转换生化指标的影响.方法 2005年1月至2007年1月前瞻性纳入北京协和医院诊断的20例男性原发性骨质疏松症患者,以20名正常男性为对照.骨质疏松症患者每周服用阿仑膦酸钠70 mg,且每日服用钙尔奇D 1片,疗程为18个月.每6个月采用双能x线骨密度仪测量腰椎和股骨近段骨密度,每3个月测量骨形成指标碱性磷酸酶和骨吸收指标Ⅰ型胶原羧基末端肽.正常男性不予干预,研究开始时和18个月时检查腰椎和股骨近端骨密度.结果 骨质疏松症组治疗前骨密度明显低于正常对照组.阿仑膦酸钠组治疗18个月时,与治疗前比较,腰椎、股骨颈、大转子、全髋和股骨干骨密度值增加6.3%、2.5%、5.8%、3.5%及4.2%(P均<0.05).骨转换生化指标碱性磷酸酶(ALP)和CTX治疗6个月时即显著下降,此后维持在较低水平,治疗18个月后ALP降低33.6%,CTX下降66.7%(P均<0.01).骨吸收指标较骨形成指标下降更明显.患者对阿仑膦酸钠的耐受性良好.正常对照组骨密度和血ALP在18个月期间无明显变化.结论 与对女性骨质疏松症患者疗效相似,阿仑膦酸钠能够明显增加男性原发性骨质疏松症患者的骨密度、降低骨转换生化指标,且安全性良好.     

老年男性骨质疏松患者阿仑膦酸钠治疗中血清骨保护素水平的变化

目的 观察阿仑膦酸钠治疗3年后骨密度、血清骨保护素(OPG)、相关骨代谢指标及性激素等的变化,探讨阿仑膦酸钠对老年男性骨质疏松患者的治疗作用及其OPG问可能的作用机制.方法 随机选取老年男性骨质疏松患者(骨质疏松组)72例及年龄匹配的健康对照者60例(对照组),检测血清OPG浓度.所有骨质疏松患者接受阿仑膦酸钠治疗3年,比较治疗前、后骨密度、血清OPG、性激素、血钙磷、甲状旁腺素、骨钙素、尿Ⅰ型胶原氨基端交联肽(NTX)、尿钙、尿肌酐等的变化. 结果 骨质疏松组血清OPG(10.56±2.56)pmol/L、骨钙素(9.54±4.40)tLg/L、甲状旁腺素(70.39±35.58)ng/L、尿NTX(72.06士9.78)nmol/L,高于对照组的OPG(8.91±2.20)pmol/L、骨钙素(6.77±2.87)μg/L,甲状旁腺素(47.11±21.80)ng/L,尿NTX(63.36±14.61)nmol/L(均为P<0.05或P<0.01).阿仑膦酸钠治疗后,骨密度明显上升,血清OPG降至(8.23±2.96)pmol/L,骨钙素降至(6.18±2.27)btg/L,甲状旁腺素降至(40.46±14.43)ng/L,尿NTX降至(64.83±11.40)nmol/L(均为P<0.05或P<0.01).Spearman相关分析显示治疗前、后骨密度的改变与OPG的变化有关. 结论 骨质疏松患者血清OPG水平明品高于对照组,阿仑膦酸钠治疗后随骨密度改善OPG浓度下降.阿仑膦酸钠能提高老年男性骨密度,改善骨代谢指标.     

右足溃疡阿仑膦酸钠治疗糖尿病合并骨质疏松的临床疗效分析

目的该文旨在探讨阿仑膦酸钠对糖尿病合并骨质疏松治疗的临床疗效,及其重要的应用价值。方法选取2012年4月—2014年7月该院收治的90例糖尿病合并骨质疏松患者作为研究对象,利用阿仑膦酸钠治疗所有90例患者。待治疗7个月后,对患者的骨密度值进行观察,并对患者治疗前后的血磷平均值和血钙平均值进行对比分析,以及观察患者是否出现不良的反应情况。结果该院通过利用阿仑膦酸钠治疗对糖尿病合并骨质疏松的90例患者,结果发现治疗后患者的骨密度值大大得到了改善,且治疗前与治疗后的骨密度值差异有统计学意义(P0.05)。此外,研究还发表,治疗前后患者的血磷和血钙等相关指标的数据无明显变化,差异无统计学意义(P0.05)。另外,除另个患者表现出一定的不良反应情况外,大部分患者表现良好,无不良反应情况。结论对于糖尿病合并骨质疏松,阿仑膦酸钠是一种很好的治疗方法,具有明显的临床治疗效果。因此,阿仑膦酸钠在治疗糖尿病合并骨质疏松上是一种十分值得大力推广的治疗方式。     

阿仑膦酸钠治疗糖尿病合并骨质疏松的临床疗效分析

目的探究阿仑膦酸钠治疗糖尿病合并骨质疏松的临床疗效,并分析其应用价值。方法选取在2012年3月—2013年7月期间该院收治的92例糖尿病合并骨质疏松患者作为研究对象,用阿仑膦酸钠对所有患者进行治疗,7个月后观察实验小组的骨密度值以及治疗前后血钙、血磷的水平值,以及患者的不良反应情况。结果从实验结果可得,治疗后患者的骨密度值得到了良好的改善,差异有统计学意义(P0.05);患者血钙、血磷的变化量不大,差异无统计学意义(P0.05),少部分患者出现不良反应现象。结论阿仑膦酸钠治疗糖尿病合并骨质疏松具有良好的临床治疗效果,明显改善了患者骨质疏松的临床症状,值得广泛推广。     

Changes in serum levels of type I collagen-related proteins after surgically induced menopause and correlations with bone loss in the lumbar spine.

The purpose of this prospective study was to characterize the changes in serum levels of two proteins produced during the synthesis and degradation of type I collagen, i.e., the carboxyterminal propeptide of type I procollagen (PICP) and the pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP), respectively, after oophorectomy, and to assess the degree of correlation between changes in the serum values of these proteins and changes in bone mineral density (BMD) of the lumbar spine. Serum levels of PICP, ICTP and bone gla protein (BGP) were determined in 18 women before oophorectomy (baseline) and at 7 days, and 1, 2, 3, 6, 9 and 12 months post-oophorectomy (PO). The BMD of the lumbar spine was measured at baseline, and at 6 months and 12 months PO. ICTP had increased significantly at 7 days PO and peaked between 1 and 3 months PO. PICP and BGP had increased significantly at 2 months PO and remained at high levels thereafter. The percent changes in lumbar BMD from baseline values (% CFB) at 6 months and at 12 months PO were significantly correlated with % CFB in ICTP, but not with % CFB in PICP or BGP. Accordingly, bone resorption is a main determinant of bone mineral loss after oophorectomy and the change in recently-developed bone resorption markers, such as ICTP, is of clinical utility in predicting a degree of subsequent bone loss after surgical menopause.     

Effects of alendronate and hormone replacement therapy, alone and in combination, on bone mass and markers of bone turnover in elderly women with osteoporosis

The aim of the study was to compare alendronate, hormone replacement therapy (HRT), and their combination in treatment of osteoporosis in elderly postmenopausal women. Ninety patients, aged 65-80 yr (mean 71), with a T-score of bone mineral density (BMD) of 2.5 or less at either the lumbar spine or the femoral neck were randomized to receive daily 10 mg alendronate (n = 30), 2 mg estradiol plus 1 mg norethisterone acetate (n = 30) (HRT), or their combination (n = 30) for 2 yr. BMD of the lumbar spine and the upper femur was measured at baseline and after 1 and 2 yr of treatment. Urinary excretion of type I collagen aminoterminal telopeptide as related to creatinine and serum type I procollagen aminoterminal propeptide was assayed at baseline and at 6-month intervals thereafter. Increases of 9.1-11.2% in lumbar spine BMD at 2 yr were similar in the study groups. Only HRT increased femoral neck BMD statistically significantly (P < 0.0001 for a change from baseline) at both 1 (+4.9%; P =NS vs. the other groups) and 2 yr (+5.8%; P < 0.05 vs. the other groups). Total hip BMD increased similarly in all study groups. Percentage reductions in urinary type I collagen aminoterminal telopeptide in the HRT group (60.2-62.7%) were significantly smaller than those in the combination group (78.1-80.4%) (P < 0.0001-0.0069) and the alendronate-only group (72.4-76.1%) (P = 0.047 at 24 months). Serum type I procollagen aminoterminal propeptide decreased less in the HRT group (53.6-59.8%) than in the other groups [73.0-75.0% in the alendronate group (P < 0.001 at 12 months); 67.0-71.5% in the combination group (P < 0.0001 at 12 months, P = 0.013 at 24 months)]. We conclude that in elderly postmenopausal women with osteoporosis, the combination of HRT and alendronate did not offer an extra gain of bone mass over either treatment alone. In terms of BMD changes, the single treatments were equally effective, but the reductions in bone markers were less with HRT than with alendronate.     

The effect of raloxifene after discontinuation of long-term alendronate treatment of postmenopausal osteoporosis

OBJECTIVE: The aim of this study was to compare bone mineral density (BMD) and biochemical markers of bone turnover in patients receiving long-term alendronate therapy who continued alendronate, were switched to raloxifene, or discontinued antiresorptive therapy. DESIGN, PATIENTS, AND INTERVENTIONS: Ninety-nine ambulatory women who were diagnosed with postmenopausal osteoporosis and treated with alendronate (10 mg/d) for a mean period of 43 months were randomized to double-blind raloxifene (60 mg/d; n = 33), placebo (n = 33), or continuation of open-label alendronate (n = 33) for 12 months. Patients continued their assigned treatment in a subsequent 12-month, open-label extension phase. All patients received supplemental calcium (500 mg/d) and vitamin D (800 IU/d). MAIN OUTCOME MEASURES: BMD (lumbar spine, total femur, femoral neck, distal forearm, and total body) and biochemical markers (serum intact amino-terminal propeptide of type I procollagen, type 1 collagen cross-linked C-telopeptide, and osteocalcin) were measured at baseline and follow-up visits. RESULTS: Discontinuation of alendronate therapy resulted in a decrease in lumbar spine BMD at 12 months (-2.66%; P < 0.05), but did not change total femur BMD (+0.35%; nonsignificant). Raloxifene and alendronate, compared with discontinuation, prevented lumbar spine BMD loss (-0.75% and -0.54% at 12 months, respectively; P < 0.05). Raloxifene and alendronate caused a similar increase in total femur BMD at 12 months (1.45% and 1.56%; both P < 0.05 vs. baseline; nonsignificant vs. discontinuation). Patients, who discontinued alendronate therapy experienced an increase in bone turnover. Bone turnover increases were less pronounced in patients taking raloxifene and were absent in those who continued alendronate. Of the three groups, mean bone turnover in raloxifene patients was the closest to premenopausal mean values. CONCLUSIONS: BMD preservation and increase were most pronounced in patients continuing alendronate. Raloxifene treatment, compared with placebo, demonstrated beneficial effects on BMD and bone turnover after discontinuation of long-term alendronate therapy.     

Effects of alendronate on bone mineral density and bone metabolic markers in postmenopausal asthmatic women treated with inhaled corticosteroids

We have recently shown that long-term use of inhaled corticosteroids decreases bone mineral density (BMD) of the lumbar spine in postmenopausal asthmatic women. The present study aimed to evaluate the efficacy of alendronate in comparison with that of alfacalcidol (1-alpha-hydroxyvitamin D(3)) for the treatment of BMD reduction in postmenopausal asthmatic patients who had inhaled corticosteroid therapy without regular use of systemic corticosteroids. Twenty-eight postmenopausal asthmatic patients with BMD T score of -1.0 or less were randomized to receive alendronate (5 mg/d) or alfacalcidol (1 microg/d). Bone mineral density was determined at baseline and 12 months after the treatment, and biochemical markers of bone metabolism were measured at baseline and after 6 and 12 months of treatment. The mean (+/-SD) BMD values at the lumbar spine, the total hip, and the Ward's triangle significantly increased by 4.9 +/- 4.5% (P = .0005), 2.4 +/- 2.2% (P = .0005), and 3.6 +/- 5.2% (P = .02) at 12 months in the alendronate group, whereas the corresponding values did not significantly change in the alfacalcidol group. In the alendronate group, urinary N-telopeptide (NTx), serum osteocalcin, and serum alkaline phosphatase concentrations significantly decreased, and serum intact parathyroid (PTH) level significantly increased, from baseline at both 6 and 12 months. In the alfacalcidol group, urinary NTx showed modest but significant decrease, although the extent of the change was smaller than that in the alendronate group. We concluded that alendronate was effective to improve reduced BMD in postmenopausal asthmatic patients on inhaled corticosteroid therapy through the mechanism of inhibiting bone resorption.     

Comparison of alendronate and intranasal calcitonin for treatment of osteoporosis in postmenopausal women

This study compared the effects of oral alendronate and intranasal calcitonin for treatment of osteoporosis in postmenopausal women. Women at least 5 yr postmenopause (n = 299) were randomized to either 10 mg alendronate, matching alendronate placebo, or open-label intranasal calcitonin 200 IU daily for 12 months. Hip and spine bone mineral density (BMD) and markers of bone turnover were measured, and safety and tolerability were assessed. Alendronate produced greater increases in BMD than calcitonin at 12 months at the lumbar spine (5.16% vs. 1.18%; P < 0.001), trochanter (4.73% vs. 0.47%; P < 0.001), and femoral neck (2.78% vs. 0.58%; P < 0.001). Changes in BMD with calcitonin were greater than with placebo at the femoral neck, but were not different from placebo at either the trochanter or lumbar spine. Greater decreases in bone turnover were seen with alendronate than with calcitonin (serum bone-specific alkaline phosphatase, 43% vs. 9%, P < 0.001; urinary N-telopeptide, 62% vs. 11%, P < 0.001). Similar percentages of patients in each group reported an adverse experience during the study. We conclude that, in postmenopausal women with osteoporosis, 12 months of therapy with alendronate produced significantly greater increases in BMD of the hip and spine and greater decreases in bone turnover than intranasal calcitonin.     

Age-related changes in bone mineral density and serum bone-related proteins in premenopausal and postmenopausal Japanese women

The purpose of this cross-sectional study was to characterize the age-related change in bone metabolism during the pre- and postmenopausal periods, and to define the standard levels of three serum markers of bone metabolism, pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP), carboxyterminal propeptide of type I procollagen (PICP), and bone gla protein (BGP), in Japanese adult women. The bone mineral density (BMD) of the lumbar spine (L2-L4) and the serum levels of ICTP, PICP and BGP were determined in a total of 207 healthy Japanese women (108 premenopausal and 99 postmenopausal). The lumbar BMD decreased significantly with increasing age not only in postmenopausal women (P<0.001) but also in premenopausal women (P=0.014). There was a clear gap in the serum levels of ICTP, PICP and BGP between the premenopausal and postmenopausal group (P<0.001), but those were absolutely the same within each group except for ICTP in the postmenopausal women. These findings and the values of serum ICTP, PICP and BGP in pre- and postmenopausal women obtained in this study are expected to be very useful for treatment of postmenopausal osteoporosis.     

Prolactinomas in adolescents: persistent bone loss after 2 years of prolactin normalization

OBJECTIVE: To evaluate the effect of hyperprolactinaemia and its treatment with dopamine-agonists on bone mass and turnover in adolescent patients compared to adults. PATIENTS: Forty patients with hyperprolactinaemia (20 with disease onset during adolescence and 20 during adulthood) and 40 healthy control subjects. DESIGN: Open transverse (in patients and controls) and open longitudinal (in the patients). MEASUREMENTS: Bone mineral density (BMD) at lumbar spine and femoral neck, serum osteocalcin (OC) and urinary cross-linked N-telopeptides of type-1 collagen (Ntx) levels were evaluated in patients and controls. In the 40 patients, bone mass and turnover were re-evaluated after 12 and 24 months of treatment with bromocriptine (BRC, dose 2.5-10 mg daily), quinagolide (CV, dose 0.075-0.3 mg daily) or cabergoline (CAB, dose 0.5-1.5 mg weekly). RESULTS: Transverse study: BMD values were significantly lower in hyperprolactinaemic patients than in controls, both at lumbar spine (0.81 +/- 0.01 vs. 1.010 +/- 0.01 g/cm2; P < 0.001) and femoral neck (0.71 +/- 0.01 vs. 0.873 +/- 0.03 g/cm2; P < 0.001). Thirty-two patients (80%) had osteoporosis and/or osteopenia at one or both skeletal sites. A significant inverse correlation was found between T score values measured at lumbar spine and femoral neck and the estimated disease duration. BMD was significantly lower in young than adult patients both at lumbar spine (T score, -2.4 +/- 0.1 vs. -1.4 +/- 0.3, P < 0.01) and at femoral neck (T score, -2.1 +/- 0.05 vs. -1.5 +/- 0.2, P < 0.05). Similarly, serum OC levels were significantly lower (2.0 +/- 0.11 vs. 9.1 +/- 2.4 micrograms/l, P < 0. 01) while Ntx levels were significantly higher in patients than in controls (129.2 +/- 1.7 vs. 80.7 +/- 2.9 nmol Bone collagen equivalent (BCE)/mmol creatinine; P < 0.001). A significant inverse correlation was found between prolactin (PRL) levels and OC levels, lumbar and femoral T score values, as well as between disease duration and OC levels, lumbar and femoral T score values. A significant direct correlation was also found between Ntx levels and PRL levels and disease duration. Longitudinal study: Normalization of serum PRL levels was obtained in all patients after 6-12 months of treatment. A significant increase of serum OC levels together with a significant decrease of Ntx levels was observed after 12 and 24 months of treatment (P < 0.01). Urinary and serum calcium, phosphorus, creatinine, and serum alkaline phosphatase and parathyroid hormone levels did not change during the study period in all patients. After 12 months of therapy OC and Ntx concentrations were restored to normal. A slight but not significant increase of BMD values was recorded after 12 and 24 months of treatment. After 12 months of treatment the percent increment of BMD values in the whole group of patients was 1.13 +/- 0.6% at lumbar spine and 1.2 +/- 0.4% at femoral neck level, whereas after 24 months, it was 2.8 +/- 0.7% at lumbar spine and 3.5 +/- 0.7% at femoral neck level. After 12 months of treatment, the percent increment of BMD values was 0.7 +/- 0.2% and 1.6 +/- 1.1% at lumbar spine and 0.9 +/- 0.5% and 1.6 +/- 0.5% at femoral neck level in the young and adult patients, respectively, whereas after 24 months, it was 2.1 +/- 0.8% and 3.4 +/- 1.3% at lumbar spine and 2.6 +/- 0.8% and 4.4 +/- 1.0% at femoral neck level in the young and adult patients, respectively. CONCLUSIONS: Adolescents with prolactinoma have osteopenia or osteoporosis, a finding that strengthens the need for a prompt diagnosis. Since normalization of PRL concentrations by dopamine agonist therapy is unable to restore the bone mass, other therapeutic approaches should be considered in order to prevent further long-term problems.     

Comparison of weekly treatment of postmenopausal osteoporosis with alendronate versus risedronate over two years

OBJECTIVE: A 1-yr extension of the Fosamax Actonel Comparison Trial was completed to compare changes in bone mineral density (BMD), bone turnover, and upper gastrointestinal tolerability over 2 yr of treatment. DESIGN: This was a randomized, double-blind extension conducted at 72 U.S. sites. PATIENTS AND METHODS: Of the 1053 women who completed yr 1, 833 postmenopausal women with low BMD entered the extension, continuing their same treatment allocation [once-weekly (OW) alendronate 70 mg or OW risedronate 35 mg]. Changes in BMD at the hip trochanter, total hip, femoral neck, and lumbar spine and in markers of bone turnover were compared at 24 months. Tolerability was assessed by adverse experience reporting. RESULTS: Alendronate produced greater increases from baseline in BMD at 24 months than did risedronate at the trochanter (alendronate, 4.6%; risedronate, 2.5%, P < 0.001) as well as at all other BMD sites. Significantly more alendronate than risedronate patients had measured BMD increases of 0% or more and 3% or more at all BMD sites (P < 0.001), and fewer alendronate patients had measured decreases of 3% or more at all BMD sites. Significantly greater reductions in all biochemical markers of bone turnover occurred with alendronate, compared with risedronate. No differences were seen in occurrence or discontinuations due to upper gastrointestinal adverse experiences. CONCLUSIONS: Patients receiving 70 mg OW alendronate had greater gains in BMD, were more likely to maintain or gain BMD, and had greater reductions in bone turnover markers than patients receiving 35 mg OW risedronate after 24 months, with no differences in upper gastrointestinal tolerability.     

Alendronate in primary hyperparathyroidism: a double-blind, randomized, placebo-controlled trial

Primary hyperparathyroidism (PHPT) is often associated with reduced bone mineral density (BMD). A randomized, double-blind, placebo-controlled trial was conducted to determine whether alendronate (ALN), 10 mg daily, maintains or improves BMD in patients with PHPT. Eligible patients had asymptomatic PHPT and did not meet surgical guidelines or refused surgery. Forty-four patients randomized to placebo or active treatment arms were stratified for gender. At 12 months, patients taking placebo crossed over to active treatment. All patients were on active treatment in yr 2. The primary outcome index, BMD, at the lumbar spine (LS), femoral neck, total hip, and distal one third radius was measured every 6 months by dual-energy x-ray absorptiometry. Calcium, phosphorous, PTH, bone-specific alkaline phosphatase (BSAP) activity, urinary calcium, and urinary N-telopeptide (NTX) excretion were monitored every 3 months. Treatment with alendronate over 2 yr was associated with a significant (6.85%; micro(d) = 0.052; +/-0.94% se; P < 0.001) increase in LS BMD in comparison with baseline. Total hip BMD increased significantly at 12 months with alendronate by 4.01% (micro(d) = 0.027; +/-0.77% se; P < 0.001) from baseline and remained stable over the next 12 months of therapy. BMD at the one third radius site did not show any statistically significant change in the alendronate-treated group at 12 or 24 months of therapy. At 24 months, the alendronate-treated group showed a 3.67% (micro(d) = 0.022; +/-1.63% se; P = 0.038) gain in bone density at the femoral neck site in comparison with baseline. The placebo group, when crossed over to alendronate at 12 months, showed a significant change of 4.1% (micro(d) = 0.034; +/-1.12% se; P = 0.003) in the LS BMD and 1.7% (micro(d) = 0.012; +/-0.81% se; P = 0.009) at the total hip site in comparison with baseline. There was no statistically significant change seen in the placebo group at 12 months at any BMD site and no significant change at 24 months for the distal one third radius or femoral neck sites. Alendronate was associated with marked reductions in bone turnover markers with rapid decreases in urinary NTX excretion by 66% (micro(d) = -60.27; +/-13.5% se; P < 0.001) at 3 months and decreases in BSAP by 49% at 6 months (micro(d) = -15.98; +/-6.32% se; P < 0.001) and by 53% at 9 and 12 months (micro(d) = -17.11; +/-7.85% se; P < 0.001; micro(d) = -17.36; +/-6.96% se; P < 0.001, respectively) of therapy. In the placebo group, NTX and BSAP levels remained elevated. Serum calcium (total and ionized), PTH, and urine calcium did not change with alendronate therapy. In PHPT, alendronate significantly increases BMD at the LS at 12 and 24 months from baseline values. Significant reductions in bone turnover occur with stable serum calcium and PTH levels. Alendronate may be a useful alternative to parathyroidectomy in asymptomatic PHPT among those with low BMD.     

Effects of 12-month GH treatment on bone metabolism and bone mineral density in adults with adult-onset GH deficiency

Serum bone-Gla protein (BGP), bone alkaline phosphatase (B-AP), and C-terminal cross-linked telopeptide of type I collagen (ICTP) levels were evaluated in 18 adults with acquired GH deficiency (GHD, 14 males and 4 females, age range: 25-59 yr) before, at 3, 6, 9 and 12 months of rec-GH treatment (0.125 IU/kg/week for the first month, followed by 0.25 IU/kg/week for 11 months) and 6 months after the withdrawal of therapy. Total body bone mineral density (BMD, g/cm2) was measured with dual energy X-ray absorptiometry (Hologic QDR 1000/W) before, at 12 months of GH treatment and 6 months after its withdrawal. Before treatment, BGP (mean+/-SE: 5.1+/-0.4 ng/ml), B-AP (59.4+/-6.5 IU/l), ICTP (3.1+/-0.3 ng/ml) levels of patients were similar to in healthy controls (BGP: 5.4+/-0.1 ng/ml; B-AP: 58.2+/-2.0 IU/l; ICTP: 4.1+/-0.3 ng/ml). GH treatment caused a significant increase of BGP, B-AP, ICTP levels, the maximal stimulation of bone resorption, occurring after 3 months of GH treatment, while the maximal effect on bone formation being evident later (at 6th month). A slight decline in BGP, B-AP, T-AP and ICTP levels occurred at 9-12 months of therapy, although the values remained significantly higher than in basal conditions and with respect to healthy controls. Before treatment, mean total body BMD of patients (1.110+/-0.027 g/cm2, range: 0.944-1.350 g/cm2) was not significantly different (z-score: +0.47+/-0.31, NS) from that observed in healthy controls (1.065+/-0.008 g/cm2, range: 1.008-1.121 g/cm2). GH therapy was associated with a significant reduction of mean total body BMD values (6th month: -1.8+/-0.5%, p<0.01; 12th month: -2.1+/-1.0%, p<0.05 vs baseline), particularly evident in the first six months of treatment. Six months after the withdrawal of GH therapy, BGP (5.9+/-0.5 ng/ml), B-AP (57.3+/-7.0 IU/l) and ICTP (3.2+/-0.1 ng/ml) levels returned similar to those recorded before treatment, while total BMD increased (+1.5+/-0.7, p<0.05), remaining however slightly lower than in basal conditions (-0.6+/-1.2, NS). In conclusion, our study shows that: a) acquired GHD in adulthood is associated with both normal bone formation/resorption indexes and normal total body BMD; b) GH therapy causes a significant rise of bone formation/resorption markers (earlier and greater for bone resorption); c) one-year GH therapy is associated with a reduction of total body BMD values, particularly evident in the first 6 months of treatment; d) the effects of GH therapy on bone turnover are transient, being completely reverted six months after the withdrawal of GH therapy; e) the increase of total body BMD (up to baseline values) after GH withdrawal might be explained as consequence of persisting effects of previous GH stimulation on bone remodeling.