Effects of raloxifene hydrochloride on bone mineral density, bone metabolism and serum lipids in Chinese postmenopausal women with osteoporosis: a multi-center, randomized, placebo-controlled clinical trial / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Raloxifene has been approved for prevention and treatment of postmenopausal osteoporosis in Caucasian women. It also has some positive effects on serum lipids in Caucasians. The objective of this study was to determine the effect of raloxifene hydrochloride on lumbar spine and total hip bone mineral density (BMD), bone metabolism, and serum lipids in Chinese postmenopausal women with osteoporosis.</p><p><b>METHODS</b>This was a multi-center, randomized, double-blind, placebo-controlled clinical trial in which 204 postmenopausal Chinese women with osteoporosis were assigned to receive raloxifene (60 mg) or placebo treatment daily for 12 months. BMD, serum bone metabolism markers, and serum lipids were measured before and after drug administration. BMD was measured by Dual-Energy X-Ray Absorptiometry (DEXA) and bone metabolism markers were analyzed by one-step enzyme-linked immunosorbent assay. Serum lipids were measured by enzymatic analysis.</p><p><b>RESULTS</b>At the end of the 12-month study, lumbar spine BMD increased in both groups with a mean increase of (3.3 +/- 4.8)% in the raloxifene group and (1.0 +/- 4.9)% in the placebo group (P < 0.001). There was a mean increase in total hip BMD of (1.4 +/- 4.8)% in the raloxifene group and a mean decrease of (0.9 +/- 5.0)% in the placebo group (P < 0.001). No subject in the raloxifene group had a new vertebral fracture and 5 placebo subjects had new fractures (P > 0.05). In the raloxifene group, the median decreases in the biochemical markers of bone metabolism serum osteocalcin and C-telopeptide were 41.7% and 61.5%, respectively. These changes were statistically significant compared with those in the placebo group (10.6% and 35.6%, P < 0.001, respectively). Both total cholesterol and low-density lipoprotein cholesterol decreased significantly in the raloxifene group compared with those in the placebo group (P < 0.001, respectively) and there was no significant effect of raloxifene on high-density lipoprotein cholesterol and triglycerides compared with placebo.</p><p><b>CONCLUSIONS</b>Raloxifene 60 mg/d for 12 months significantly increases lumbar spine and total hip BMD, significantly decreases bone turnover, and has favourable effects on serum lipids in Chinese postmenopausal women with osteoporosis.</p>

Influence of androgen and estrogen deprivation therapy on bone metabolism and bone mineral density in men with prostate cancer / 中华老年医学杂志

Objective To investigate the effects of castration treatment by luteinizing hormonereleasing hormone(LHRH)analog(goserelin)on bone loss and bone resorption in men with prostate cancer.Methods Serum sex hormones,bone mineral density(BMD),serum and urine concentrations of bone turnover markers were determined in men with prostate cancer(n=36) and in age-matched controls(n=13).BMD in the lumbar spine(L2-4),femoral neck,trochanter,Ward's triangle and total femoral was determined by dual energy X-ray absorptiometry(DEXA).Results After 12 months of LHTH analog therapy,the BMD of the femoral neck,total femoral and Ward's triangle decreased significantly in men with prostate cancer compared with the controls,all P＜0.05. No significant bone loss was observed in the control subjects.The concentrations of the serum markers of bone formation,i.e.bone alkaline phosphatase(BALP),and urine markers of bone resorption,i. e.DPD,Cros,Ca/Cr were significantly increased in patients treated with LHRH analog compared with control subjects,all P＜0.05,respectively.Conclusions These findings demonstrate that a significant increase of bone turnover and loss of bone mass in men with prostate cancer after receiving LHRH analog therapy were correlated with the decreased levels of serum androgen and estrogen,and suggest that measuring BMD by DEXA and assesing the bone turnover markers can early detect the bone loss and osteoporosit induced by goserelin castration treatment.