Management of male osteoporosis

The objective of this study was to evaluate the efficacy of treatments for male osteoporosis selected based on the cause of the disease. METHODS: Sixty-three men with osteoporosis (T-score at the lumbar spine and/or femoral neck lower than -2.5) with a mean age of 53+/-11 years were studied. Forty-three (68.3%) had a history of fracturing without trauma (vertebral fractures, 37 patients, 57%). Treatments were as follows: idiopathic osteoporosis: calcium and vitamin D supplements (N = 10) or cyclical etidronate for 2 weeks followed by calcium and vitamin D supplements for 76 days (N = 29); moderate idiopathic phosphate diabetes: calcitriol and phosphate (N = 15); idiopathic hypercalciuria: hydrochlorothiazide (N = 6); and hypogonadism: testosterone (N = 3). RESULTS: Percentage change in bone mineral density (mean +/- standard error of the mean) after 18 months: calcium and vitamin D (lumbar spine: 0.6+/-2; femoral neck: 2.2+/-2.2); etidronate (lumbar spine: 3.6+/-1.4*; femoral neck: 0.5+/-1); calcitriol (lumbar spine: 7.0+/-3.5*; femoral neck: 0.0+/-1.4); thiazide diuretic (lumbar spine: 1+/-3.2; femoral neck: -2.3+/-3.7); and testosterone (lumbar spine: 6.8+/-6.4; femoral neck: 2.5+/-2.7), where *P < 0.05 versus baseline. Gastrointestinal side effects occurred in three patients (4.8%), including two on calcitriol-phosphate therapy and one on etidronate therapy. Of the six (9.5%) patients who experienced incident fractures, four were on etidronate, one on calcitriol-phosphate, and one on calcium-vitamin D. No patients discontinued their treatment because of side effects. CONCLUSION: Etidronate and the combination of calcitriol-phosphate produce a significant increase in lumbar spine bone mass in men with idiopathic osteoporosis or moderate idiopathic phosphate diabetes.     

Preventive effect of risedronate on bone loss and frailty fractures in elderly women treated with anastrozole for early breast cancer

The aim of this study was to assess the effect of adjuvant anastrozole, alone or associated with risedronate, on BMD and bone fracture risk in women more than 70 years old with hormone receptor-positive early breast cancer (EBC). In a group of 51 elderly women (aged 76.4 ± 5.0 years) considered for adjuvant aromatase inhibitors for EBC, 24 patients with T-scores ≥ -2 and no prevalent fractures received anastrozole 1 mg/day (group A), and 27 patients with T-scores < -2, or with T-scores ≥ -2 and prevalent fractures (group B), received anastrozole (1 mg/day) plus risedronate (35 mg/week). Both groups received supplementation with 1 g calcium carbonate and 800 IU vitamin D per day. Differences in BMD and frailty fractures were evaluated after 1 and 2 years. In group A, significant decreases in BMD were observed in the lumbar spine (Δ BMD, -0.030 ± 0.04 g/cm(2), P < 0.05), femoral neck (Δ BMD, -0.029 ± 0.05 g/cm(2), P < 0.05), and trochanter (Δ BMD, -0.026 ± 0.03 g/cm(2), P < 0.01) after 2 years. The greatest percent reduction in height (Hpr) emerged in the thoracic spine (3.6 ± 2.4%, P < 0.01), although only one incident vertebral fracture was observed. In group B, BMD increased in the lumbar spine (Δ BMD, 0.038 ± 0.04, P < 0.001), although no significant changes were seen in the hip regions. The decline in Hpr was negligible (about 1%). No incident fractures were observed at follow-up. In conclusion, anastrozole treatment for EBC in elderly women seems to have only mild negative effects on the femoral bone. Risedronate makes the use of anastrozole safer, even for osteopenic or osteoporotic elderly patients.     

Clodronate reduces vertebral fracture risk in women with postmenopausal or secondary osteoporosis: results of a double-blind, placebo-controlled 3-year study.

The efficacy of oral clodronate 800 mg daily to reduce vertebral fractures was studied in 593 women with postmenopausal or secondary osteoporosis. The incidence of vertebral fractures was significantly reduced by 46%. The effect was not modified by the underlying cause of osteoporosis or other baseline factors including bone mineral density, QUS, weight, and smoking. INTRODUCTION: This study aimed to determine if the bisphosphonate, clodronate (Bonefos), reduced the incidence of vertebral fractures in osteoporotic women. MATERIALS AND METHODS: Women fulfilling the WHO criteria for osteoporosis at the lumbar spine (T-score 相似文献   

Fracture site-specific deficits in bone size and volumetric density in men with spine or hip fractures.

To study the structural basis of bone fragility in men, we compared bone size and volumetric bone mineral density (vBMD) of the third lumbar vertebra and femoral neck in 95 men with spine fractures, 127 men with hip fractures, and 395 healthy controls using dual-energy X-ray absorptiometry (DXA). The results were expressed in absolute terms and age-specific SD scores (mean +/- SEM). In controls, vertebral body and femoral neck width increased across age, being 0.46 +/- 0.11 SD and 0.91 +/- 0.08 SD higher in elderly men than in young men, respectively (both,p < 0.001). Men with spine fractures had reduced vertebral body width (-0.45 +/- 0.10 SD;p < 0.01) but not femoral neck width (-0.15 +/- 0.10 SD, NS). Men with hip fractures had reduced femoral neck width (-0.45 +/- 0.11 SD; p < 0.01) and vertebral body width (-0.25 +/- 0.10 SD; p < 0.05). The deficits in bone volume (BV) exaggerated the deficits in bone mineral content (BMC) by 40% at the vertebrae in men with spine fractures and by 9% at the femoral neck in men with hip fractures. vBMD deficits were greater at the vertebrae in men with spine fractures than in men with hip fractures (-1.37 +/- 0.08 SD vs.-0.70 +/- 0.10 SD, respectively; p < 0.01) but were similar at the femoral neck (-0.93 +/- 0.10 SD and -0.76 +/- 0.11 SD, respectively, NS), despite the men with spine fracture being 10 years younger. Bone fragility leading to spine or hip fractures in men may be the result of fracture site-specific deficits in bone size and vBMD that have their origins in growth, aging, or both.     

Treatment of Glucocorticoid-Induced Osteoporosis with Alfacalcidol/Calcium Versus Vitamin D/Calcium

Vitamin D/calcium substitution is generally regarded as an effective first step treatment for glucocorticoid-induced osteoporosis (GIOP). The aim of our study was to evaluate the efficacy of the active vitamin D metabolite alfacalcidol (1α) compared with the native vitamin D₃ in patients with established GIOP with or without vertebral fractures. Patients on long-term corticoid therapy were given either 1 μg alfacalcidol plus 500 mg calcium per day (group A, n = 43) or 1000 IU vitamin D₃ plus 500 mg calcium (group B, n = 42). The two groups were alike in age range, sex ratio, percentages of underlying diseases, average initial bone density values (lumbar spine: mean T-score −3.28 and −3.25, respectively), and rates of vertebral and nonvertebral fractures. During the 3-year study we found a small but significant increase of lumbar spine density in group 1α (+2.0%, P < 0.0001) and no significant changes at the femoral neck. In the D₃ group, there were no significant changes at both sites. At the end of the study, 12 new vertebral fractures had occurred in 10 patients of the group 1α and 21 in 17 patients of the D₃ group. In accordance with the observed fracture rates, the alfacalcidol group showed a significant decrease in back pain (P < 0.0001) whereas no change was seen in the vitamin D group. We conclude that with the doses used in this trial, alfacalcidol is superior to vitamin D in the treatment of established GIOP.     

Prevalence of osteoporosis, osteopenia, and vertebral fractures in long-term renal transplant recipients

BACKGROUND: Osteopenia and osteoporosis are frequent complications early after transplantation. Their long-term prevalences and associations with the risk of fractures are not well known. The objective of the present work was to determine the incidence of osteopenia and osteoporosis versus vertebral fractures in renal transplant recipients with stable graft function and with a follow-up of at least 10 years. PATIENTS AND METHODS: Forty renal transplant recipients, 24 men and 16 women, were included in the study. The mean age was 41.8 years and the follow-up was 130 +/- 14 months. Initial immunosuppression consisted of cyclosporine with or without an antiproliferative agent. Measurements of bone mass density (BMD) were performed by dual-energy X-ray absorptiometry (DEXA). The assessment of vertebral fracture using conventional radiography was evaluated by semiquantitative criteria. RESULTS: Eleven patients (27.5%) displayed lumbar spine osteoporosis (T-score < -2.5); 21 (52.5%), osteopenia (T-score > -2.5 and < -1) and 8 (20.0%), normal BMD. However, BMD was better preserved at the femoral neck: 14 patients (35.0%) had normal BMD; 20 (50.0%) osteopenia, and 6 (15.0%), osteoporosis. When analyzed together, patients with osteoporosis or osteopenia showed worse graft function at 1 and 8 years compared with normal BMD patients (1.75 +/- 0.634 vs 1.32 +/- 0.33 mg/dL at 1 year; P < .014) and (1.7 +/- 0.4 vs 1.2 +/- 0.2 mg/dL at 5 years; P < .01) and a greater number were prescribed vitamin D (50% vs 23%). Mild vertebral fractures were observed in 60.0% patients with osteoporosis; 70% with osteopenia; and 43% with normal lumbar BMD. Peripheral fractures were more common in patients with osteoporosis (P = .053). CONCLUSIONS: Osteoporosis and osteopenia are common among long-term renal transplant recipients are associated with poorer graft function. Lumbar spine BMD osteoporosis is associated with peripheral fractures. However, mild vertebral deformities are not associated with the presence of osteopenia or osteoporosis.     

The effects of three-month intravenous ibandronate on bone mineral density and bone remodeling in Klinefelter's syndrome: the influence of vitamin D deficiency and hormonal status

The aim of this study was to evaluate the effects of a 2-year treatment with intravenous ibandronate (2 mg every 3 months) and calcium (1000 mg daily) on bone mineral density (BMD) and bone markers in 14 patients with Klinefelter's syndrome who served as their own controls. During the follow-up of 5.9 years before the treatment was started, the mean rates of bone loss per year were 1.3, 0.9, and 0.6% in the lumbar spine, femoral neck, and total body, respectively. The rate of bone loss from the spine was significantly inversely related to both serum estradiol and testosterone. At the onset of treatment, the average age of the patients was 55.2 years (48-64 years), and T score, mean +/- SD, at the lumbar spine was -2.6 +/- 1.0. After 6 months, the mean serum CTX and PINP decreased by 39 and 55% below the pretreatment concentrations, respectively (P < 0.05). After 12 months of treatment, the patients gained mean +/- SD, 7.8 +/- 2.3% of BMD in the lumbar spine, 3.8 +/- 4.0% in the femoral neck, and 4.7 +/- 2.2% in the total body (P < 0.05). During the second year of treatment, all patients also received 700 IU of vitamin D daily. After 24 months of treatment, the patients gained 10.1 +/- 4.3% of BMD in the lumbar spine, 6.7 +/- 5.5% in the femoral neck, and 5.5 +/- 2.5% in the total body. The increase in BMD in the second year of ibandronate treatment was not significant. The rate of gain of BMD in the femoral neck was positively related to serum concentrations of testosterone and inversely related to 25-hydroxyvitamin D (P < 0.005). After the discontinuation of treatment, serum CTX and PINP increased to the pretreatment levels, and the lumbar spine and femur neck BMD decreased (P < 0.05). In conclusion, ibandronate was effective in increasing BMD at all sites, but the effects were adversely influenced by vitamin D insufficiency or deficiency. The overall changes in biochemical markers of bone remodeling were consistent with the antiresorptive effect of the drug.     

Treatment with vitamin D and calcium reduces bone loss after renal transplantation: a randomized study

A decrease in bone mineral density (BMD) is a major complication of renal transplantation (RTx), predominantly occurring within the first 6 mo after RTx. The most important causative factor is the use of corticosteroids, but persisting hyperparathyroidism and abnormalities in vitamin D metabolism play a role too. This study examines the effect of treatment with calcium and active vitamin D on the loss of BMD in the first 6 mo after RTx. A total of 111 renal transplant recipients (65 men, 46 women; age, 47 +/- 13 yr) were randomized to either treatment with active vitamin D (0.25 microg/d) plus calcium (1000 mg/d) (CaD group), or to no treatment (NoT group). Immunosuppressive therapy consisted of cyclosporine, prednisone, and mycophenolate mofetil. Laboratory parameters and BMD (lumbar spine and hip) were measured at 0, 1 (laboratory only), 3, and 6 mo after RTx. Lumbar BMD was nearly normal at the time of RTx. In both groups, a significant decrease in lumbar BMD was observed during the first 3 mo (CaD, -3.3 +/- 4.3%; P < 0.0001; NoT, -4.1 +/- 4.8%; P < 0.0001). Between the third day and sixth month, lumbar BMD slightly recovered in the CaD group, but it decreased further in the NoT group (total loss 0 to 6 mo: CaD, -2.6 +/- 5.0% [P < 0.001]; NoT, -5.0 +/- 4.7% [P < 0.0001]). As a result, the amount of bone loss at 6 mo was significantly lower in the CaD group (P = 0.02). Loss of BMD at the different femoral sites was also significantly reduced in the CaD group. Apart from a trend toward more frequent hypercalcemia in the CaD group, no clinical or biochemical differences existed between the groups. Treatment with a low dose of active vitamin D and calcium partially prevents bone loss at the lumbar spine and proximal femur during the first 6 mo after RTx.     

Glucocorticoid-induced osteoporosis: is the bone density decrease the only explanation?

BACKGROUND: Glucocorticoids may increase bone fragility via mechanisms independent from their bone mass reducing effect. OBJECTIVE: To study relationships between osteoporotic fractures and bone mineral density in patients on long-term glucocorticoid therapy. PATIENTS AND METHODS: We studied 121 women with a mean age of 60.4 +/- 14.3 years on long-term glucocorticoid therapy (cumulative dose > or = 1 g of prednisone equivalent, duration > or = 6 months) for rheumatoid arthritis (n = 38), polymyalgia rheumatica or giant cell arteritis (n = 26), connective tissue disease (n = 15), asthma (n = 14), another inflammatory joint disease (n = 14), or another condition (n = 14). The control group was composed of 125 subjects who had the same mean age and met the same exclusion criteria as the case group. Bone mineral density was measured at the lumbar spine and femoral neck using a Hologic QDR 4500 unit. In subjects with back pain, radiographs of the thoracic and lumbar spine were obtained to look for fractures. RESULTS: The odds ratio for a bone mineral density decrease of one standard deviation at the femoral neck was 1.68 (1.20-2.35) in patients with a cumulative glucocorticoid dose of 10 g of prednisone equivalent and 1.67 (1.22-2.29) in those with a glucocorticoid therapy duration of 2 years. Sixty-eight fractures were recorded in 56 patients (46% of the overall patient group). Even after adjustment on age, glucocorticoid therapy duration, and dose, mean bone mineral density values at the lumbar spine and femoral neck were significantly lower in the subgroup of patients with fractures than in the subgroup without fractures. Sensitivity and specificity of bone mineral density at the femoral neck and/or lumbar spine for the diagnosis of vertebral fracture and/or peripheral fracture were 73% and 51%, respectively. In the stepwise logistic regression model, factors explaining the presence of fractures were as follows, in hierarchical order: age; absence of calcium/vitamin D supplementation, femoral neck T-score, and glucocorticoid dose. CONCLUSION: Our data are compelling evidence that bone mineral density is a major determinant of the fracture risk in patients with glucocorticoid-induced osteoporosis.     

Efficacy and safety of daily risedronate in the treatment of corticosteroid-induced osteoporosis in men and women: a randomized trial. European Corticosteroid-Induced Osteoporosis Treatment Study.

Long-term use of high-dose corticosteroids often results in bone loss, which may lead to osteoporosis-related fractures. This was a multicenter, double-blind study in which 290 ambulatory men and women receiving high-dose oral corticosteroid therapy (prednisone > or = 7.5 mg/day or equivalent) for 6 or more months were randomized to receive placebo, risedronate 2.5 mg/day, or risedronate 5 mg/day for 12 months. All patients received calcium 1 g and vitamin D 400 IU daily. The primary endpoint was lumbar spine bone mineral density (BMD) at month 12. Additional measurements included BMD at the femoral neck and trochanter and the incidence of vertebral fractures. Overall, there were statistically significant treatment effects on BMD at 12 months at the lumbar spine (p < 0.001), femoral neck (p = 0.004), and trochanter (p = 0.010). Risedronate 5 mg increased BMD at 12 months by a mean (SEM) of 2.9% (0.49%) at the lumbar spine, 1.8% (0.46%) at the femoral neck, and 2.4% (0.54%) at the trochanter, whereas BMD was maintained only in the control group. Although not powered to show fracture efficacy, we observed a reduction in the incidence of vertebral fractures of 70% in the combined risedronate treatment groups, relative to placebo (p = 0.042). Risedronate was well tolerated, had a good safety profile, and was not associated with gastrointestinal adverse events. We conclude that risedronate increases BMD and potentially reduces the incidence of vertebral fractures in patients with corticosteroid-induced osteoporosis.     

The effect of intranasal salmon calcitonin therapy on bone mineral density in idiopathic male osteoporosis without vertebral fractures--an open label study

The aim of this study was to examine the effect of intranasal salmon calcitonin therapy on bone mineral density (BMD) in idiopathic male osteoporosis without vertebral fractures. We conducted a randomized, open label, controlled trial in 71 male patients (mean age 59 +/- 6 years) suffering from idiopathic osteoporosis (femoral neck T-score < -2.5) without vertebral deformity. Patients in the control group (n = 31) received 400 IU Vitamin D + 1000 mg elemental calcium daily while the treatment group (n = 40) received 400 IU Vitamin D, 1000 mg elemental calcium plus 200 IU calcitonin nasal spray daily during alternate months. The study period was 18 months. Compared to controls, nasal calcitonin was associated with significant increases in bone mineral density at the lumbar spine (+3.5 +/- (-4.3%) vs. +0.83 +/- 6.4%, P = 0.04) and the femoral neck (+3.2 +/- 3.9% vs. +0.68 +/- 5.7%, P = 0.004). No significant difference was observed at the radius between the treatment groups (+1.4 +/- 8.8% vs. +1.4 +/- 10.9%, P = 0.98). Treatment was well tolerated with no premature discontinuations or significant side effects compared to the control group. We conclude that 200 IU salmon calcitonin nasal spray used daily, intermittently proved to be an effective and safe therapy in male idiopathic osteoporosis.     

Risedronate Increases Bone Density and Reduces Vertebral Fracture Risk Within One Year in Men on Corticosteroid Therapy

Limited information is available on the effect of bisphosphonates in men receiving corticosteroid therapy. We studied 184 men among the patients enrolled in two, double-blind, placebo-controlled, 1-year studies with similar protocols. The studies evaluated the effects of risedronate in patients beginning corticosteroid treatment at a dose of at least 7.5 mg per day of prednisone or equivalent (prevention study) or continuing long-term treatment of corticosteroid at that dose (treatment study). The men received either placebo or risedronate (2.5 mg or 5 mg) daily, along with calcium supplementation (500-1000 mg). Endpoints included differences in bone mineral density (BMD) at the lumbar spine, femoral neck, and femoral trochanter, assessment of vertebral fractures, changes in biochemical markers of bone turnover, and overall safety. In the treatment study, risedronate 5 mg significantly (P < 0.01) increased lumbar spine BMD by 4.8% at the lumbar spine, 2.1% at the femoral neck, and 2.6% at the femoral trochanter compared with baseline values. In the prevention study, bone loss was prevented with risedronate 5 mg; in the placebo group, BMD decreased significantly (P < 0.01) by 3.4%, 3.3%, and 3.4% in the lumbar spine, femoral neck, and trochanter, respectively, at 1 year. The differences between risedronate 5 mg and placebo groups were significant at all skeletal sites in the prevention study (P < 0.01) and at the lumbar spine in the treatment study (P < 0.001). The 2.5 mg dose also had a positive effect on BMD, although of a lesser magnitude than the 5 mg dose. When the data from the two studies were combined, the incidence of vertebral fractures decreased 82.4% (95% confidence interval, 36.6%-95.1%) in the pooled risedronate groups compared with placebo (P = 0.008). Risedronate was well tolerated in men, with a similar incidence of upper gastrointestinal adverse events in the placebo and treatment groups. Daily treatment with risedronate increases bone density and decreases vertebral fracture risk within 1 year in men receiving corticosteroid therapy.     

Alendronate in kidney transplant patients: a single-center experience

INTRODUCTION: Osteoporosis following a renal transplant is an important cause of morbidity. Several studies have demonstrated the efficiency of diphosphonates for the prevention and treatment of osteoporosis. METHODS: We evaluated the effect of alendronate treatment on bone mineral density (BMD) in patients with osteoporosis (lumbar spine and/or hip t-scores < or = -2.5). Two study groups were established: group A (n = 13), patients treated orally with vitamin D, calcium, and alendronate (70 mg/week) and group B (n = 12) patients receiving only vitamin D and calcium. The immunosuppression regimen mostly used was steroids and cyclosporine. BMD was determined at the lumbar spine and hip using a Hologic 4500 QDR densitometer at the start of treatment and after 1 year. RESULTS: The study groups showed no significant differences in age, sex, menopause, or transplant time. Group A received a mean of 1.80 +/- 1.3 microg vitamin D/week and 1.3 +/- 2.1 g calcium/d, compared to 1.1 +/- 1 microg and 1.25 +/- 2.3 g, respectively for group B (NS). After a mean of 411.15 +/- 107.75 days of treatment, a significant increase in BMD at the femoral neck was recorded in group A, but not at the level of the spine (+5.57% +/- 3.5%, P < .05 and -0.42% +/- 12%, NS, respectively). No significant changes were observed in group B (-1.45% +/- 8% femoral neck and +1.69% +/- 3.5% hip, NS). Dyspepsia was reported by 7% of patients. CONCLUSIONS: In this preliminary analysis, alendronate produced, improvements are so far limited to an increased BMD in the hip.     

A randomized controlled trial of salmon calcitonin to prevent bone loss in corticosteroid-treated temporal arteritis and polymyalgia rheumatica

Patients treated with high-dose or long-term corticosteroids are at risk of accelerated osteoporosis and spontaneous vertebral and traumatic fractures. To assess the efficacy of salmon calcitonin in preventing corticosteroid-induced osteoporosis, 48 patients with newly diagnosed polymyalgia rheumatica, temporal arteritis, and other vasculitides were enrolled in a 2-year, double-blind, randomized, controlled trial. Patients were randomized to receive subcutaneous injections t.i.w. of either 100 IU of salmon calcitonin (25 patients) or placebo (23 patients). After 2 years, 19 and 21 patients, respectively, were evaluable. All patients also received supplemental calcium carbonate (1500 mg daily in divided doses) and vitamin D₃ (400 IU daily). Baseline and serial radiologic assessments included dual-energy X-ray absorptiometry (DXA) of the lumbar spine and hip, and spine radiographs to detect vertebral fractures. There were no significant baseline differences between the two study groups. The mean within-subject percentage change in DXA lumbar spine density in the two groups over the 2-year period of the study was only −0.1% (calcitonin plus calcium) versus −0.2% (placebo plus calcium) a nonsignificant difference despite the high mean cumulative corticosteroid doses of 5371 mg and 4680 mg, respectively (NS). The incidence of vertebral fracture was 12.5% (calcitonin plus calcium: 11%, versus placebo plus calcium: 14%, NS), with four fractures in the first year and one fracture in the second year. Higher cumulative corticosteroid dose was associated with a greater loss in bone density. In rheumatic disease patients starting high-dose, long-term corticosteroids, salmon calcitonin with calcium and vitamin D₃ provided no greater bone preservation than that observed with calcium and vitamin D₃ alone. Deceased. This report is dedicated to Patricia Schwartzberg, R.N., who gave life to the study, and without whom it could not have been accomplished.     

Effects of clodronate on vertebral fracture risk in osteoporosis: a 1-year interim analysis

The aim of this study was to determine whether clodronate reduced the incidence of vertebral fractures in patients with osteoporosis. We report here the interim analysis after 1 year of a 3-year double-blind placebo-controlled study. The objectives of the interim analysis were to determine whether there was a trend in fracture frequency and to examine the effects of clodronate on bone mineral density (BMD). Patients with densitometrically proven osteoporosis (T-score <-2.5 and <-3 for women and men, respectively) or with at least one prevalent vertebral fracture were recruited to a 3-year double-blind, controlled study. Patients were randomized to three strata, namely women with postmenopausal osteoporosis (stratum I, n = 483), women with secondary osteoporosis (II, n = 110), and men with osteoporosis of any causation (III, n = 84). They received either clodronate 800 mg daily by mouth or an identical placebo, and all patients received a calcium supplement of 500 mg daily. BMD was measured at six monthly intervals, and lateral spine radiographs for vertebral morphometry were obtained at baseline and 1 year. Treatment with clodronate was associated with a significant increase in BMD at the spine of 3.2 +/- 0.3% (p < 0.0001 vs. baseline) compared with a nonsignificant change of 0.5 +/- 0.3% in the placebo group (p < 0.0001 between treatments). At the hip, clodronate was associated with a significant increase in total hip BMD of 1.3 +/- 0.3% (p = 0.018 vs. baseline) compared with a small decrease of 0.4 +/- 0.3% in the placebo group (p = 0.027 for the difference between treatment groups). The mean changes at the spine and hip were similar in all three strata. Incident vertebral fractures were observed in 27 patients at 1 year in the placebo group (9.0%) and in 14 patients receiving clodronate (4.9%) (relative risk 0.54; 95% CI 0.29-1.02; p = 0.07). A trend was observed in all treatment strata. Treatment was well tolerated, with no significant adverse events attributable to clodronate treatment. We conclude that clodronate 800 mg daily is effective in preventing bone loss, and at 1 year, there is a trend consistent with antifracture efficacy in patients with established osteoporosis regardless of causation.     

Prise en charge thérapeutique de l’ostéoporose masculine

The objective of this study was to evaluate the efficacy of treatments for male osteoporosis selected based on the cause of the disease. Methods. Sixty-three men with osteoporosis (T-score at the lumbar spine and/or femoral neck lower than –2.5) with a mean age of 53 ± 11 years were studied. Forty-three (68.3%) had a history of fracturing without trauma (vertebral fractures, 37 patients, 57%). Treatments were as follows: idiopathic osteoporosis: calcium and vitamin D supplements (N = 10) or cyclical etidronate for 2 weeks followed by calcium and vitamin D supplements for 76 days (N = 29); moderate idiopathic phosphate diabetes: calcitriol and phosphate (N = 15); idiopathic hypercalciuria: hydrochlorothiazide (N = 6); and hypogonadism: testosterone (N = 3). Results. Percentage change in bone mineral density (mean ± standard error of the mean) after 18 months: calcium and vitamin D (lumbar spine: 0.6 ± 2; femoral neck: 2.2 ± 2.2); etidronate (lumbar spine: 3.6 ± 1.4*; femoral neck: 0.5 ± 1); calcitriol (lumbar spine: 7.0 ± 3.5*; femoral neck: 0.0 ± 1.4); thiazide diuretic (lumbar spine: 1 ± 3.2; femoral neck: –2.3 ± 3.7); and testosterone (lumbar spine: 6.8 ± 6.4; femoral neck: 2.5 ± 2.7), where *P < 0.05 versus baseline. Gastrointestinal side effects occurred in three patients (4.8%), including two on calcitriol-phosphate therapy and one on etidronate therapy. Of the six (9.5%) patients who experienced incident fractures, four were on etidronate, one on calcitriol-phosphate, and one on calcium-vitamin D. No patients discontinued their treatment because of side effects. Conclusion. Etidronate and the combination of calcitriol-phosphate produce a significant increase in lumbar spine bone mass in men with idiopathic osteoporosis or moderate idiopathic phosphate diabetes.     

Cyclical etidronate versus sodium fluoride in established postmenopausal osteoporosis: a randomized 3 year trial

To compare the effects of sodium fluoride and etidronate in severe postmenopausal osteoporosis, we conducted a 3 year, prospective, trial in 118 postmenopausal osteoporotic women with at least one vertebral fracture, who were randomly assigned to receive sodium fluoride (25 mg twice daily, as enteric-coated tablets) plus calcium (1000 mg/day) or intermittent etidronate (400 mg/day for 14 days) followed by calcium (1000 mg/day for 76 days). Lateral spine X-ray films and dual-energy X-ray absorptiometry (DXA) measurements of the lumbar spine and proximal femur were performed at enrollment and yearly. Nonvertebral fractures were recorded every 6 months. Thirty-one women in the fluoride group and 47 in the etidronate group completed the trial. At 36 months, the mean change from baseline of the lumbar bone density in the fluoride group was 8.5 +/- 2.04% (p = 0.001) and in the etidronate group was of 3.6 +/- 0. 84% (p < 0.001). The changes in the fluoride group were significantly higher than in the etidronate group (p = 0.01). Both groups showed nonsignificant changes in femoral neck bone density. There was no significant difference between groups in the cumulative proportion of women with new vertebral fractures, with an incidence in the fluoride group of 16% vs. 17% in the etidronate group. However, the number of new vertebral fractures was significantly lower in the fluoride group (6 fractures) than in the etidronate group (19 fractures) (p = 0.05). The number of patients with nonvertebral fractures was similar in both groups. A high incidence of side effects, mainly gastrointestinal symptoms and lower extremity pain syndrome, was observed in the fluoride group. Etidronate was well tolerated. We conclude that, in women with severe osteoporosis, although sodium fluoride is more favorable than cyclical etidronate for increasing lumbar bone mass, no differences were observed in the incidence of fractures.     

Abdominal injuries associated with lumbar spine fractures in blunt trauma

BACKGROUND: Specific analysis of the relationship between abdominal injuries and lumbar spine fractures has not yet been reported. METHODS: A retrospective review of 258 blunt trauma patients with lumbar spine fractures treated between 1991 and 1996. RESULTS: 26 patients sustained concomitant lumbar spine fractures and abdominal injuries. The mechanism of injury was motor vehicle collision (73%), pedestrian-struck (11%), fall (8%) and assault (8%) resulting in ISS, RTS and mortality of 27 +/- 4, 6.5 +/- 0.4 and 8%, respectively. Forty-four lumbar spine fractures were identified (1.7/pt) in association with splenic (54%), renal (41%), hepatic (32%) and small bowel (23%) injuries and no retroperitoneal involvement. Multilevel lumbar spine fractures were associated with a higher organ injury/fracture ratio compared with single level fractures (p < 0.01) including a twofold higher incidence of solid organ (spleen, liver and kidney) injury (p < 0.01). The level and type of fracture did not affect the incidence of total and individual organ injury. Patients with abdominal injuries were more severely injured mainly due to increased incidence of associated thoracic injuries although no significant difference in mortality was observed. CONCLUSION: Abdominal injuries occurred only in the minority of blunt trauma patients with lumbar spine fractures. These injuries, which followed a similar distribution pattern as in blunt trauma in general, occurred most commonly due to motor vehicle collisions and in association with multilevel vertebral fractures. No correlation with fracture type or level was identified.     

Primary biliary cirrhosis and osteoporosis: a case-control study

Osteoporosis is a common complication of chronic liver disease, from cholestatic disorders to autoimmune, alcoholic, and posthepatitic cirrhosis. Osteoporosis appears more striking in patients with primary biliary cirrhosis (PBC) because the disease usually affects elderly women, who are naturally prone to osteoporosis. Our aims were (1) to compare the prevalence of osteoporosis (T-score <-2.5 SD) between PBC patients and a group of age-and sex-matched controls consisting of healthy subjects from the general population; and (2) to identify the main risk factors for the development of bone loss. Thirty-three women with PBC (mean age, 47.3 +/- 10.4 years) and 66 healthy subjects were enrolled in the study. Bone mineral density (BMD) was assessed at the lumbar spine by dual-photon X-ray absorptiometry. Bone metabolism was evaluated by measuring serum calcium corrected for serum albumin, 25-hydroxyvitamin D (25-OH vit D), parathyroid hormone, and osteocalcin. Vertebral fractures were analyzed using vertebral fracture assessment (VFA). The mean T-score was lower in the PBC group compared to healthy controls, with a significant statistical difference (-2.39 +/- 0.93 and -1.47 +/- 0.99 in lumbar spine and total hip, respectively, in the PBC group versus -0.99 +/- 0.51 and -0.56 +/- 1.14 in healthy controls (P < 0.001). The prevalence of osteoporosis was 51.5% in the PBC group versus 22.7% in healthy controls with a statistically significant difference (P = 0.004). BMD of the PBC group was significantly correlated positively with body mass index (BMI) and 25-OH vit D, and negatively with menopausal status, duration of disease, and parathyroid hormone (PTH) levels. Vertebral fractures were present in 9% of the patients. We found that osteoporosis is more prevalent in women with PBC than in the general population. BMI, menopausal status, duration of the disease, and vitamin D deficiency are the main risk factors for osteoporosis in this liver disease.