Calcium regulation and bone mass loss after total gastrectomy in pigs.

OBJECTIVE: Total gastrectomy often results in postgastrectomy bone disease with decreased bone mass and increased fracture risk. To further elucidate the mechanisms of postgastrectomy bone disease, the authors investigated calcium metabolism and bone mineral density after total gastrectomy in pigs. SUMMARY BACKGROUND DATA: Postgastrectomy bone disease can present as osteomalacia, osteoporosis in excess of normal aging, or a combination of both. The underlying mechanisms are insufficiently understood and need further investigation. METHODS: Growing minipigs were gastrectomized and compared with fed-matched, sham-operated control p gs for 1 year. Calcium absorption, serum calcium, parathyroid hormone, 25-(OH)-vitamin D, 1,25-(OH)2-vitamin D, alkaline phosphatase, and computed tomography bone mineral density were measured in three monthly intervals. RESULTS: Total gastrectomy resulted in impaired calcium absorption, reduced serum calcium and 25-(OH)-vitamin D, increased parathyroid hormone and 1,25-(OH)2-vitamin, and reduced bone mineral density compared with fed-matched, sham-operated control pigs. CONCLUSIONS: The authors data indicate that a reduced serum calcium activates counter-regulatory mechanisms, resulting in calcium mobilization from the bone. Possibly, calcium and vitamin D supplementation after total gastrectomy might prevent postgastrectomy bone mass loss.     

Randomised double blind placebo controlled trial investigating the effect of calcium and vitamin D supplementation on bone mineral density and bone metabolism in adult patients with cystic fibrosis

BACKGROUND: Low bone mineral density (BMD) is prevalent in adults with cystic fibrosis and might be related to calcium and vitamin D malabsorption from the gastrointestinal tract. The aim of this study was to investigate the effect of calcium and vitamin D supplementation on BMD and bone metabolism in these subjects. METHODS: Patients were invited to participate if they had a BMD Z score of -1 or less in the lumbar spine, proximal femur or distal forearm. Patients were randomised to receive calcium 1 g+vitamin D 800 IU or placebo daily, in addition to their regular vitamin D supplements (900 IU/day). BMD and bone biochemical markers were measured before and after 1 year of treatment. RESULTS: After 12 months, the treatment group (n=15) showed a reduced rate of bone loss compared with the control group (n=15) in the lumbar spine (mean difference 1.9% [CI -0.9% to 4.6%]), total hip (mean difference 0.7% [CI -2.2% to 3.5%]) and distal forearm (mean difference 1.7% [CI -2.2% to 5.5%]), but these changes did not reach statistical significance. There was also a trend towards a reduction in bone turnover in the treatment group. CONCLUSIONS: Calcium and vitamin D supplementation reduced the rate of bone turnover and bone loss in adult patients with cystic fibrosis, but these changes did not reach statistical significance. These data suggest that a longer term trial of this simple intervention would be justified.     

Comparison of the effects of calcium loading with calcium citrate or calcium carbonate on bone turnover in postmenopausal women

Calcium supplementation is known to increase bone mineral density and decrease fractures, but the relative efficacy of different forms of calcium supplementation is not established. We compared the effects of calcium carbonate and calcium citrate on markers of bone resorption in older postmenopausal women in an open-labeled crossover study. Forty women were randomized to receive 1000 mg/day of either calcium citrate or calcium carbonate for 12 weeks, followed by a 2-week washout without calcium supplements and 12 weeks treatment with the alternate calcium supplement. All women received vitamin D (900 IU/day). Thirty-four women (25 Caucasian, nine Hispanic) completed the study. No significant differences in the decrease in parathyroid hormone (PTH) or bone specific alkaline phosphatase or the increase in urinary calcium/creatinine were detected between the two treatments. However, calcium citrate supplementation decreased the collagen cross-link resorption markers, urinary N-telopeptide (–30%), C-telopeptide (–31%), free deoxypyridinoline (19%) and serum N-telopeptide (–8%), compared to no significant change following calcium carbonate supplementation (+2%, +3%, +2% and +2%, respectively; P<0.05). Calcium citrate decreased markers of bone resorption significantly more than calcium carbonate in postmenopausal women, although no differences in their effects in calcium excretion or PTH were detected.     

A comparison of the effects of alfacalcidol treatment and vitamin D2 supplementation on calcium absorption in elderly women with vertebral fractures

Although vitamin D supplementation in the frail elderly improves calcium absorption, suppresses parathyroid hormone, decreases bone loss and reduces the risk of fractures, such treatment may be ineffective in patients with vertebral osteoporosis, because of impaired vitamin D metabolism or resistance to the action of vitamin D metabolites on the bowel. We have therefore performed a randomized, single masked study comparing the effects of alfacalcidol treatment (0.25 µg twice daily) and vitamin D₂ supplementation (500-1000 units daily) on calcium absorption and bone turnover in 46 elderly women (median age 69 years, range 64–79 years) with radiological evidence of vertebral fractures. Serum 25-hydroxyvitamin D increased significantly after 3 and 6 months of treatment with vitamin D₂ (p<0.001), but was unchanged in the group receiving alfacalcidol. Serum 1,25-dihydroxyvitamin D did not change significantly in either group over the study period. Fractional⁴⁵Ca absorption increased after 3 months of treatment with alfacalcidol (p<0.05), but was unchanged with vitamin D₂. There was also a reduction in plasma intact parathyroid hormone and serum alkaline phosphatase after 6 months of treatment with alfacalcidol (p<0.05) which was not seen in the group receiving vitamin D₂. Our study shows that vitamin D₂ supplementation is ineffective in stimulating calcium absorption in elderly women with vertebral osteoporosis. By increasing calcium absorption in such patients, alfacalcidol may prove more effective than vitamin D in the management of vertebral osteoporosis.     

Effects on bone mineral density of calcium and vitamin D supplementation in elderly women with vitamin D deficiency

OBJECTIVE: Calcium and vitamin D deficiency is common in older individuals, particularly those who live in nursing homes, and increases the risk of osteoporosis and fractures. METHODS: We conducted a randomized double-blind placebo-controlled study of combined supplementation with 500 mg of elemental calcium, as carbonate, and 400 IU of vitamin D bid for 12 months in women older than 65 years of age with vitamin D deficiency, defined as serum 25(OH)D concentrations 相似文献   

Prophylactic calcium and vitamin D treatments in steroid-treated children with nephrotic syndrome

Steroid treatment has several side effects, including the deterioration of the bone and mineral metabolism in children with nephrotic syndrome. This randomized prospective study was conducted to determine the effects and prophylactic role of calcium plus vitamin D treatment on bone and mineral metabolism in children receiving prednisolone treatment. 40 children (27 boys and 13 girls) with NS (18 new onset and 22 relapsing) were included in the study. Their mean age was 4.6±1.8 years. All patients received prednisolone treatment (2 mg/kg/day for 4 weeks followed by alternate days at the same dose for 4 weeks). The patients were randomized into treatment (vitamin D 400 IU plus calcium 1 g daily) and non-treatment groups. Bone mineral density, serum Ca, P, alkaline phosphatase and urinary Ca and P excretions were analyzed at the beginning and 2 months after the treatment. The XR36 Norland device was used for bone mineral density analysis. Bone mineral density was significantly decreased in both the treatment (0.54±0.15 to 0.51±0.1 g/cm², P =0.001) and non-treatment (0.52±0.18 to 0.45±0.16 g/cm², P <0.001) group. But the percentage of bone mineral density decrease was found to be significantly lower in the treatment group than in the non-treatment group (4.6±2.1% vs. 13.0±4.0%, respectively; P <0.001). Serum calcium and urinary calcium excretion increased in the treatment group (8.0±1.0 to 10.0±0.5 mg/dl and 1.1±0.5 to 3.2±1.0 mg/kg/day) and non-treatment group (8.1±0.8 to 10.0±0.6 mg/dl and 1.4±0.9 to 3.8±3.3 mg/kg/day) after prednisolone treatment (P <0.001). Steroid treatment decreases bone mineral density in children with nephrotic syndrome. Vitamin D plus calcium therapy at the current doses reduces but does not completely prevent bone loss, with no additional adverse effects.     

Alendronate in combination with calcium and vitamin D prevents bone loss after orthotopic liver transplantation: a prospective single-center study.

Bone loss is a common complication in patients before and after liver transplantation (LT). The aim of this study was to investigate the efficacy of prophylactic treatment with bisphosphonates after LT in preventing progressive bone loss in LT patients. We included 136 patients with end-stage liver diseases awaiting LT. Bone mineral density (BMD) (by dual X-ray absorptiometry) and markers of bone metabolism were determined before, and 4, 12, 24, 36, and 48 months after LT. All patients received vitamin D and calcium supplementation before and after LT, those with osteopenia or osteoporosis prior to LT were additionally treated with alendronate following LT. Decreased BMD was seen in a high percentage of patients undergoing LT (osteopenia 48.5%, osteoporosis 23.5%). Reduced BMD before LT was not related to gender, underlying liver disease, or Child-Turcotte-Pugh classification. Body mass index (BMI) prior to LT, however, correlated significantly with the fracture risk. Alendronate prevented the ubiquitously observed bone loss after LT in patients with osteoporosis and osteopenia and, in addition, led to an increase in BMD in patients with osteoporosis within 24 months after LT. In conclusion, our study suggests that alendronate is efficacious in preventing the natural course of bone loss associated with LT.     

Effect of low-calcium hemodialysate on bone metabolism

In the present study, we investigated the kinetics of bone metabolism by determining serum bone metabolic markers and quantifying bone mineral density by dual-energy X-ray absorptiometry to clarify the effect of long-term use of low-calcium hemodialysate on bone metabolism. After changing the calcium concentration in the dialysate from 3.0 mEq/l to 2.5 mEq/l, serum intact parathyroid hormone level, serum highly sensitive parathyroid hormone level, and serum bone metabolic markers were determined in ten patients with chronic nondiabetic renal insufficiency during 1 year. The doses of an oral phosphate binder and activated vitamin D were carefully regulated to control serum ionized calcium levels and serum inorganic phosphorus levels. Bone mineral density was determined at the distal 1/3 and 1/6 of the radius on the nonshunt side. As a result, the required amount of oral phosphate binder was increased; however, there was no need to significantly increase the amount of activated vitamin D. Intact parathyroid hormone showed no significant variation, but the highly sensitive parathyroid hormone was significantly increased. There were no significant changes in any bone metabolic markers or in bone mineral density. From these study results, it was found that it was difficult to increase the dose of activated vitamin D even if low-calcium hemodialysate was used, and that during use of the low-calcium hemodialysate the serum level of parathyroid hormone tended to increase but led to neither acceleration of bone turnover nor a decrease in bone mineral density. Received: Feb. 22, 1999 / Accepted: July 6, 1999     

The Effect of Pregabalin on Bone Metabolism

The aim of the study was to determine the effect of pregabalin as monotherapy on biochemical markers and bone mineral density. 40 patients diagnosed with neuropathic pain or fibromyalgia syndrome who were using pregabalin for at least 6 months and age and sex matched 40 healthy individuals were recruited for this cross-sectional study. Bone mineral density of both groups were measured by dual energy x ray absorbsiometry(DXA), bone biochemical markers, serum calcium, and vitamin D levels were investigated. Association between pregabalin use and bone biochemical markers, serum calcium, vitamin D levels were evaluated. The mean age of 40 patients (27 females, 13 males) was 40.6 ± 7.1 years and the mean age of 40 healthy individuals (27 females, 13 males) was 40.4 ± 7.3 years. The other demographic data were similar. There were no significant differences in lumbar and femur neck BMD scores between 2 groups. Also, there were no associations neither between pregabalin use and biochemical markers including serum calcium levels nor between pregabalin use and vitamin D levels. However, the patients who had been used pregabalin less than 24 months had low lumbar t and z scores than patients who had been used pregabalin more than 24 months. This effect was more prominent in male patients. Although no negative effect of pregabalin was found on bone metabolism in these group of patients, we have suggested that further prospective controlled studies with large sample size in different age groups could provide new data about the effects of pregabalin on bone metabolism. We suggest to investigate the bone metabolism especially in male patients on pregabalin treatment who had been used pregabalin treatment less than 24 months.     

Supplementation with oral vitamin D3 and calcium during winter prevents seasonal bone loss: a randomized controlled open-label prospective trial.

Bone metabolism follows a seasonal pattern with high bone turnover and bone loss during the winter. In a randomized, open-label 2-year sequential follow-up study of 55 healthy adults, we found that supplementation with oral vitamin D3 and calcium during winter abolished seasonal changes in calciotropic hormones and markers of bone turnover and led to an increase in BMD. Supplementation with oral vitamin D3 and calcium during the winter months seems to counteract the effects of seasonal changes in vitamin D and thus may be beneficial as a primary prevention strategy for age-related bone loss. INTRODUCTION: Bone metabolism follows a seasonal pattern characterized by high bone turnover and bone loss during winter. We investigated whether wintertime supplementation with oral vitamin D3 and calcium had beneficial effects on the circannual changes in bone turnover and bone mass. MATERIALS AND METHODS: This prospective study comprised an initial observation period of 12 months ("year 1"), followed by an intervention during parts of year 2. Fifty-five healthy subjects living in southwestern Germany (latitude, 49.5 degrees N) were randomized into two groups: 30 subjects were assigned to the treatment group and received oral cholecalciferol (500 IU/day) and calcium (500 mg/day) during the winter months of year 2 (October-April), while 25 subjects assigned to the control group obtained no supplements. Primary endpoints were changes in calciotropic hormones [serum 25(OH)D, 1,25(OH)2D, and parathyroid hormone], markers of bone formation (serum bone-specific alkaline phosphatase) and of bone resorption (urinary pyridinoline and deoxypyridinoline), and changes in lumbar spine and femoral neck BMD. RESULTS: Forty-three subjects completed the study. During year 1, calciotropic hormones, markers of bone turnover, and BMD varied by season in both groups. During the winter months of year 1, bone turnover was significantly accelerated, and lumbar spine and femoral BMD declined by 0.3-0.9%. In year 2, seasonal changes in calciotropic hormones and markers of bone turnover were either reversed or abolished in the intervention group while unchanged in the control cohort. In the subjects receiving oral vitamin D3 and calcium, lumbar and femoral BMD increased significantly (lumbar spine: +0.8%, p = 0.04 versus year 1; femoral neck: +0.1%, p = 0.05 versus year 1), whereas controls continued to lose bone (intervention group versus control group: lumbar spine, p = 0.03; femoral neck, p = 0.05). CONCLUSIONS: Supplementation with oral vitamin D3 and calcium during winter prevents seasonal changes in bone turnover and bone loss in healthy adults. It seems conceivable that annually recurring cycles of low vitamin D and mild secondary hyperparathyroidism during the winter months contributes, at least in part and over many years, to age-related bone loss. Supplementation with low-dose oral vitamin D3 and calcium during winter may be an efficient and inexpensive strategy for the primary prevention of bone loss in northern latitudes.     

Bone mineral density and urine calcium excretion among subjects with and without nephrolithiasis

BACKGROUND: Bone mineral density (BMD) is reduced among patients with idiopathic hypercalciuria (IH) and nephrolithiasis. To disentangle effects of diet, stone formation, and physiology upon BMD, we studied vertebral and femoral neck BMD among relatives of hypercalciuric stone formers, and contrasted those with to those without stones. METHODS: Among 59 subjects from 11 families, vertebral and femoral neck BMD, diet calcium intake, urine excretions of calcium, sodium, ammonium, titratable acid, sulfate, urea nitrogen, and serum levels of calcitriol and markers of bone turnover were studied. RESULTS: Stone formers (SF) consumed less calcium than non-stone formers (NSF). Spine and femoral neck BMD z-scores varied inversely with urine calcium loss and urine ammonium excretion among SF but not NSF. No correlations of BMD z-score were found for bone markers, calcitriol, or any of the other measurements. CONCLUSION: SF consumed less calcium, presumably to prevent more stones, and displayed a bone mineral responsiveness to calcium loss and ammonium excretion not present among NSF, who ate more calcium. Lowered calcium consumption in IH, perhaps in response to stone formation, alters bone responses in a direction that can predispose to mineral loss and eventual fracture.     

椎体成形术后应用唑来膦酸联合维生素K2治疗老年性椎体压缩骨折

目的观察椎体成形术后应用唑来膦酸联合维生素K2治疗老年性椎体压缩性骨折的3年临床疗效。 方法2013年1月至2015年1月共收治老年性椎体压缩性骨折患者525例,其中女412例,男113例;年龄64～91岁,平均( 79 ± 11)岁。所有患者均予CT引导下椎体成形术手术治疗,术后2～4 d给予唑来膦酸静脉输注,同时补充维生素K2以及钙剂、维生素D。获得术前、术后1周和术后3年腰背痛视觉模拟评分(VAS)评分、Oswestry功能障碍指数(ODI),术前及术后3年骨密度、骨代谢指标的数据。采用配对样本t检验的方法对术后与术前,术后不同时间获得的各组数据进行统计分析。 结果坚持1年随访为189(36%)人,2年随访为131(25%)人,坚持3年随访的患者为56(10.7%)人,56例中17例为发生再次椎体骨折。经3年随访,患者腰背痛VAS评分(t＝3.01)、ODI评分(t＝0.98)、骨密度同术前比较均有明显改善,且差异有统计学意义(P<0.05) 。骨代谢指标中,骨钙素较术前明显提高(t＝5.75),β-CTX较术前显著下降(t＝3.06),差异有统计学意义(P<0. 05),其他指标变化无统计学差异。 结论老年性椎体压缩性骨折患者长期随访治疗的依从性不高。经过椎体成形术后联合多种抗骨质疏松药物3年的干预治疗,可以明显缓解患者临床症状、改善生活质量、促进骨形成、抑制骨吸收、提高骨密度。     

Litiasis renal cálcica y densidad mineral ósea. Importancia del metabolismo óseo en la litiasis urinaria

ContextCalcium Nephrolithiasis is a multifactorial disease; in its pathophysiology is involved various minerals and metabolic factors that may be altered, including bone and phosphor-calcium metabolism.ObjectiveTo establish the scientific evidence and demonstrate the relationship between calcium nephrolithiasis and bone mineral density loss, through the use of bone turnover markers, serum and urinary metabolites.Evidence acquisitionWe performed a PubMed literature review using different MeSH Terms like «Nephrolithiasis» «Bone mineral density»,«Urinary stones», «Calcium», «Bone resorption» and «Bone formation», with different combinations. We only selected articles with abstracts in English or Spanish and discarded clinical cases and articles with inappropriate statistical study. A total of 40 articles were selected.Evidence synthesisIn different studies reviewed have been observed that patients with hypercalciuria have a higher bone mineral density loss with respect to normocalciuric. Among patients with calcium stones (normocalciuric or hypercalciuric), there is loss of bone mineral density, being more evident in patients with stones and hypercalciuria. This mineral density loss is marked and important in patients with recurrent calcium stones. Increased markers like fasting calcium/creatinine and β-CrossLaps are determinant of nephrolithiasis and mineral density loss in these patients.ConclusionWe recommend perform markers of bone turnover and fasting calcium/creatinine in patients with recurrent calcium stones by the significant presence of bone mineral density loss, with a level of evidence III.     

A positive dose-response effect of vitamin D supplementation on site-specific bone mineral augmentation in adolescent girls: a double-blinded randomized placebo-controlled 1-year intervention.

The effect of vitamin D supplementation on bone mineral augmentation in 212 adolescent girls with adequate calcium intake was studied in a randomized placebo-controlled setting. Bone mineral augmentation determined by DXA increased with supplementation both in the femur and the lumbar vertebrae in a dose-responsive manner. Supplementation decreased the urinary excretion of resorption markers, but had no impact on formation markers. INTRODUCTION: Adequate vitamin D intake protects the elderly against osteoporosis, but there exists no indisputable evidence that vitamin D supplementation would benefit bone mineral augmentation. The aim of this 1-year study was to determine in a randomized double-blinded trial the effect of 5 and 10 microg vitamin D3 supplementation on bone mineral augmentation in adolescent girls with adequate dietary calcium intake. MATERIALS AND METHODS: Altogether, 228 girls (mean age, 11.4 +/- 0.4 years) participated. Their BMC was measured by DXA from the femur and lumbar spine. Serum 25-hydroxyvitamin D [S-25(OH)D], intact PTH (S-iPTH), osteocalcin (S-OC), and urinary pyridinoline (U-Pyr) and deoxypyridinoline (U-Dpyr) were measured. Statistical analysis was performed both with the intention-to-treat (IT) and compliance-based (CB) method. RESULTS: In the CB analysis, vitamin D supplementation increased femoral BMC augmentation by 14.3% with 5 microg and by 17.2% with 10 microg compared with the placebo group (ANCOVA, p = 0.012). A dose-response effect was observed in the vertebrae (ANCOVA, p = 0.039), although only with the highest dose. The mean concentration of S-25(OH)D increased (p < 0.001) in the 5-microg group by 5.7 +/- 15.7 nM and in the 10-microg group by 12.4 +/- 13.7 nM, whereas it decreased by 6.7 +/- 11.3 nM in the placebo group. Supplementation had no effect on S-iPTH or S-OC, but it decreased U-DPyr (p = 0.042). CONCLUSIONS: Bone mineral augmentation in the femur was 14.3% and 17.2% higher in the groups receiving 5 and 10 microg of vitamin D, respectively, compared with the placebo group, but only 10 mug increased lumbar spine BMC augmentation significantly. Vitamin D supplementation decreased the concentration of bone resorption markers, but had no impact on bone formation markers, thus explaining increased bone mineral augmentation. However, the positive effects were noted with the CB method but not with IT.     

Bsm1 Vitamin D Receptor Polymorphism and Calcium Homeostasis Following Bariatric Surgery

Purpose/Aim: To evaluate the association between the Bsm1 vitamin D receptor polymorphism and the calcium-vitamin D-parathormone axis following bariatric surgery. Materials and Methods: This cross-sectional study included 86 morbidly obese patients, who underwent either gastric bypass or sleeve gastrectomy, with a mean follow-up of four years. Calcium metabolism indices and bone turnover markers were assessed according to the presence of secondary hyperparathyroidism and the Bsm1 vitamin D receptor genotypes. Results: Secondary hyperparathyroidism (42.2% of sample) was associated with lower levels of 25hydroxyvitamin D and elevated markers of bone turnover. In subjects without secondary hyperparathyroidism, presence of the unfavorable B allele resulted in higher levels of parathormone (Bb and BB vs. bb genotype: 50.3 ± 8.2 pg/dl vs. 44.4 ± 10.7 pg/dl, p = .011, adjusted for weight loss, baseline body mass index, 25hydroxyvitamin D, surgical procedure, and duration after surgery). In the whole sample, patients bearing the unfavorable B allele exhibited lower weight loss, a parameter that was negatively associated with markers of bone resorption. Conclusions: Secondary hyperparathyroidism is highly prevalent after bariatric surgery. Bsm1 vitamin D receptor polymorphism may have an effect in early stages of calcium metabolism imbalance, while no association is detected in patients who have already developed secondary hyperparathyroidism. Moreover, vitamin D receptor polymorphism is associated with post-surgery weight loss, a process related to bone turnover.     

The remodeling transient and the calcium economy

SUMMARY: The remodeling transient describes a change in bone mass that lasts one remodeling cycle following an intervention that disturbs the calcium economy. We demonstrated the transient in a study of the response of bone density to calcium/vitamin D3 supplementation and show the hazards of misinterpretation if the transient is not considered. INTRODUCTION: The remodeling transient describes a change in bone mass that lasts for one remodeling cycle following an intervention that disturbs the calcium economy. METHODS: We report an intervention with calcium and vitamin D supplementation in 208 postmenopausal African-American women where the remodeling transient was considered a priori in the study design. Both groups (calcium alone vs. calcium + 20 microg (800 IU) vitamin D3) were ensured a calcium intake in excess of 1200 mg/day. RESULTS: There were no differences between the two groups in changes in BMD over time. These BMD changes were therefore interpreted to reflect increased calcium intake in both groups but not any influence of vitamin D. A transient increase in bone mineral density was observed during the first year of study, followed by a decline. The remodeling period was estimated at about 9 months, which is similar to histomorphometric estimates. CONCLUSION: It is problematic to draw conclusions concerning interventions that influence the calcium economy without considering the remodeling transient in study design. Studies of agents that effect bone remodeling must be carried out for at least two remodeling cycles and appropriate techniques must be used in data analysis.     

Addressing the Musculoskeletal Components of Fracture Risk with Calcium and Vitamin D: A Review of the Evidence

Osteoporotic fractures are an extremely common and serious health problem in the elderly. This article presents the rationale for calcium and vitamin D supplementation in the prevention and treatment of osteoporotic fractures and reviews the literature evidence on the efficacy of this strategy. Two musculoskeletal risk factors are implicated in osteoporotic fractures in the elderly: the loss of bone mass due to secondary hyperparathyroidism and the increased propensity to falls. Calcium and vitamin D reverse secondary hyperparathyroidism with resultant beneficial effects on bone mineral density (BMD). Additionally, calcium and vitamin D supplementation significantly improves body sway and lower extremity strength, reducing the risk of falls. The effects of combined calcium and vitamin D on parathyroid function and BMD provide a strong rationale for the use of this therapy in the prevention and treatment of osteoporosis and osteoporotic fractures. There is general agreement that, in patients with documented osteoporosis, calcium and vitamin D supplementation should be an integral component of the management strategy, along with antiresorptive or anabolic treatment. Frail elderly individuals constitute another major target population for calcium and vitamin D because evidence from randomized studies in institutionalized elderly subjects demonstrates that these supplements reduce osteoporotic fracture risk, particularly in the presence of dietary deficiencies. However, the results of trials in community-dwelling subjects have been equivocal. Within the primary-care setting, further research is required to establish appropriate target subgroups for calcium and vitamin D supplementation; overall, the data are consistent with a benefit individuals with insufficient calcium and/or vitamin D, although patients with documented osteoporosis will derive further benefit in terms of fracture prevention from the addition of an antiresorptive agent.     

Mineral Metabolism in Obese Patients Following Vertical Banded Gastroplasty

Background Bone disease has been described in patients after surgical treatment for obesity, but few studies have dealt with the impact of vertical banded gastroplasty on mineral metabolism. We have examined bone mineral metabolism in morbidly obese patients before and after 3 months after vertical banded gastroplasty without vitamin D supplementation. Methods Sixteen morbidly obese patients (14 women, 2 men) with a mean (±SD) age of 38 ± 9 years and a body mass index (BMI) of 47.1 ± 8.1 kg/m² were studied. No vitamin D supplementation was given. Body weight, fat mass, calcium, 25OHD, iPTH, bone remodeling markers, and leptin levels were measured at baseline and after weight loss. Results Mean weight loss was 28 ± 11 kg; BMI and body fat mass decreased by 20 and 35%, respectively. Bone resorption markers and albumin-corrected serum calcium increased after operation, whereas iPTH fell. Serum 25OHD levels rose. Leptin levels decreased. Serum iPTH was positively correlated with weight, BMI, and fat mass before operation (p < 0.05), and its decline after weight reduction was negatively associated with the increase in bone resorption markers (p < 0.01). Leptin concentration was correlated with BMI and body fat mass (p < 0.05) both before and after surgery. Conclusions Weight reduction obtained in morbidly obese subjects 3 months after vertical banded gastroplasty increases bone turnover markers and decreases PTH secretion. Serum 25OHD levels rose. Therefore, no reasons for a metabolic bone disease related to hypovitaminosis D were readily apparent. However, an increase in bone turnover, which is generally regarded as a potential risk factor for osteoporosis, was observed. Further work is needed to clarify the importance of this turnover increase in the long run.     

Effects of cholecalciferol and calcium on experimental hepatic osteodystrophy in rats

To investigate cholecalciferol (vitamin D) metabolism disorders in hepatic osteodystrophy (HOD) and the effects of vitamin D, its metabolites, and calcium (Ca) on HOD, an experimental HOD model in rats was developed using carbon tetrachloride. In the serum level of 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, and 24R,25-dihydroxycholecalciferol, there were no significant differences between normal and control cirrhotic rats. Vitamin D supplementation significantly inhibited the atrophy of intestinal villi, reduction of bone calcium content, elevation of bone resorption, reduction of osteoid volume, and reduction of bone volume. Ca supplementation significantly increased the serum free Ca index and inhibited the elevation of bone resorption, the reduction of bone ash and Ca content, and the reduction of bone volume. This experimental study demonstrates that: (1) no marked vitamin D hydroxylation disorder was found in HOD; (2) vitamin D supplementation was effective in inhibiting HOD; and (3) sufficient Ca supplementation was also effective in inhibiting HOD.A portion of this work was presented at the 13th Annual Meeting of the Japanese Society for Bone and Mineral Research, July 1995, Fukuoka, Japan.