Serum bone markers in patients with loosening of cemented total hip endoprosthesis]

Serum levels of bone markers N-mid osteocalcin (OCN-Mid) and Cross-Laps in 20 patients (8 men and 12 women) with loosening of at least one element of total hip endoprosthesis confirmed during operation were compared with age and sex matched group with OA. Marker levels were measured by direct chemoluminescency using Modular E-170. Statistical analysis were done with t-Student test (alpha = 0.05). There were no significant differences in OCN-Mid, Cross-Laps levels and OCN-Mid/Cross-Laps ratio between both groups. Implant loosening is a slow process taking place on a relatively small surface in comparison to whole skeleton, so bone markers have no clinical value in diagnostics of total hip loosening.     

The short-term changes of bone mineral metabolism following bone marrow transplantation

Organ transplantation is now the treatment of choice for many patients with life-threatening chronic diseases. A new set of side effects unique to these groups of patients has become recognized, and bone disease is one of these complications. However, little is known about the effects of myeloablative treatment followed by bone marrow transplantation (BMT) on bone mineral metabolism. We have prospectively investigated 31 patients undergoing BMT for hematologic diseases. Serum concentrations of calcium, phosphorus, creatinine, gonadotropins, sex hormones, and the biochemical markers of bone turnover were measured. The samples were collected before BMT and 1, 2, 3, 4, and 12 weeks, 6 months, and 1 year after BMT. Bone mineral density (BMD) was measured with dual-energy X-ray absorptiometry before BMT and 1 year after BMT. The serum carboxy-terminal cross-linked telopeptide of type I collagen increased progressively until 4 weeks after BMT. Thereafter, it began to decrease and reached basal values after 1 year. Serum osteocalcin decreased progressively until 3 weeks after BMT. After that, it increased and reached basal values after 3 months. No distinct differences were observed in the serum biochemical turnover markers between males and females, or between patients who received total body irradiation and those who did not. One year after BMT, lumbar spine BMD had decreased by 2.2%, and total proximal femoral BMD had decreased by 6.2%. Eighty-six percent of the women (12/14) went into a menopausal state immediately after BMT. This was caused by high gonadotropin levels and low estradiol levels. In contrast, gonadotropin levels and testosterone levels did not change significantly in the male patients after BMT. In conclusion, the rapid impairment of bone formation and the increase in bone resorption, as shown by the biochemical markers in this study, might play a role in post-BMT bone loss.     

Serum osteocalcin and bone mineral metabolism following successful renal transplantation

Serum osteocalcin (bone gla protein, BGP), a vitamin K-dependent non-collagenous bone protein and its relationship to other markers of bone and mineral metabolism were studied cross-sectionally in varying numbers of patients before and over 240 days following renal transplantation. Marked elevation of serum creatinine (11.9 +/- 0.76 mg/dl), osteocalcin (216.9 +/- 7 ng/ml), parathyroid hormone (PTH, mid-molecule fragment) (24.5 +/- 3.6 ng/ml), alkaline phosphatase (255.2 +/- 54.7 IU/l) and phosphorus (5.6 +/- 0.3 mg/dl) were noted preoperatively. Serum calcium levels remained normal throughout the study period while phosphate levels normalized within one week after transplantation. PTH levels progressively decreased postoperatively over the study period but were still elevated well above normal. Serum osteocalcin decreased to near normal values at 60-90 days after surgery. Both PTH and alkaline phosphatase correlated significantly with osteocalcin preoperatively and postoperatively. The relatively depressed values of osteocalcin in the face of still elevated PTH levels post-transplantation was attributed to the effect of immunosuppressive corticosteroid therapy. The significant correlation between PTH and osteocalcin suggests that osteocalcin may be as or more sensitive a measurement of bone turnover than alkaline phosphatase pre- and post-transplantation.     

原发性甲状旁腺机能亢进症手术治疗后骨量和骨代谢指标的变化

目的 了解甲状旁腺切除术对原发性甲状旁腺机能亢进症病人的骨矿密度及骨代谢指标变化的影响。方法 ４０例病人,其中３０例未治疗组（男：女＝３：２７）;１０例已手术治疗组（男：女＝３：７）,手术后时间１～２４月（平均５．３±７．９月）。用ＤＥＸＡ测量腰椎及股骨颈的骨矿密度,同时,测定血清中的甲状旁腺素（ＰＴＨ）,骨钙素（ＯＣ）,及骨唾液酸蛋白（ＢＳＰ）。结果 在已手术组病人其腰椎及股骨颈骨矿密度再没有明     

A short course of recombinant human growth hormone treatment stimulates osteoblasts and activates bone remodeling in normal human volunteers

The effects of recombinant human growth hormone (rhGH) on biochemical markers of bone turnover and bone mineral content (BMC) were investigated in 20 normal male volunteers (aged 22-31 years) randomized to treatment for 7 days with either rhGH (0.1 IU/kg subcutaneously twice a day) or placebo. Serum somatomedin C rose during treatment (p less than 0.001) but was not significantly different from baseline at day 14. The fasting urinary hydroxyproline/creatinine (p less than 0.001) and calcium/creatinine ratios (p less than 0.01) increased during treatment and remained elevated for 4 and 2 weeks, respectively. Serum bone gamma-carboxyglutamic acid-containing protein (BGP) increased during treatment (p less than 0.001) and remained elevated for 6 months (p less than 0.02). Serum bone alkaline phosphatase (B-AP), after an initial fall in the treatment period (p less than 0.001), increased slightly in the following months (p less than 0.01). In the rhGH group BMC was significantly higher than the prestudy value at day 14 (p less than 0.05) but was unaltered at the end of study. The simultaneous increase in markers of bone resorption and formation during rhGH treatment followed by a decline in resorption parameters within a few weeks and the prolonged effect on BGP and B-AP demonstrate that rhGH treatment stimulates osteoblasts and activates bone remodeling.     

Mechanisms of rapid bone loss following cardiac transplantation

Rapid bone loss after orthoptic cardiac transplantation (OHTX) is a major problem; however, the mechanisms are poorly understood. To investigate these mechanisms we measured biochemical and hormonal indices of bone turnover serially in 25 patients (21 men, 4 women) after OHTX. Serum osteocalcin was reduced immediately post-OHTX (2.2±0.5 ng/ml) but rose significantly by 6 and 12 months (14.1±2.5 and 15.7±2.2 respectively). Bone resorption indices (urinary hydroxyproline/creatinine and calcium/creatinine ratios) were increased immediately post-OHTX but fell by 6 months. Serum testosterone was reduced in males but recovered towards normal values by 6–12 months. Regression analysis showed lumbar bone loss was predicted independently by the change in both serum osteocalcin and testosterone. The data suggest that bone loss post-OHTX is due to a combination of accelerated turnover and hypogonadism.     

Implant design affects markers of bone resorption and formation in total hip replacement.

Concentrations of the bone resorption markers pyridinoline and deoxypyridinoline and the bone formation marker osteocalcin were measured in 24-h urine collections from 30 subjects who underwent unilateral total hip replacements for monoarticular symptomatic osteoarthrosis and 10 controls. The patient groups were divided based on the femoral implant type (cemented cobalt alloy stem, cementless porous coated cobalt alloy stem, and cementless porous coated titanium alloy stem). Urine collections were performed before surgery and then at 3, 6, 12, 24, and 36 months. There were significant changes over time in the three patient groups for pyridinoline, deoxypyridinoline, and the ratio of osteocalcin to deoxypyridinoline (p < or = 0.01), but the control group values did not change over time. The resorption markers tended to peak at 3 months and the osteocalcin to deoxypyridinoline ratio was more variable, having depressed values in the cementless cobalt alloy group and elevated values in the other two groups compared with baseline. The cementless cobalt alloy group had higher resorption marker levels than the cemented cobalt alloy group at 6, 12, 24, and 36 months and higher levels than the cementless titanium alloy group at all postoperative times (p < 0.05). The osteocalcin to deoxypyridinoline ratio was lower in the cementless cobalt alloy group than in the cemented cobalt alloy group at 3, 6, and 24 months and the cementless titanium alloy group at 6, 12, and 24 months (p < 0.05). For the cemented cobalt chrome group, the baseline-normalized resorption marker values at 3 months and 6 months were correlated with the severity of radiographically assessed bone loss at 36 months (0.749 < r < 0.840; p < 0.05). For the cementless titanium alloy group, baseline-normalized osteocalcin/ deoxypyridinoline ratios at 3 months and 6 months were related inversely to radiographic bone loss at 36 months (0.687 < r < 0.749; p < 0.05). Thus, body fluid markers of bone metabolism change after total hip replacement. In addition, the changes in the marker concentrations were sensitive to implant design and were correlated with subsequent stress-shielding-induced bone loss.     

Time-dependent changes in biochemical bone markers and serum cholesterol in ovariectomized rats: Effects of raloxifene HCl, tamoxifen, estrogen, and alendronate

Bone loss associated with postmenopausal osteoporosis can be reduced by treatment with antiresorptive agents such as estrogen or bisphosphonates. Whereas bisphosphonates primarily affect bone loss, estrogens have an advantage of also lowering serum cholesterol levels, although they have a detrimental effect in the uterus. Recently, raloxifene HCl, a selective estrogen receptor modulator (SERM), has been shown to decrease both bone loss and cholesterol levels without the negative uterine effects. These antiresorptive agents reduce bone turnover, which can be evaluated by measuring bone turnover markers. To compare the effects of estrogen, two SERMs (raloxifene HCl and tamoxifen), and alendronate, a bisphosphonate that inhibits bone loss by an estrogen-independent pathway, on metabolic bone markers and cholesterol levels, rats were ovariectomized 2 weeks prior to 3 weeks of daily oral treatment with raloxifene HCl (3 mg/kg), ethynyl estradiol (0.1 mg/kg), tamoxifen (3 mg/kg), or alendronate (3 mg/kg). Raloxifene HCl, tamoxifen, and ethynyl estradiol reduced serum cholesterol to levels below control values within 4 days after initiation of treatment, whereas alendronate had no effect. After 3 weeks of treatment, serum cholesterol values in ethynyl estradiol treated animals, although still below the control value, had risen 6.4-fold; raloxifene HCl and tamoxifen values rose by only 1.4–1.5-fold. Therefore, compared with estrogen, SERMs may have a longer-term suppressive effect on serum cholesterol. At 4 days of treatment, ovariectomized rats had a 1.4-fold increase in serum osteocalcin level compared with controls. Ethynyl estradiol lowered this level within 1 week of treatment by 18%, with a more pronounced reduction of 34% at 3 weeks. In contrast, raloxifene HCl, tamoxifen, or alendronate had very little effect after the first week (6% to 13% reduction), although there was an 18% to 25% reduction by 3 weeks. Urinary pyridinoline levels, elevated 1.4-fold in the ovariectomized rat compared with controls 2 weeks after surgery, were reduced to control values after 2 weeks of treatment with raloxifene HCl, ethynyl estradiol, tamoxifen, or alendronate. These data support the concept that estrogen, raloxifene HCI, tamoxifen, and alendronate inhibit bone loss in the ovariectomized animal by reducing bone resorption. The results also indicate that for treatment of postmenopausal osteoporosis, raloxifene HCl may have an advantage over the other antiresorptives studied in having both non-uterotrophic and hypocholesterolemic effects in addition to its ability to inhibit bone resorption.     

Changes in bone mineral density,insulin-like growth factor-1 and insulin-like growth factor binding protein-3 in kidney transplant recipients. A longitudinal study

BACKGROUND: Osteopenia is a major complication of renal transplantation (RTx). This cross-sectional and longitudinal study was planned to better define long-term bone status and relationship to IGF system components. METHODS: Serial measurements of bone mineral density (BMD) and serum markers were performed in 30 patients prior to RTx and at 6 and 12 months following RTx. Serum concentrations of insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), vitamin D, and intact parathyroid hormone (iPTH) were measured. RESULTS: Serum creatinine, phosphate, alkaline phosphatase and osteocalcine levels decreased, serum calcium levels increased and serum iPTH levels did not change significantly after transplantation. The mean BMD of the vertebrae was 0.97 +/- 0.22 g/cm(2) at the time of RTx, 0.87 +/- 0.21 g/cm(2) 6 months post-RTx (p < 0.05), and 0.81 +/- 0.21 g/cm(2) 12 months post-RTx (p < 0.05). Femur BMD also declined from 0.79 +/- 0.16 to 0.72 +/- 14 g/cm(2) at 12 months (p < 0.05). There was a significant increase in the IGF-1 and a significant reduction in the IGFBP-3 concentrations at 6 months post-RTx (p < 0.05). Significant correlations between serum IGF-1 concentrations and vitamin D concentrations were noted only at 6 months. There was no significant correlation between the BMD and serum IGF system. CONCLUSIONS: These results demonstrate a significant loss of BMD after RTx. The circulating levels of IGF-1 and IGFBP-3 stimulated by the reduction in BMD and IGF-1 secretion are increased in order to restore bone formation.     

Changes in Bone Mass and Bone Turnover Following Distal Forearm Fracture

Bone loss occurs close to a fracture and is associated with increased bone turnover. Fracture healing itself results in increased markers of bone turnover. But the exact patterns of these changes after different fractures are unclear. We aimed to investigate the changes in bone density and biochemical markers following distal forearm fracture. Twenty women (mean age 63 years) were recruited following fracture of the distal radius and ulna. Bone mineral density (BMD) of the hand and forearm were measured by dual-energy X-ray absorptiometry (DXA) and quantitative ultrasound (QUS) of the fingers was measured at 0, 6, 12, 26 and 52 weeks after fracture. Serum and urine samples were collected at 0, 3 and 7 days and at 2, 4, 6, 12, 26 and 52 weeks after fracture to measure markers of bone turnover. For bone formation we measured: bone alkaline phosphatase (iBAP), osteocalcin (Oc), procollagen type I N-terminal propeptide (PINP); and for bone resorption: tartrate-resistant acid phosphatase (TRAcP), free deoxypyridinoline (iFDpd), N-telopeptides of type I collagen (NTx). We used the nonfractured limb to calculate values for baseline BMD and amplitude-dependent speed of sound (AD-SoS). There was a decrease in BMD at the hand and in AD-SoS of the fingers after forearm fracture (p<0.001). This bone loss was maximal for BMD by 6 weeks at 9% (p<0.001) and remained decreased at 52 weeks. AD-SoS decreased at 12 weeks by 3% (p<0.01) and recovered completely by 52 weeks. Bone formation markers increased between 2 and 4 weeks by 13–52% (p<0.001), and were still elevated at 52 weeks. Bone resorption markers increased between 2 and 6 weeks by 18–35% and returned to baseline at 52 weeks (TRAcP remained elevated). We conclude that BMD decreased distal and immediately proximal to the fracture line when measured with DXA and QUS. Bone loss after distal forearm fracture did not recover by 52 weeks and most bone turnover markers did not return to baseline. Received: 27 January 1999 / Accepted: 19 April 1999     

Changes in bone turnover following gonadotropin-releasing hormone (GnRH) agonist administration and estrogen treatment in cynomolgus monkeys: a short-term model for evaluation of antiresorptive therapy

In this study we determine the early time course of estrogen deficiency-induced bone loss in the cynomolgus monkey and examine the potential of this method for evaluating antiresorptive therapies. In two groups of animals, estrogen deficiency was induced by the administration of a gonadotropin-releasing hormone agonist (GnRHa) and bone turnover was measured using biochemical markers. Two weeks after receiving GnRHa, serum estradiol decreased to below the detection limit in most animals and remained there through 6 months or until estrogen replacement started (months 4-6). Relative to untreated animals, urinary deoxypyridinoline (dPyr), as well as C- and N-telopeptides of type I collagen, were significantly elevated 4 weeks after receiving GnRHa. Serum osteocalcin increased in GnRHa-treated animals as early as week 4 and the level was significantly higher than in untreated control animals from weeks 8-24. Estradiol treatment returned all measures of bone turnover to control levels within 2 weeks. The use of biochemical markers as surrogates of bone turnover and loss was validated by measurement of bone mineral density (BMD), which showed a significant reduction at 6 months in estrogen-deficient animals. However, lumbar BMD in animals that received GnRHa and estradiol was similar to that in animals that had not received GnRHa. In conclusion, a monthly depot injection of GnRHa resulted in increased bone turnover due to estrogen deficiency, as early as 4 weeks after treatment. Estrogen administration returned bone turnover to control levels in 2 weeks. This method represents a valid model for evaluating antiresorptive agents in the short term in a nonhuman primate. Furthermore, the data suggest that changes in biochemical markers in response to antiresorptive therapy in humans may be detectable at much earlier timepoints than commonly used.     

Early response in biochemical markers predicts long-term response in bone mass during hormone replacement therapy in early postmenopausal women

Based on data from 153 early postmenopausal women who completed a double-blind, randomized 3 year study of graded hormone replacement therapy (HRT) doses or placebo, we investigated the value of bone markers to predict prevention of bone loss. Absolute values of serum and urinary CrossLaps (S-CTX and U-CTX) after 2 weeks of treatment were significantly correlated to 3 year bone mass response (r = −0.28/−0.35; p < 0.001). These associations were fully expressed at 6 months (r = −0.61/−0.64; p < 0.001). Receiver operating characteristic analyses revealed that the predictive capacity of one measurement of a resorption marker after 6 months’ treatment performed similarly as assessment of hip bone mass over 3 years in predicting preservation of spinal bone mass over 3 years. Comparable results were obtained using percent change from baseline in resorption markers at both 6 and 12 months, whereas for formation markers percent change was superior to absolute value at 6 months but not at 12 months. Values of accuracy for S-CTX for a cutoff of 1881 pmol/L at 6 months were 85.2% (sensitivity), 74.3% (specificity), 90.5% (positive predictive value), and 63.4% (negative predictive value); U-CTX performed similarly, whereas the values for the formation markers were slightly lower. A cutoff for S-CTX of 1245 pmol/L eliminated false-positive individuals (those who had a decrease below the cutoff but lost bone). In the false-negative group, which was composed of individuals whose S-CTX did not decrease below the cutoff but had preserved bone mass, S-CTX was significantly associated with spinal bone mass response (r = −0.41; p < 0.01), indicating these women had been treated with a dose that was not at its optimum for their individual bone turnover. For this cutoff, the values were 49.5% (sensitivity), 97.1% (specificity), 98% (positive predictive value), and 40% (negative predictive value). In conclusion, early bone marker measurements predict long-term preservation of bone mass during HRT. Resorption markers seem superior to formation markers, which reflects that the primary effect of HRT is on bone resorption. A strategy with two cutoff levels may optimize the use of bone markers to predict bone mass response. Whether resorption markers can be used to guide individualized treatment remains to be investigated.     

Sclerostin antibody stimulates bone regeneration after experimental periodontitis

The reconstruction of large osseous defects due to periodontitis is a challenge in regenerative therapy. Sclerostin, secreted by osteocytes, is a key physiological inhibitor of osteogenesis. Pharmacologic inhibition of sclerostin using sclerostin‐neutralizing monoclonal antibody (Scl‐Ab) thus increases bone formation, bone mass and bone strength in models of osteopenia and fracture repair. This study assessed the therapeutic potential of Scl‐Ab to stimulate alveolar bone regeneration following experimental periodontitis (EP). Ligature‐induced EP was induced in rats to generate localized alveolar bone defects. Following 4 weeks of disease induction, Scl‐Ab (+EP) or vehicle (+/? EP) were systemically delivered, twice weekly for up to 6 wks to determine the ability of Scl‐Ab to regenerate bone around tooth‐supporting osseous defects. 3 and 6 wks after the initiation of Scl‐Ab or vehicle treatment, femur and maxillary jawbones were harvested for histology, histomorphometry, and micro‐computed tomography (micro‐CT) of linear alveolar bone loss (ABL) and volumetric measures of bone support, including bone volume fraction (BVF) and tissue mineral density (TMD). Serum was analyzed to examine bone turnover markers during disease and regenerative therapy. Vehicle + EP animals exhibited maxillary bone loss (BVF, TMD and ABL) at ligature removal and thereafter. 6 weeks of Scl‐Ab significantly improved maxillary bone healing, as measured by BVF, TMD and ABL, when compared to vehicle + EP. After 6 weeks of treatment, BVF and TMD values in the Scl‐Ab + EP group were similar to those of healthy controls. Serum analysis demonstrated higher levels of bone formation markers osteocalcin and PINP in Scl‐Ab treatment groups. Scl‐Ab restored alveolar bone mass following experimental periodontitis. These findings warrant further exploration of Scl‐Ab therapy in this and other oral bone defect disease scenarios. © 2013 American Society for Bone and Mineral Research.     

应用脱钙骨基质和硫酸钙颗粒治疗骨缺损的初期结果

目的探讨使用骨移植替代物脱钙骨基质（DBM）和硫酸钙颗粒（OSTEOSET）治疗骨缺损的疗效。方法对同期手术治疗的52例骨缺损患者的缺损处,分别于术后第1、4、8周及3、6、12个月进行随访并摄X线片直至骨缺损愈合。统计分析患者的临床资料、X线片辅助分析骨缺损修复程度和并发症。结果随访8-12个月,植骨术后6、12个月分别有95%和99%患者的骨缺损显示有明显的新骨形成,修复水平为60%-100%。并发症为3例（5.77%）,经换药后治愈,未发生骨缺损不愈合。结论DBM和OSTEOSET在骨愈合早期可加速骨缺损的修复,并可作为新鲜自体髂骨的替代物。     

Increases in bone turnover marker levels at an early phase after starting zoledronic acid predicts skeletal-related events in patients with prostate cancer with bone metastasis

Study Type – Prognosis (case series) Level of Evidence 4 What’s known on the subject? and What does the study add?

相似文献   

Tartrate-resistant acid phosphatase 5b (TRAP 5b) as a marker of osteoclast activity in the early phase after cementless total hip replacement

Background After total hip replacement, increased bone metabolism is seen. A local periprosthetic osteopenia can be measured by dual-energy X-ray absorptiometry (DXA), but it is still unkown whether biochemical markers can be used to monitor the local remodeling at an earlier stage.

Patients and methods In this prospective study we compared the biochemical markers tartrate-resistant acid phosphatase 5b (TRAP 5b), bone ALP, osteocalcin and CrossLaps with periprosthetic DXA in 17 consecutive patients after uncemented total hip replacement.

Results We found a highly significant early increase in TRAP 5b after 2 weeks and 6 weeks, which was followed by a densitometrically detectable decrease in bone mineral density after 26 weeks, especially in periprosthetic section Gruen zone 7. Bone ALP and osteocalcin levels as markers of osteoblast activity, and also Cross-Laps as a further marker of osteoclast activity, did not appear to allow any significant prediction of local bone remodeling.

Discussion Our findings show that TRAP 5b is a sensitive parameter for monitoring of osteoclast activity after cementless total hip replacement, and may predict local osteopenia.     

Changes of the biochemical markers of bone turnover and periprosthetic bone remodeling after cemented hip arthroplasty

Do periprosthetic bone loss and postoperative levels of the biochemical markers of bone turnover correlate? The femoral bone mineral density of 53 patients was measured by dual-energy x-ray absorptiometry 1 week and 2, 4, 6, and 12 months after cemented total hip arthroplasty (THA). Biochemical markers of bone turnover were assayed preoperatively and 3, 8, 16, and 24 weeks post-THA. Greatest bone loss was detected in the calcar region (region of interest 7), on average, 16% after 1 year. A marker of bone resorption, C-terminal telopeptides of type I collagen, increased 21% 3 weeks after THA. A significant correlation between periprosthetic bone loss in region of interest 7 after 1 year and type I collagen at 3 weeks was seen (r = −0.42, P = .003). Data suggest that periprosthetic bone loss is induced by an early postoperative high activity of osteoclasts. Counteracting this osteoclast activity with a limited and timely postoperative antiresorptive treatment may be concluded for clinical application.     

Markers of Bone and Calcium Metabolism Following Gastric Bypass and Laparoscopic Adjustable Gastric Banding

BACKGROUND: Several studies have suggested that morbid obesity is associated with vitamin D deficiency and elevated parathyroid hormone (PTH). Studies have also suggested that there is an increase in vitamin D deficiency, bone resorption, and elevated PTH after gastric bypass surgery. Few studies have evaluated markers of bone and calcium metabolism after laparoscopic adjustable gastric banding or compared these results to those after gastric bypass. METHODS: Data on all patients undergoing primary gastric bypass (GBP; n = 979) and laparoscopic adjustable gastric banding (LAGB; n = 269) procedures at a tertiary-referral center from June 1996 through March 2005 were reviewed from a prospective database. Only patients with 25OH vitamin D levels available were included in this study (n = 534; GBP = 403, LAGB = 131). All patients were advised to take at least 1,200 mg calcium and 800-1,200 IU of vitamin D daily before and subsequent to their operation. Markers for bone metabolism [25OH Vitamin D, corrected serum calcium, alkaline phosphatase (AP), and PTH] were evaluated preoperatively and 3, 6, 12, and 24 months postoperatively. An analysis of variance and chi-square were performed to determine differences between the operative groups. Linear regression analysis was performed to evaluate the relationship between preoperative body mass index (BMI) and 25OH vitamin D and PTH levels and between percent excess weight loss and 25OH vitamin D and PTH after surgery. RESULTS: Sixty-four percent of all patients presented with vitamin D deficiency (<20 ng/ml) and 14% presented with elevated PTH preoperatively. Mean 25OH vitamin D levels and AP levels increased significantly after GBP surgery (vitamin D, 17 to 25 ng/ml 12 months post-op; AP, 80 to 90 IU/L 24 months post-op). Corrected calcium levels remained within normal limits and showed no change over time after both procedures. AP levels significantly increased from 76 IU/l preoperatively to 82 IU/l 6 months after LAGB surgery and then decreased to 59 IU/l 24 months after LAGB surgery. Linear regression analysis of preoperative vitamin D, PTH, and BMI values showed a significant positive relationship between initial BMI and PTH (r = 0.29) and a significant negative relationship between vitamin D and initial BMI (r = -0.19). A significant positive linear relationship between vitamin D and percent excess weight loss was evident 12 and 24 months after GBP surgery (r = 0.39 and 0.57, respectively). A negative relationship was evident between PTH and vitamin D 6 months after GBP surgery (r = -0.35) and 12 months after LAGB surgery (r = -0.61). CONCLUSIONS: These findings suggest that morbid obesity is associated with vitamin D deficiency, and elevated PTH and with adequate supplementation, GBP, and particularly LAGB, patients can improve their bone metabolism abnormalities related to obesity. Furthermore, adequate supplementation for GBP patients may attenuate the increased risk for bone loss associated with malabsorption from the bypass.     

Factors influencing bone mineral density around the femoral stem after cementless total hip arthroplasty]

Factors influencing bone mineral density around the femoral stem after PM cementless total hip arthroplasty were evaluated in longitudinal study of 18 hips in 18 patients who had undergone surgery due to unilateral hip osteoarthritis. Bone mineral density in the femoral neck was determined by dualenergy X-ray absorptiometry measurement performed preoperatively and in periprosthetic femoral Gruen's zones prospectively 2 weeks, 3, 6, 12 and 24 months after surgery. The concentrations of calcium, magnesium and fluoride were measured in cortical and trabecular bone samples taken from resected femoral head and neck. At 12 and 24 months after the operation the regional bone mineral density measurement showed significant, maximum decrease but after 12 months bone mineral density appeared to be stabilized. The analysis of preoperative femoral neck density and fluoride content in trabecular bone proved that osteopenia and lower fluoride concentrations correlated significantly with greater bone density decrease after total hip arthroplasty. No other factors (age, sex, weight, calcium and magnesium concentrations in bone and fluoride concentration in cortical bone) showed significant associations.     

Significance of time-course changes of serum bone markers after parathyroidectomy in patients with uraemic hyperparathyroidism.

BACKGROUND: The increase of bone mineral density in cortical bone after parathyroidectomy is smaller than that in cancellous bone. Changes of serum bone markers reflect those of bone metabolism both in cortical and cancellous bone after parathyroidectomy. The present study was undertaken to investigate changes of histomorphometric parameters of cortical and cancellous bone together and their correlation with those of serum bone markers. METHODS: Iliac bone biopsy was performed before and 1 week after parathyroidectomy in Group I (n = 13), and before and 4 and 12 weeks after in Group II (n = 11). Moreover, changes of histomorphometric parameters of the endocortical, intracortical and periosteal surfaces as well as in cancellous bone were monitored. Serum levels of intact parathyroid hormone and bone markers were measured simultaneously. Results. In cancellous bone, osteoclast surface (Oc.S/BS) decreased to 0% within 4 weeks after parathyroidectomy, while osteoblast surface (Ob.S/BS) transiently increased at 1 week, followed by a reduction at 4 weeks to levels below the pre-surgical level. In cortical bone, Oc.S/BS was not reduced to 0%, while a significant and temporary increase of Ob.S/BS was observed only on the endocortical and intracortical surfaces at 4 weeks, but not at 1 week. Serum bone resorption markers did not completely disappear and significant and sustained increases of bone formation markers were observed until 4 weeks after parathyroidectomy. CONCLUSIONS: Changes of bone formation markers lagged behind those of histomorphometric parameters in cancellous bone because changes of cortical bone were observed later and were incomplete compared with those of cancellous bone.