scholarly journals Acute and 3-month effects of microcrystalline hydroxyapatite, calcium citrate and calcium carbonate on serum calcium and markers of bone turnover: a randomised controlled trial in postmenopausal women

2014 ◽  
Vol 112 (10) ◽  
pp. 1611-1620 ◽  
Author(s):  
Sarah M. Bristow ◽  
Greg D. Gamble ◽  
Angela Stewart ◽  
Lauren Horne ◽  
Meaghan E. House ◽  
...  

Ca supplements are used for bone health; however, they have been associated with increased cardiovascular risk, which may relate to their acute effects on serum Ca concentrations. Microcrystalline hydroxyapatite (MCH) could affect serum Ca concentrations less than conventional Ca supplements, but its effects on bone turnover are unclear. In the present study, we compared the acute and 3-month effects of MCH with conventional Ca supplements on concentrations of serum Ca, phosphate, parathyroid hormone and bone turnover markers. We randomised 100 women (mean age 71 years) to 1 g/d of Ca as citrate or carbonate (citrate–carbonate), one of two MCH preparations, or a placebo. Blood was sampled for 8 h after the first dose, and after 3 months of daily supplementation. To determine whether the acute effects changed over time, eight participants assigned to the citrate dose repeated 8 h of blood sampling at 3 months. There were no differences between the citrate and carbonate groups, or between the two MCH groups, so their results were pooled. The citrate–carbonate dose increased ionised and total Ca concentrations for up to 8 h, and this was not diminished after 3 months. MCH increased ionised Ca concentrations less than the citrate–carbonate dose; however, it raised the concentrations of phosphate and the Ca–phosphate product. The citrate–carbonate and MCH doses produced comparable decreases in bone resorption (measured as serum C-telopeptide (CTX)) over 8 h and bone turnover (CTX and procollagen type-I N-terminal propeptide) at 3 months. These findings suggest that Ca preparations, in general, produce repeated sustained increases in serum Ca concentrations after ingestion of each dose and that Ca supplements with smaller effects on serum Ca concentrations may have equivalent efficacy in suppressing bone turnover.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 358.2-358
Author(s):  
S. Shevchuk ◽  
L. Denyshchych

Background:Osteoporosis and fractures associated with it are considered to be one of the most severe complications of systemic lupus erythematosus (SLE). The role of a systemic inflammatory process, vitamin D deficiency, hypogonadism and peculiarities of disease treatment in reduced bone mineral density (BMD) is being discussed. Even though the frequency of osteoporosis in patients with SLE is being studied extensively by scientists from different countries, data on the peculiarities of bone tissue metabolism and the factors that provoke disorders of bone remodeling in such individuals are quite limited. The association between markers of bone tissue metabolism and BMD, and how they change during an inflammatory process is poorly studied.Objectives:The objective of our research is to study the levels of osteocalcin (OC) and procollagen type I C-terminal propeptide (PICP) in patients with systemic lupus erythematosus and to estimate their association with BMD and inflammatory activity based on the levels of interleukin-6 (IL-6).Methods:A total of 58 women with SLE (the average age was 45.11 ± 1.03 years old) and 29 individuals from the control group (the average age was 46.79 ± 2.30 years old) were examined. The diagnosis of SLE was established on the basis of 2019 EULAR/ACR classification criteria for SLE. Levels of IL-6, OC and PICP in serum were determined by enzyme immunoassay. Changes in BMD of the lumbar spine at the level of L1-L4 and the proximal femur were determined by dual-energy X-ray absorptiometry. In postmenopausal women, the diagnosis of osteoporosis was established by the T-score ≤ -2.5 SD. Osteopenia met T-score from -1 to -2.5 SD. In women of reproductive age, the Z-score was used to determine BMD. Values of the Z-score ≤ -2.0 SD were considered as “below expected range for age”.Results:The average OC level in serum of practically healthy individuals equaled 17.64 ± 0,59 ng/ml, and in patients with SLE it was 13.96 ± 0.40 ng/ml, i.e. it was 20.9% lower. The average PICP level in the control group equaled 107.8 ± 4.28 ng/ml, in the main group it was 92.9 ± 5.01 ng/ml, i.e. 16% lower. Overall, the decrease in the bone turnover markers (PICP and/or OC) was noticed in 28 patients with SLE (48.3%) and only in 4 practically healthy individuals (13.8%).In women with decreased bone turnover markers, the T-score of the lumbar spine and hip was 2.3-2.6 times lower (p < 0.05) than in the group with adequate levels of bone turnover markers. Z-score was also lower among patients with decreased levels of OC and PICP. In this group, the average BMD level was 0.81 ± 0.05 g/cm2and was 13.8% lower than in the group of patients with no signs of bone tissue metabolism disorder – 0.94 ± 0.02 g/cm2. Among the group of women with signs of suppression of biosynthetic processes in bone tissue, there were twice more individuals with decreased BMD. In patients with critically high levels of IL-6 (above 20.0 ng/L), OC level was lower than in patients with high (12.5-20.0 ng/L) and adequate (< 12.5 ng/L) levels of IL-6 (by 17.3 and 19% respectively). The proportion of individuals with low OC levels increased from 31.2% in the last group to 70.6% among patients with critically high levels of IL-6.PICP level was also lower (38.1% and 39.7% respectively) in case of critically high IL-6 levels compared to its high and adequate levels. The proportion of individuals with low PICP levels increased from 6.3% in the group with adequate IL-6 level to 58.8% in the group with critically high IL-6 level.Conclusion:Women with SLE have bone tissue metabolism disorder in the form of decreased bone turnover markers (procollagen type I C-terminal propeptide and osteocalcin) associated with the inflammatory activity. In the group of patients with the signs of suppression of biosynthetic processes in the bone tissue, there were more individuals with decreased BMD.Disclosure of Interests:Sergii Shevchuk Grant/research support from: Celltrion, Inc, Liudmyla Denyshchych: None declared


2003 ◽  
Vol 88 (10) ◽  
pp. 4867-4873 ◽  
Author(s):  
Jackie A. Clowes ◽  
Heather C. Allen ◽  
Donna M. Prentis ◽  
Richard Eastell ◽  
Aubrey Blumsohn

Abstract Feeding or oral intake of glucose results in an acute suppression of bone turnover. This does not appear to be mediated by insulin. Several gastrointestinal hormones modulate bone turnover in vitro and may mediate this response. We examined whether inhibiting the production of gastrointestinal hormones using octreotide could block glucose-mediated suppression of bone turnover. Fifteen subjects were each studied on four occasions in a randomized, single-blind, crossover study after receiving 1) oral placebo, iv saline; 2) oral glucose, iv saline; 3) oral glucose, iv octreotide; or 4) iv octreotide alone. We measured serum C-terminal telopeptide of type I collagen, urinary N-terminal telopeptide of type I collagen, osteocalcin, procollagen type I N-terminal propeptide, PTH, insulin, ionized calcium, and glucose over 4 h. All bone turnover markers decreased significantly after oral glucose (P &lt; 0.001). At 120 min serum C-terminal telopeptide decreased by 45 ± 2%, urinary N-terminal telopeptide by 31 ± 7%, osteocalcin by 16 ± 1%, and procollagen type I N-terminal propeptide by 8 ± 1%. There was no significant decrease in bone turnover in response to oral glucose during octreotide infusion. Octreotide alone resulted in a significant increase in all bone turnover markers (P &lt; 0.05) and PTH (P &lt; 0.01). We conclude that octreotide completely abolishes the bone turnover response to glucose intake and increases PTH secretion. The apparent bone turnover response to feeding is probably mediated by an octreotide-inhibitable endocrine factor.


2011 ◽  
Vol 164 (4) ◽  
pp. 643-648 ◽  
Author(s):  
Maria Luchavova ◽  
Vit Zikan ◽  
Dana Michalska ◽  
Ivan Raska ◽  
Ales A Kubena ◽  
...  

BackgroundWe hypothesized that with the administration of teriparatide (TPTD) treatment at different times, we would be able to modify the physiological circadian rhythm of bone turnover.MethodsThe concentration of serum C-terminal telopeptide of collagen type I (βCTX), serum N-terminal propeptide of procollagen type I (P1NP), serum ionized calcium (iCa), and plasma PTH were measured every 3 h over a 24 h period in 14 postmenopausal osteoporotic women (aged 72.4±9.3 years) treated with 20 μg TPTD for long term, given at different times of the day. General linear model-repeated measurements (GLM RM) were performed to analyze the circadian rhythms as well as intergroup comparisons.ResultsGLM-RM for both related groups showed a significant influence of time of day on all measured variables except P1NP. The analysis for each group separately provided a powerful model for βCTX (P<0.001, η2=0.496), serum iCa (P<0.001, η2=0.423), plasma PTH (P<0.001, η2=0.283), and serum PINP (P<0.001, η2=0.248). While the evening TPTD treatment showed a marked circadian rhythm for serum βCTX, the morning TPTD treatment rather suggested circasemidian rhythm. The P1NP rhythm followed a much smaller amplitude of the rhythm than βCTX. Changes in serum iCa were positively related to changes in serum βCTX (P<0.001) and negatively related to changes in PTH (P<0.001).ConclusionTiming of TPTD administration may significantly change the 24 h variation in bone turnover markers as well as calcium-parathyroid axis in postmenopausal osteoporotic women.


2011 ◽  
Vol 55 (4) ◽  
pp. 272-278 ◽  
Author(s):  
André Gonçalves da Silva ◽  
José Gilberto H. Vieira ◽  
Ilda Sizue Kunii ◽  
Janaína Martins de Lana ◽  
Marise Lazaretti-Castro

OBJECTIVE: To assess bone turnover markers (BTM) and bone mineral density (BMD) after discontinuation of alendronate treatment used for five or more years. SUBJECTS AND METHODS: 40 patients (pt) with post-menopausal osteoporosis treated with alendronate (10 mg/d) for at least five years (Group 1, G1) had their medication discontinued. Group 2 (G2): 25 pt treated with alendronate for at least one year. Group 3 (G3): 23 treatment-naïve osteoporotic pt. BMD was evaluated in G1 and G2 at baseline and after 12 months. Collagen type I cross-linked C-telopeptide (CTX) and procollagen type 1 N-terminal propeptide (P1NP) levels were measured in all pt at baseline, and in G1 and G2 every three months for 12 months. Data were analyzed using ANOVA on ranks and Mann-Whitney tests. RESULTS: Mean BMD values in G1 and G2 did not differ during follow-up. However, 16 pt (45.7%) in G1 and one (5.2%) in G2 lost BMD (P < 0.001). BTM at baseline was not different between G1 and G2, and both were lower than G3. A significant increase in BTM levels was detected in G1 pt after three months, but not in G2. CONCLUSION: Observed BMD loss and BTM rise after alendronate withdrawal imply that bone turnover was not over suppressed, and alendronate discontinuation may not be safe.


2002 ◽  
Vol 87 (7) ◽  
pp. 3324-3329 ◽  
Author(s):  
Jackie A. Clowes ◽  
Robert T. Robinson ◽  
Simon R. Heller ◽  
Richard Eastell ◽  
Aubrey Blumsohn

Bone turnover is acutely suppressed after feeding or oral glucose. Insulin infusion suppresses bone turnover and might mediate this effect, but this is confounded by a possible direct effect of hypoglycemia. We examined the effect of euglycemic hyperinsulinemia and hypoglycemic hyperinsulinemia on bone turnover using an insulin clamp. Sixteen men participated in this double-blind crossover study. Clamp induction involved infusion of insulin (80 mU/m2·min) while maintaining euglycemia (5 mmol/liter) for 40 min with a variable rate dextrose infusion. Glucose was lowered to 2.5 mmol/liter (hypoglycemic clamp) or maintained at 5 mmol/liter (euglycemic clamp) for a further 105 min. Nine controls received a matched saline infusion. Measurements included serum C-terminal telopeptide of type I collagen, procollagen type I N-terminal propeptide, osteocalcin, and PTH. Induction of hyperinsulinemia resulted in a reduction in PTH (27% ± 5; P &lt; 0.01), but no significant change in bone turnover from baseline. Hypoglycemic clamp resulted in suppression of serum C-terminal telopeptide of type I collagen by 34% ± 3, procollagen type I N-terminal propeptide by 15% ± 1, osteocalcin by 5% ± 1, and PTH by a further 12% ± 5 (all P &lt; 0.05). By contrast, there was no significant change in any marker of bone turnover during euglycemic clamp. Postprandial hyperinsulinemia is unlikely to explain the acute suppression of bone turnover with feeding. The reduction in bone turnover during hypoglycemia may be related to hypoglycemia itself, acute changes in PTH, or other hormones released in response to hypoglycemia.


Bone ◽  
2010 ◽  
Vol 47 ◽  
pp. S193
Author(s):  
R. Eastell ◽  
A. Rogers ◽  
X. Ni ◽  
J.H. Krege

2018 ◽  
Vol 56 (10) ◽  
pp. 1603-1607 ◽  
Author(s):  
Samuel Vasikaran

Abstract An imbalance between bone formation and bone resorption is a factor in the development of osteoporosis. Bone turnover markers (BTM) are useful in assessing bone remodeling at the cellular level. Measurement of BTM is useful for assessing bone turnover and therefore fracture risk as well as for monitoring response to treatment response. This paper describes the steps that have been taken so far and the ongoing work to harmonize the total testing process for the assessment of bone turnover in osteoporosis internationally and collaboratively between the clinical and laboratory professions. The International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) in collaboration with the International Osteoporosis Foundation (IOF) as well as the National Bone Health Association (NBHA) in the US have designated procollagen type I N propeptide (s-PINP), and cross-linked β-isomerized type I collagen C-telopeptide (s-βCTX), in blood as reference standard BTM. Collaborative efforts are ongoing in order to standardize preanalytical steps as well as the analysis of s-PINP and s-CTX by standardizing or harmonizing their measurement as appropriate and reporting of values. Reporting units have been standardized. Reference interval studies and examination of appropriate decision thresholds, reference change values and treatment targets are ongoing with the aim of harmonizing the total testing process for the assessment of bone turnover in osteoporosis.


Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 364
Author(s):  
Pramod B. Umarji ◽  
Pankaj Verma ◽  
Vivek Garg ◽  
Marian Schini ◽  
Richard Eastell

Young Indian women may be at risk of poor bone health due to malnutrition. The aim of this study was to examine the effects on bone metabolism of a nutritional supplement in women aged 25 to 44. The nutritional supplement was a protein-rich beverage powder fortified with multi-micronutrients including calcium (600 mg), vitamin D (400 IU), and vitamin K (55 mcg) per daily serving, while a placebo supplement was low-protein non-fortified isocaloric beverage powder. This 6-month randomised, controlled trial showed favorable changes in bone turnover markers (decreased) and calcium homeostasis; such changes in older adults have been associated with slowing of bone loss and reduced fracture risk. For example, serum CTX decreased by about 30% and PINP by about 20% as a result of the increase in calcium intake. There were also changes in the ratio of carboxylated to undercarboxylated osteocalcin and such changes have been linked to a slowing of bone loss in older subjects. For example, the ratio increased by about 60% after 3 months as a result in the improvement in vitamin K status. Finally, there were improvements in the status of B vitamins, and such changes have been associated with reductions in homocysteine, but it is uncertain whether this would affect fracture risk. The product was generally well tolerated. This study shows the nutritional supplement holds promise for improved bone health among young Indian women.


2019 ◽  
Vol 6 (1) ◽  
pp. e000352 ◽  
Author(s):  
Sara K. Tedeschi ◽  
Cynthia Aranow ◽  
Diane L. Kamen ◽  
Meryl LeBoff ◽  
Betty Diamond ◽  
...  

ObjectiveBone health in SLE is adversely affected by vitamin D deficiency, inflammatory cytokines and glucocorticoid use. We hypothesised that vitamin D supplementation would increase markers of bone formation and decrease markers of bone resorption in SLE subjects.MethodsWe studied 43 vitamin D-deficient SLE subjects who participated in a 12-week randomised controlled trial of 2000–4000 IU/day vitamin D supplementation versus placebo. Subjects had inactive SLE (SLE Disease Activity Index ≤4) and were taking <20 mg prednisone daily at baseline. We assayed baseline and week 12 serum 25-hydroxyvitamin D, N-terminal propeptide of type 1 collagen (P1NP) and C-telopeptide (CTX). We tested the effect of vitamin D versus placebo on change (Δ) in P1NP and ΔCTX in an intention-to-treat analysis. Secondary analyses evaluated whether vitamin D affected bone turnover among subjects achieving vitamin D repletion (≥30 ng/mL) or currently taking glucocorticoids.Results28 subjects were randomised to vitamin D and 15 to placebo. Mean age was 39 years and 40% were using glucocorticoids at enrolment. Repletion was achieved by 46% in the vitamin D group versus none in the placebo group. Changes in bone turnover markers were not significantly different in the vitamin D group versus placebo group (median ΔP1NP −0.2 vitamin D group vs −1.1 placebo group (p=0.83); median ΔCTX +3.5 vitamin D group vs −37.0 placebo group (p=0.50)). The effect of vitamin D did not differ based on achieving vitamin D repletion or baseline glucocorticoid use.ConclusionVitamin D supplementation did not affect the 12-week change in bone turnover markers among SLE subjects in this trial.


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