Use of bone turnover markers in postmenopausal osteoporosis

In prolonged critical illness, increased bone resorption and osteoblast dysfunction have been reported facing low 25 hydroxy vitamin D [25(OH)D] concentrations. The current study investigates the extent to which lack of nutritional vitamin D and time in intensive care contribute to bone loss in the critically ill. Prolonged critically ill patients (n = 22) were compared with matched controls and then randomized to daily vitamin D supplement of either +/- 200 IU (low dose) or +/- 500 IU (high dose). At intensive care admission, serum concentrations of 25(OH)D, 1,25 dihydroxyvitamin D(3), vitamin D-binding protein, ionized calcium, IL-1, and soluble IL-6-receptor were low, and PTH was normal. Circulating type-I collagen propeptides were high, alkaline phosphatase was normal, and osteocalcin was low. Bone resorption markers [(carboxy terminal cross-linked telopeptide of type I collagen (betaCTX), pyridinoline, deoxypyridinoline (DPD)] were 6-fold increased. Serum C-reactive protein (CRP) was 40-fold, IL-6 400-fold, TNFalpha levels 5-fold, and osteoprotegerin concentrations 3-fold higher than in controls. Soluble receptor activator of nuclear factor kappaB ligand was undetectable. High-dose vitamin D only slightly increased circulating 25 hydroxy vitamin D (P < 0.05), but 1,25 dihydroxyvitamin D(3) was unaltered. High-dose vitamin D slightly increased serum osteocalcin (P < 0.05) and decreased carboxy terminal propeptide type-I collagen (P < 0.05) but did not affect other bone turnover markers. Bone-specific alkaline phosphatase, urinary pyridinoline and DPD, and serum betaCTX markedly increased with time (P < 0.01). Circulating CRP and IL-6 decreased with time, whereas TNFalpha and IL-1 remained unaltered. The fall in CRP and IL-6 was more pronounced with the high- than low-dose vitamin D (P < 0.05). Except for a mirroring of betaCTX rise by a fall in osteoprotegerin, cytokines were unrelated to the progressively aggravating bone resorption. In conclusion, prolonged critically ill patients were vitamin D deficient. The currently recommended vitamin D dose did not normalize vitamin D status. Furthermore, severe bone hyperresorption further aggravated (up to 15-fold the normal values) with time in intensive care and was associated with impaired osteoblast function.

/pdf/bone-turnover-in-prolonged-critical-illness-effect-of-2kqwwd4mk0.pdf

Bone Turnover in Prolonged Critical Illness: Effect of Vitamin D

The aim was to analyse data on the use of biochemical bone turnover markers (BTM) in postmenopausal osteoporosis. We carried out a comparative analysis of the most important papers concerning BTM in postmenopausal osteoporosis that have been published recently. The BTM levels are influenced by several factors. They are moderately correlated with BMD and subsequent bone loss. Increased levels of bone resorption markers are associated with a higher risk of fracture. Changes in the BTM during the anti-osteoporotic treatment (including combination therapy) reflect the mechanisms of action of the drugs and help to establish their effective doses. Changes in the BTM during the anti-resorptive treatment are correlated with their anti-fracture efficacy. Biological samples should be obtained in a standardised way. BTM cannot be used for prediction of the accelerated bone loss at the level of the individual. BTM help to detect postmenopausal women who are at high risk of fracture; however, adequate practical guidelines are lacking. BTM measurements taken during the anti-resorptive therapy help to identify non-compliers. They may improve adherence to the anti-resorptive therapy and the fall in the BTM levels that exceeds the predefined threshold improves patients’ persistence with the treatment. There are no guidelines concerning the use of BTM in monitoring anti-osteoporotic therapy in postmenopausal women.

Biochemical markers of bone turnover: potential use in the investigation and management of postmenopausal osteoporosis

This chapter reviews the recent development in bone marker technology and also discusses the use of markers for the management of osteoporosis. There are basically two types of biomarkers for bone remodelling: for bone formation and for bone resorption. Biomarkers for bone formation consists of skeletal alkaline phosphatase (ALP), osteocalcin, and procollagen type I propeptides (PICP). ALP activity may provide information of bone metabolism within specific bone envelopes. Serum total alkaline phosphatase activity is the most commonly used marker of bone formation, but for the above reasons, it lacks sensitivity and specificity. PICP concentrations correlate weakly with histological bone formation in patients with vertebral osteoporosis. Biochemical markers of bone resorption consists of tartrate-resistant acid phosphatase, free pyridinoline and deoxypyridinoline, C-terminal cross-linking telopeptide of type I, N-terminal and C-terminal (S-CTX) crosslinking telopeptide of type I collagen, and bone sialoprotein. In osteoporosis, bone turnover markers have been suggested to predict the rate of postmenopausal bone loss, to predict the occurrence of osteoporotic fractures, and to monitor the efficacy of treatment, especially anti-resorptive therapy (hormone replacement therapy, bisphosphonates, and calcitonin). It has also been suggested that measurement of bone turnover before treatment might be useful to select the type of therapy (anti-resorptive or bone stimulating agent) and to predict the amplitude of the response to estrogen and bisphosphonate treatment.

Biochemical markers of bone turnover in osteoporosis.

We have compared the analytical performance and biological variability of three commercially available bone resorption assays: Pyrilinks-D, Osteomark, and CrossLaps, for the measurement of urinary free deoxypyridinoline (Dpd), cross-linked N-telopeptides of type I collagen (NTx), and linear C-telopeptides of type I collagen (CTx), respectively. The intraassay and interassay CVs for precision of the Dpd and NTx assays were < 10% for analyte concentrations greater than the second calibrator (i.e., 3 nmol/L Dpd or 30 nmol bone collagen equivalents/L NTx). The CTx assay demonstrated poor precision for analyte concentration lower than the third calibrator (i.e., 200 micrograms/L). The NTx assay exhibited nonlinear recovery for sample dilutions prepared in buffer; however, this nonlinear recovery could be corrected for sample dilutions made in urine at a low analyte concentration. Supplement recoveries of each of the three assays were within 100% +/- 10% on average. All three analytes showed stability through five freeze-thaw cycles. The mean day-to-day variations were 16% for Dpd, and 23% for both NTx and CTx. Similar diurnal rhythm was observed for all three assays on average, with the peak in the early morning and the nadir in the afternoon. Mean amplitude of the diurnal variation was 37% for Dpd and NTx, and 57% for CTx. Variations within the reference intervals for a healthy premenopausal population were 28% for Dpd, 57% for NTx, and 56% for CTx. Pyrilinks-D has demonstrated analytical precision and accuracy equal or superior to Osteomark and CrossLaps in all areas. Dpd exhibits the least biological variability day-to-day, within individuals across the diurnal cycle, and within a healthy premenopausal population.

/pdf/comparison-of-analytical-performance-and-biological-56f454hfbk.pdf

Comparison of analytical performance and biological variability of three bone resorption assays

The pyridinium cross-links of collagen pyridinoline (Pyd) and deoxypyridinoline (Dpd) are released during bone resorption and are neither metabolized nor absorbed from the diet. The aim of this study was to validate their use in osteoporosis. We studied 19 women with osteoporosis and estimated the bone resorption rate from a combined calcium balance/kinetics technique without (R) and with partial (RH) and “complete” (Res) correction for long-term exchange. The strongest correlation was observed between the bone-specific marker (Dpd) and with complete correction for long-term exchange (Res) (r = 0.71, p < 0.001). The intercept was not different from zero, suggesting that bone was the major source for Dpd. The crude ratio of Dpd to Res in the 19 women was 54.5; but the regression coefficient relating Dpd as the dependent variable to Res was 31.8 (95% CI 15.6–48.0), which was higher, but not significantly, than the ratio between Dpd and calcium (16.4) in 10 bone samples (cortical and trabecular bone). The weakest correlations between a biochemical marker and a kinetic index were those between hydroxyproline (a nonspecific marker of bone resorption) and R or RH. Treatment with hormone replacement therapy (HRT) or HRT and parathyroid hormone peptide 1–38 in seven women over 1 year resulted in similar percent changes in the biochemical markers and estimates of bone resorption. We conclude that the measurement of Dpd provides a reasonably accurate assessment of bone resorption in osteoporosis, and in the context of several repeat 24-h collections of urine offers measurement precision that is similar to that obtainable with methods depending on the use of radioisotopic tracers and the assessment of metabolic calcium balance.

https://asbmr.onlinelibrary.wiley.com/doi/pdf/10.1359/jbmr.1997.12.1.59

Biochemical Markers of Bone Resorption Compared with Estimates of Bone Resorption from Radiotracer Kinetic Studies in Osteoporosis

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Biochemical Markers of Bone Resorption Compared with Estimates of Bone Resorption from Radiotracer Kinetic Studies in Osteoporosis