7-84 PTH or aluminum antagonism in the resistance of uremic bone to the remodeling effect of endogenous PTH?

Fournier, A; Solal, Martine-Esther Cohen; Oprisiu, Roxana; Choukroun, Gabriel; Morinière, P; Bouillon, Roger

doi:10.1046/j.1523-1755.2001.00761.x

Cited by 2 publications

(1 citation statement)

References 5 publications

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“…Serum concentrations of 24,25(OH) 2 D were measured by LC-MS/MS as described [33]. Serum intact PTH was measured by a two-site immunometric assay that detects only PTH (1-84) but not the large PTH (7-84) fragments [34,35]. sCD163 was measured with an in-house enzyme-linked immunosorbent assay (ELISA), as described in reference [36].…”

Section: Blood Analysesmentioning

confidence: 99%

Effect of Intravenous 25OHD Supplementation on Bone Turnover and Inflammation in Prolonged Critically Ill Patients

et al. 2020

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Critically ill patients have low circulating 25-hydroxyvitamin D (25OHD), vitamin D binding protein (DBP), and 1,25-dihydroxyvitamin D [1,25(OH)2D]. Low 25OHD is associated with poor outcomes, possibly explained by its effect on bone and immunity. In this prospective, randomized double-blind, placebo-controlled study, we investigated the feasibility of normalizing 25OHD in prolonged (>10 days) critically ill patients and the effects thereof on 1,25(OH)2D, bone metabolism, and innate immunity. Twenty-four patients were included and compared with 24 matched healthy subjects. Patients were randomized to either intravenous bolus of 200 μg 25OHD followed by daily infusion of 15 μg 25OHD for 10 days, or to placebo. Parameters of vitamin D, bone and mineral metabolism, and innate immune function were measured. As safety endpoints, ICU length of stay and mortality were registered. Infusion of 25OHD resulted in a sustained increase of serum 25OHD (from median baseline 9.2 –16.1 ng/ml at day 10), which, however, remained below normal levels. There was no increase in serum 1,25(OH)2D but a slight increase in serum 24,25(OH)2D. Mineral homeostasis, innate immunity and clinical safety endpoints were unaffected. Thus, intravenous 25OHD administration during critical illness increased serum 25OHD concentrations, though less than expected from data in healthy subjects, which suggests illness-induced alterations in 25OHD metabolism and/or increased 25OHD distribution volume. The increased serum 25OHD concentrations were not followed by a rise in 1,25(OH)2D nor were bone metabolism or innate immunity affected, which suggests that low 25OHD and 1,25OHD levels are part of the adaptive response to critical illness.

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Section: Blood Analysesmentioning

confidence: 99%

Effect of Intravenous 25OHD Supplementation on Bone Turnover and Inflammation in Prolonged Critically Ill Patients

et al. 2020

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Influence of PTH assay methodology on differential diagnosis of renal bone disease

Reichel¹,

Esser²,

Roth³

et al. 2003

Nephrology Dialysis Transplantation

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With respect to information about bone turnover we were not able to find differences between whole PTH and intact PTH assays. Our data also suggest that whole PTH and intact PTH assays give similar information. (i) The correlation between all PTH assays was very high. (ii) The rank order between whole PTH and Nichols intact PTH assays was comparable. (iii) The association between intact PTH assays and non-PTH(1-84) was very high. Albeit non-PTH(1-84) was mostly determined by the prevailing intact PTH concentration, diagnostic information on parathyroid activity provided by whole PTH or intact PTH, respectively, may differ in individual patients. How often this would happen cannot be answered with the currently available data. Unequivocal structural identification of the non-PTH(1-84) fraction would facilitate the answer to that question. The use of the whole PTH/non-PTH(1-84) ratio as a biochemical bone marker in renal bone disease requires further investigation.

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7-84 PTH or aluminum antagonism in the resistance of uremic bone to the remodeling effect of endogenous PTH?

Cited by 2 publications

References 5 publications

Effect of Intravenous 25OHD Supplementation on Bone Turnover and Inflammation in Prolonged Critically Ill Patients

Effect of Intravenous 25OHD Supplementation on Bone Turnover and Inflammation in Prolonged Critically Ill Patients

Influence of PTH assay methodology on differential diagnosis of renal bone disease

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