Supplementation, optimal status, and analytical determination of vitamin D: Where are we standing in 2012?

There is a growing interest for vitamin D in the medical and scientific community as well as in the public medias as illustrated by a huge number of publications. Most experts claim that vitamin D deficiency/insufficiency is widespread with potential important public health consequences. It may seem surprising for many persons that a deficiency in a vitamin may be so frequent in countries where food is so diversified and easily available. In fact, vitamin D is not a vitamin stricto sensu as it is mainly synthesized in the skin under the action of UVB rays, while its food sources are scarce. Furthermore, UVB rays are absent during a marked part of the year at latitudes greater than 35-40°, while pollution and cloud cover reduce the number of UVB reaching the earth, and many factors such as age, skin pigmentation, covering clothes, sun creams reduce the capacity of the skin to synthesize vitamin D3. Vitamin D must be hydroxylated to form 1,25dihydroxyvitamin D (1,25OH2D), the active metabolite. As 1,25OH2D is released into the bloodstream and binds to a receptor present in several distant tissues, it may be considered as a hormone, vitamin D being thus a pre-prohormone. In the present article, we review briefly the metabolism and various effects of vitamin D as well as the vitamin D assays and vitamin D treatments. We define vitamin D deficiency/insufficiency considerin

Overestimation of the 25OHD serum concentration with the automated IDS EIA kit.

We have recently observed an increasing number of patients presenting very high serum levels of 25-hydroxyvitamin D [25(OH)D] (> 150 ng/mL), which, in all cases, had been measured with the IDS EIA kit adapted on different "open" automated platforms. We performed a comparison between the IDS EIA kit adapted on two different "open"automated platforms and the DiaSorin RIA. We found a systematic bias (higher levels with the IDS EIA kit) for concentrations more than 50-60 ng/mL that was less obvious when the IDS EIA was used in its manual procedure. We thus suggest to use the IDS EIA kit in its manual procedure rather than to adapt it on an automated platform, and to interpret cautiously a 25(OH)D greater than 100 ng/mL with this kit

Validation of the Abbott Architect 25(OH)-vitamin D assay

peer reviewe

Inhibition of markers of bone resorption by consumption of vitamin D and calcium-fortified soft plain cheese by institutionalised elderly women

Acceleration of bone remodelling increases the risk of fragility fractures. The objective of the present study was to explore in elderly women whether a vitamin D and Ca-fortified dairy product providing about 17-25% of the recommended intakes in vitamin D, Ca and proteins would reduce secondary hyperparathyroidism and bone remodelling in a way that may attenuate age-related bone loss in the long term. Thirty-seven institutionalised women, aged 84·8 (sd 8·1) years, with low serum 25-hydroxyvitamin D (5·5 (sd 1·7) ng/ml) were enrolled into a multicentre open trial to consume during 1 month two servings of soft plain cheese made of semi-skimmed milk providing daily 686kJ (164kcal), 2·5μg vitamin D, 302mg Ca and 14·2g proteins. The primary endpoint was the change in serum carboxy terminal cross-linked telopeptide of type I collagen (CTX), selected as a marker of bone resorption. Thirty-five subjects remained compliant. Mean serum changes were: 25-hydroyvitamin D, +14·5% (P=0·0051); parathyroid hormone (PTH), −12·3% (P=0·0011); CTX, −7·5% (P=0·01); tartrate-resistant acid phosphatase isoform 5b (TRAP 5b), −9·9% (P<0·0001); albumin, +6·2% (P<0·0001); insulin-like growth factor-I (IGF-I),+16·9% (P<0·0001); osteocalcin, +8·3% (P=0·0166); amino-terminal propeptide of type 1 procollagen (P1NP),+19·3% (P=0·0031). The present open trial suggests that fortified soft plain cheese consumed by elderly women with vitamin D insufficiency can reduce bone resorption markers by positively influencing Ca and protein economy, as expressed by decreased PTH and increased IGF-I, respectively. The rise in the bone formation marker P1NP could be explained by a protein-mediated increase in IGF-I. Thus, such a dietary intervention might uncouple, at least transiently, bone resorption from bone formation and thereby attenuate age-related bone los

Inhibition of bone turnover by milk intake in postmenopausal women

Increased postmenopausal bone turnover leads to bone loss and fragility fracture risk. In the absence of osteoporosis, risk preventive measures, particularly those modifying nutritional lifestyle, are appropriate. We tested the hypothesis that milk supplementation affects bone turnover related to biochemical markers in a direction that, in the long term, may be expected to reduce postmenopausal bone loss. Thirty healthy postmenopausal women aged 59·3 (sd 3·3) years were enrolled in a prospective crossover trial of 16 weeks. After a 4-week period of adaptation with diet providing 600mg calcium plus 300mg ingested as 250ml semi-skimmed milk, participants were maintained during 6 weeks under the same 600mg calcium diet and randomized to receive either 500ml semi-skimmed milk, thus providing a total of 1200mg calcium, or no milk supplement. In the next 6 weeks they were switched to the alternative regimen. At the end of the each period, i.e. after 4, 10 and 16 weeks, blood and urinary samples were collected. The changes in blood variables between the periods of 6 weeks without and with milk supplementation were: for parathyroid hormone, −3·2pg/ml (P=0·0054); for crosslinked telopeptide of type I collagen, −624pg/ml (P<0·0001); for propeptide of type I procollagen, −5·5ng/ml (P=0·0092); for osteocalcin, −2·8ng/ml (P=0·0014). In conclusion, a 6-week period of milk supplementation induced a decrease in several biochemical variables compatible with diminished bone turnover mediated by reduction in parathyroid hormone secretion. This nutritional approach to postmenopausal alteration in bone metabolism may be a valuable measure in the primary prevention of osteoporosi

Update on vitamin D and evaluation of vitamin D status.

Knowledge about vitamin D has greatly improved during the last few years. Vitamin D cannot any more be considered as exclusively necessary to prevent ricket/osteomalacia. Its role in the prevention of some osteoporotic fractures in the elderly (in association with calcium nutrition) is now well demonstrated and many epidemiologic and laboratory data argue for a role in the prevention of several diseases or anomalies (cancer, auto-immune diseases, cardiovascular events, sarcopenia...). A few intervention studies confirming some of these effects also exist. Vitamin D status can easily be assessed by measuring serum 25 hydroxy vitamin D (25OHD) level. However, many experts have claimed that the population-based reference values for 25OHD are too low and that the cut-off value below which vitamin D insufficiency can be present is somewhere between 20 and 40ng/mL with a clear tendency to target values above 30ng/mL (75nmol/L). The main consequences are that vitamin D insufficiency is highly frequent whereas the currently recommended supplementation doses are not sufficient

Standardization of DiaSorin and Roche automated third generation PTH assays with an international standard: impact on clinical populations

Background: Standardization of parathyroid hormone (PTH) assays is a major issue, especially in hemodialyzed (HD) patients. Two automated third generation PTH assays (Roche Elecsys and DiaSorin Liaison) are now available. These assays are specific for the (1-84) PTH and do not cross-react with the (7-84) fragment, contrary to second generation (intact) assays. We aimed to calibrate the two methods against the WHO International PTH Standard (IS) 95/646 to see if the two assays could provide comparable results in a population of healthy subjects, HD patients and patients suffering from primary hyperparathyroidism (PHP). Methods: We selected 79 healthy subjects and two populations of patients presenting PTH disorders: 56 HD and 27 PHP patients. We reconstituted the IS in a pool of human serum containing undetectable levels of 1-84 PTH and prepared 13 serum standards ranging from 0 to 2000 pg/mL. The standards were run on the two instruments to calibrate the assays on the IS. The different populations were run before and after restandardization. Results: As these kits were differently calibrated, the results obtained after restandarization were significantly different. Restandardization process improved concordance between assays and, taking the analytical variability of the two kits into account, the results could be considered to be similar. Conclusions: Restandardization of automated third generation PTH assays with the WHO 1-84 PTH Standard significantly reduces inter-method variability. Reference ranges and raw values are totally transposable from one method to the other in healthy subjects, but also in diseased patients, e.g., with HD or those suffering from PHP