Impact of a single oral dose of 100,000 IU vitamin D3 on profiles of serum 25(OH)D3 and its metabolites 24,25(OH)2D3, 3-epi-25(OH)D3, and 1,25(OH)2D3 in adults with vitamin D insufficiency

Saleh, Lanja; Tang, Jonathan; Gawinecka, Joanna; Boesch, Lukas; Fraser, William D.; Eckardstein, Arnold von; Nowak, Albina

doi:10.1515/cclm-2016-1129

Cited by 12 publications

(8 citation statements)

References 31 publications

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“…Saleh et al performed an RC.T. of 4 weeks with 107 participants receiving a single 100,000 IU dose of vitamin D or placebo [11]. The VMR could not predict the increase of 25(OH)D after 4 weeks, whereas 25(OH)D did predict this increase with a similar R 2 -value to our data.…”

Section: Discussionsupporting

confidence: 68%

“…In addition, it has been speculated that the ratio could provide useful information regarding bone health [7]. Interestingly, several studies show that the VMR can predict the change seen in 25(OH)D after vitamin D supplementation, although results are inconclusive [6,8,9,10,11]. The CYP24A1 activity could be partially responsible for the individual differences seen in the effect of vitamin D supplementation on serum levels of 25(OH)D. Theoretically, if CYP24A1 activity is a major predictor of the effect of vitamin D supplementation, the VMR could be used to personalize the treatment dosage.…”

Section: Introductionmentioning

confidence: 99%

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The Effect of Vitamin D Supplementation on its Metabolism and the Vitamin D Metabolite Ratio

et al. 2019

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25-hydroxyvitamin D (25(OH)D) is commonly measured to assess vitamin D status. Other vitamin D metabolites such as 24,25-dihydroxyvitamin D (24,25(OH)2D) provide additional insights into vitamin D status or metabolism. Earlier studies suggested that the vitamin D metabolite ratio (VMR), calculated as 24,25(OH)2D/25(OH)D, could predict the 25(OH)D increase after vitamin D supplementation. However, the evidence for this additional value is inconclusive. Therefore, our aim was to assess whether the increase in 25(OH)D after supplementation was predicted by the VMR better than baseline 25(OH)D. Plasma samples of 106 individuals (25(OH)D < 75 nmol/L) with hypertension who completed the Styrian Vitamin D Hypertension Trial (NC.T.02136771) were analyzed. Participants received vitamin D (2800 IU daily) or placebo for 8 weeks. The treatment effect (ANCOVA) for 25(OH)D3, 24,25(OH)2D3 and the VMR was 32 nmol/L, 3.3 nmol/L and 0.015 (all p < 0.001), respectively. Baseline 25(OH)D3 and 24,25(OH)2D3 predicted the change in 25(OH)D3 with comparable strength and magnitude. Correlation and regression analysis showed that the VMR did not predict the change in 25(OH)D3. Therefore, our data do not support routine measurement of 24,25(OH)2D3 in order to individually optimize the dosage of vitamin D supplementation. Our data also suggest that activity of 24-hydroxylase increases after vitamin D supplementation.

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Section: Discussionsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

The Effect of Vitamin D Supplementation on its Metabolism and the Vitamin D Metabolite Ratio

et al. 2019

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“…Out of the numerous randomized clinical trials conducted on the effect of oral vitamin D supplementation on serum 25(OH)D, only a few trials present data that allow a rough assessment of the variation in the individual 25(OH)D response to vitamin D 3 supplementation. [4][5][6][7][8] These trials suggest that the inter-individual variation is wide [9][10][11][12][13][14] and may be confounded by additional ambient solar exposure (season, sun habits and clothing habits), 15,16 ethnicity, 17 BMI 18 genetics, 16 weight and physical activity. 19…”

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confidence: 99%

Serum 25(OH)D levels after oral vitamin D₃ supplementation and UVB exposure correlate

Datta

Philipsen

Olsen

et al. 2019

Photoderm Photoimm Photomed

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Background The inter‐individual variation in 25(OH)D3 increase (Δ25(OH)D3) after vitamin D3 supplementation was determined and compared with the UVB irradiation response. Methods Nineteen Danish participants received 85 μg vitamin D3 (cholecalciferol) daily for nine weeks with regular serum 25(OH)D3 measurements. These participants had three years earlier taken part in a 9‐week controlled UVB study. The Δ25(OH)D3 was not confounded by ambient UVB, BMI or ethnicity. Results Δ25(OH)D3 was 53 nmol L−1 and almost identical to Δ25(OH)D3 (52 nmol L−1) after UVB. Δ25(OH)D3 ranged from 17 to 91 nmol L−1 (span 74 nmol L−1) and was about half of that observed after UVB irradiation (span 136 nmol L−1). The interquartile ranges for vitamin D3 supplementation (38.8‐71.4 nmol L−1, span: 32.6 nmol L−1) and UVB irradiation (35.7‐65.4 nmol L−1, span: 29.7 nmol L−1) were similar indicating a comparable response of the two interventions. As the 25(OH)D3 start levels (R2 = 0.398, P = 3.8 × 10−3), 25(OH)D3 end levels (R2 = 0.457, P = 1.5 × 10−3) and Δ25(OH)D3 (R2 = 0.253, P = 0.028) between both interventions were correlated, this suggested a possible common individual background for the variation. Four pigment SNPs influenced the variation in the vitamin D3‐induced and UVB‐induced Δ25(OH)D3. A combined model including the influence of these four SNPs and the 25(OH)D3 start level explained 86.8% (P = 1.6 × 10−35) of the individual variation after vitamin D3 supplementation. Conclusion The inter‐individual variation in the two interventions was comparable and had no common demographic but a partly common genetic background.

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“…There is a balance between net Ca absorption from the intestine and calcium excretion in the kidney. An excessive production of the active 1.25(OH)D3 results in an adequate production of the catabolic enzyme 24-hydroxylase ( CYP24A1 ), largely avoiding VD toxicity 117. A possible (theoretical) mechanism of VD toxicity could be based on changes in the metabolic pathway by displacement of 1.25(OH)D from its binding protein (DBP).…”

Section: Monitoring Of the Safety Of (Long-term) Vd Therapymentioning

confidence: 99%

“…Another possible cause of VD hypervitaminosis may be low activity of the catabolic enzyme 24-hydroxylase ( CYP24A1 ). Mutations in the CYP24A1 gene are associated with a partial or total loss of 24-hydroxylase activity, which may result in hypercalcemia 117. In addition, nontoxic VD levels (<375 nmol/L) or nonhypervitaminotic levels (<250 nmol/L) have shown very rare cases of intoxication.…”

Section: Monitoring Of the Safety Of (Long-term) Vd Therapymentioning

confidence: 99%

<p>Comorbidities in multiple sclerosis—a plea for interdisciplinary collaboration to improve the quality of life of MS patients</p>

Goischke¹

2019

DNND

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The negative influence of comorbidities on the quality of life of people with multiple sclerosis is evident and the problem is increasingly acknowledged by numerous international studies in long-term care. One therapeutic option would be an add-on therapy with vitamin D (VD), with the aim of achieving a therapeutically effective dose. The individually required VD dose must be tested, since the response to a certain dose is subject to variations between individuals. A possible toxicity with increased 1.25(OH)D3 (active VD metabolite) is largely prevented by increased activity of 24-hydroxylase ( CYP24A1 ). Monitoring of serum VD levels as well as serum calcium and phosphate levels (optional Ca excretion in 24-hour urine, Ca creatinine ratio in urine) provides safety and is necessary because possible mutations on the (catabolic) CYP24A1 gene can lead to a partial or total loss of 24-hydroxylase activity and provoke hypercalcemia/hyperphosphatemia. The main therapeutic objective is to maintain functional and social independence by using drugs with a high safety profile. The prevention and optimal management of comorbidities can influence the quality of life of patients with MS (PwMS) when included in patient care. Adequate measures can reduce the burden of MS only if the risk of comorbidity is reduced through targeted monitoring, early detection and diagnosis. Such a strategy will contribute to influencing the premature mortality of patients with MS. If VD is recognized as a “multipurpose steroid hormone”, it could also be used to maintain cognitive function and prevent premature possible dementia, especially as there is evidence that VD deficiency correlates with brain atrophy (hippocampus). At present, MS therapy is still a balancing act between therapeutically efficient action and the management of unexpected side effects, with VD add-on therapy being almost unproblematic and most likely to be accepted by PwMS.

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Impact of a single oral dose of 100,000 IU vitamin D3 on profiles of serum 25(OH)D3 and its metabolites 24,25(OH)2D3, 3-epi-25(OH)D3, and 1,25(OH)2D3 in adults with vitamin D insufficiency

Cited by 12 publications

References 31 publications

The Effect of Vitamin D Supplementation on its Metabolism and the Vitamin D Metabolite Ratio

The Effect of Vitamin D Supplementation on its Metabolism and the Vitamin D Metabolite Ratio

Serum 25(OH)D levels after oral vitamin D₃ supplementation and UVB exposure correlate

<p>Comorbidities in multiple sclerosis—a plea for interdisciplinary collaboration to improve the quality of life of MS patients</p>

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Impact of a single oral dose of 100,000 IU vitamin D3 on profiles of serum 25(OH)D3 and its metabolites 24,25(OH)2D3, 3-epi-25(OH)D3, and 1,25(OH)2D3 in adults with vitamin D insufficiency

Cited by 12 publications

References 31 publications

The Effect of Vitamin D Supplementation on its Metabolism and the Vitamin D Metabolite Ratio

The Effect of Vitamin D Supplementation on its Metabolism and the Vitamin D Metabolite Ratio

Serum 25(OH)D levels after oral vitamin D3 supplementation and UVB exposure correlate

<p>Comorbidities in multiple sclerosis—a plea for interdisciplinary collaboration to improve the quality of life of MS patients</p>

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Serum 25(OH)D levels after oral vitamin D₃ supplementation and UVB exposure correlate