Abstract
Vitamin D has reported anti-cancer and anti-inflammatory properties modulated through gene transcription and non-genomic signaling cascades. The purpose of this review was to summarize the available research on interactions and pharmacokinetics between vitamin D and the pharmaceutical drugs used in patients with cancer. Hypercalcemia was the most frequently reported side effect that occurred in high dose calcitriol. The half-life of 25(OH)D3 and/or 1,25(OH)2D3 was found to be impacted by cimetidine; rosuvastatin; prednisone and possibly some chemotherapy drugs. No unusual adverse effects in cancer patients; beyond what is expected from high dose 1,25(OH)2D3 supplementation, were revealed through this review. While sufficient evidence is lacking, supplementation with 1,25(OH)2D3 during chemotherapy appears to have a low risk of interaction. Further interactions with vitamin D3 have not been studied.
Highlights
Vitamin D’s role and importance in bone metabolism has been known for many years
The objective of this review is to summarize the available evidence on the interactions between vitamin D and pharmaceutical drugs used in patients with cancer including the impact of vitamin D on the pharmacokinetics of these drugs and any changes in vitamin D pharmacokinetics due to the drugs themselves
Of the hundred or so pharmaceutical drugs that are used in the treatment of cancer patients only a handful of these drugs have been studied in combination with vitamin D, primarily calcitriol
Summary
Vitamin D’s role and importance in bone metabolism has been known for many years. The influence of vitamin D status and the associated impact on health and disease represents yet another important potential role for vitamin D. In a recent meta-analysis on vitamin D status and the associated risk of cardiovascular disease (CVD) found a direct inverse association between circulating (25(OH)D3 levels and CVD risk to 60 nmol/L [1]. Vitamin D is synthesized by the action of UVB radiation activating the 7-dehydrocholesterol molecule in the skin and converting it to pre-vitamin Vitamin D3 (cholecalciferol). In this form, it is transported in the blood to the liver, bound to either albumin or vitamin D binding protein (DBP) [6]. It is thought to be hydroxylated by 25-hydroxylase, a member of the CYP2R1 enzyme family, through specific enzyme(s) that still need to be elucidated, to 25-dehydroxyvitamin D3 [25(OH)D3, calcidiol] [7]
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