Drug–Vitamin D Interactions

Abstract

Extensive media coverage of the potential health benefits of vitamin D supplementation has translated into substantial increases in supplement sales over recent years. Yet, the potential for drug-vitamin D interactions is rarely considered. This systematic review of the literature was conducted to evaluate the extent to which drugs affect vitamin D status or supplementation alters drug effectiveness or toxicity in humans. Electronic databases were used to identify eligible peer-reviewed studies published through September 1, 2010. Study characteristics and findings were abstracted, and quality was assessed for each study. A total of 109 unique reports met the inclusion criteria. The majority of eligible studies were classified as Class C (non-randomized trials, case-control studies, or time series) or D (cross-sectional, trend, case report/series, or before-and-after studies). Only two Class C and three Class D studies were of positive quality. Insufficient evidence was available to determine whether lipase inhibitors, antimicrobial agents, antiepileptic drugs, highly active antiretroviral agents or H2 receptor antagonists alter serum 25(OH)D concentrations. Atorvastatin appears to increase 25(OH)D concentrations, while concurrent vitamin D supplementation decreases concentrations of atorvastatin. Use of thiazide diuretics in combination with calcium and vitamin D supplements may cause hypercalcemia in the elderly, or those with compromised renal function or hyperparathyroidism. Larger studies with stronger study designs are needed to clarify potential drug-vitamin D interactions, especially for drugs metabolized by cytochrome P450 3A4 (CYP3A4). Health care providers should be aware of the potential for drug-vitamin D interactions.

The effects of first-line anti-tuberculosis drugs on the actions of vitamin D in human macrophages

“…Several drugs may potentially impact the metabolism of vitamin D. Any drug that interferes with vitamin D absorption, metabolism and/or excretion process could potentially alter the action of vitamin D [35]. Several drugs are known to impact one of the two hydroxylation steps of vitamin D: (1) the hydroxylation of vitamin D to 25-hydroxyvitamin D (25(OH)D) via cytochrome P450 vitamin D 25-hydroxylase (25-OHase or CYP27A1) or (2) the hydroxylation of 25(OH)D to 1,25-dihydroxyvitamin D (1, 25(OH) 2 D) via the cytochrome P450 D-1-α-hydroxylase (1-OHase or CYP27B1) [36].…”

“…In a classic endocrine feedback loop, high blood concentrations of vitamin D also induces its own catabolism by increasing the expression of the 25-hydroxyvitamin D-24-hydroxylase (CYP24A1) which plays an important role in the catabolism of vitamin D [37]. Anti-convulsive medications such as phenytoin and phenobarbital can increase CYP24A1 expression, which results in the lowering of serum vitamin D [35].…”

Low vitamin D levels are common in patients with epilepsy

“…Vitamin D status in adults with epilepsy is less clear. Several studies have failed to find that patients on EIAEDs have lower vitamin D levels than those on non-enzyme-inducing AEDs (Non-AEDs) (Vestergaard, 2005; Pack et al, 2005; Pack et al, 2011a), and a recent systematic review found insufficient evidence to determine if AEDs alter serum 25-hydroxyvitamin D levels (Robien et al, 2013). The prevalence of vitamin D deficiency in adults with epilepsy and its relationship to specific AEDs remain uncertain.…”

The Role of Vitamin D and Omega-3 PUFAs in Islet Transplantation

“…Notably, vitamin D deficiency is highly prevalent and severe during the immediate post-transplant period following solid organ transplantation (e.g., heart, liver or kidney transplantation) and persists in long-term allograft recipients [87][88][89][90][91][92][93][94]. This may be due to several factors, namely: (i) inadequate vitamin D dietary intake or supplementation after transplantation [91,95]; (ii) reduced sun exposure (usually recommended to organ transplant recipients in order to prevent the risk of skin cancer related to long-term immunosuppression) [96,97]; and (iii) increased vitamin D catabolism or reduced vitamin D hydroxylation induced by glucocorticoids and/or immunosuppressive drugs [87,[98][99][100][101]. Therefore, vitamin D deficiency should be promptly diagnosed and treated in organ transplant recipients, since it can potentially result in secondary hyperparathyroidism and bone loss [102,103], which can be further exacerbated by the detrimental skeletal effects mediated by immunosuppressive drugs [104].…”