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Aberger, S; Schreiber, N; Pilz, S; Eller, K; Rosenkranz, AR; Kirsch, AH.
Targeting Calcitriol Metabolism in Acute Vitamin D Toxicity-A Comprehensive Review and Clinical Insight.
Int J Mol Sci. 2024; 25(18): 10003 Doi: 10.3390/ijms251810003 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz
Aberger Simon Michael
Kirsch Alexander
Co-Autor*innen der Med Uni Graz
Eller Kathrin
Pilz Stefan
Rosenkranz Alexander
Schreiber Nikolaus
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Abstract:
High-dose vitamin D supplementation is common in the general population, but unsupervised high-dose supplementation in vitamin D-replete individuals poses a risk of severe toxicity. Susceptibility to vitamin D toxicity shows a significant inter-individual variability that may in part be explained by genetic predispositions (i.e., CYP24A1 polymorphism). The classic manifestation of vitamin D toxicity is hypercalcemia, which may be refractory to conventional therapy. Its causes include the endogenous overaction of 1α-hydroxylase, monogenic alterations affecting vitamin D metabolizing enzymes and exogenous vitamin D intoxication. In this manuscript, we include a literature review of potential pharmacological interventions targeting calcitriol metabolism to treat vitamin D intoxication and present a case of severe, exogenous vitamin D intoxication responding to systemic corticosteroids after the failure of conventional therapy. Systemic glucocorticoids alleviate acute hypercalcemia by inhibiting enteric calcium absorption and increasing the degradation of vitamin D metabolites but may cause adverse effects. Inhibitors of 1α-hydroxylase (keto/fluconazole) and inducers of CYP3A4 (rifampicin) may be considered steroid-sparing alternatives for the treatment of vitamin D intoxication.
Find related publications in this database (using NLM MeSH Indexing)
Humans - administration & dosage
Calcitriol - therapeutic use, metabolism
Hypercalcemia - metabolism, drug therapy, chemically induced
Vitamin D - metabolism, therapeutic use
Vitamin D3 24-Hydroxylase - metabolism, genetics

Find related publications in this database (Keywords)
vitamin D
drug toxicity
CYP polymorphism
pharmacogenetics
nutrients
calcitriol
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