Levocarnitine-Induced Hypophosphatemia in a Hemodialysis Patient With Acute Valproic Acid Toxicity
L-carnitine acts as a cofactor for VPA metabolism, increasing beta-oxidation of VPA and limiting hepatotoxic metabolites.1 Hypercalcemia is a known metabolic adverse effect with L-carnitine;2 however, a study in hemodialysis patients reported decreased phosphorus levels after its use.3 We present a...
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Veröffentlicht in: | The journal of neuropsychiatry and clinical neurosciences 2012, Vol.24 (1), p.E18-E19 |
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Sprache: | eng |
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Zusammenfassung: | L-carnitine acts as a cofactor for VPA metabolism, increasing beta-oxidation of VPA and limiting hepatotoxic metabolites.1 Hypercalcemia is a known metabolic adverse effect with L-carnitine;2 however, a study in hemodialysis patients reported decreased phosphorus levels after its use.3 We present a case in which L-carnitine was administered for acute VPA toxicity and subsequently may have contributed to hypophosphatemia. Hyperphosphatemia decreases production of 1,25-hydroxyvitamin D because of direct and indirect inhibition of the renal enzyme 1[alpha]-hydroxylase.4 Over time, secondary hyperparathyroidism develops, resulting in hypocalcemia, hypophosphatemia, and vitamin D deficiency.5 Our patient's laboratory values were consistent with this. |
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ISSN: | 0895-0172 1545-7222 |
DOI: | 10.1176/appi.neuropsych.11010023 |