Abstract
IntroductionAn epileptic child had been long treated with valproic acid and lamotrigine. After a few years of treatment, he manifested severe clinical signs of hypocalcemia. We retain that valproic acid could have caused such metabolic dysfunction.Case presentationWe report here the involvement of valproic acid in symptomatic hypocalcemia in an 11-year-old epileptic white patient in treatment with valproic acid and lamotrigine. During the treatment the patient developed hypocalcemia associated with high plasma levels of valproic acid, parathyroid hormone and alkaline phosphatase, indicating increased bone turnover. Plasma levels of Vitamin D were normal. Plasma calcium values significantly correlated with valproic acid haematic levels; reduction of valproic acid dose was accompanied by prompt normalization of calcemia.The specific mechanism through which valproic acid causes hypocalcemia is unknown, although the relationship between valproic acid dose and haematic levels of calcium appears very likely.ConclusionsIt seems necessary, during long term therapy with valproic acid, to monitor plasma calcium and alkaline phosphatase plasma levels. Also, these patients should undergo treatment and perhaps prescribe vitamin D and calcium treatment.
Highlights
An epileptic child had been long treated with valproic acid and lamotrigine
Case presentation: We report here the involvement of valproic acid in symptomatic hypocalcemia in an 11-year-old epileptic white patient in treatment with valproic acid and lamotrigine
Plasma calcium values significantly correlated with valproic acid haematic levels; reduction of valproic acid dose was accompanied by prompt normalization of calcemia
Summary
Hypocalcemia is defined as low calcium levels in the blood, usually taken as less than 8.5 mg/dL. A growing body of evidence suggests a relationship between this condition and long-term anticonvulsant therapy This association has been initially confirmed only for those anti-epileptic drugs (AEDs) inducing the cytochrome P450 enzyme system due to the defective vitamin D metabolism and consequent reduction of intestinal absorption of calcium We report the case of an 11-year-old white, epileptic patient treated with valproic acid and lamotrigine who developed symptomatic hypocalcemia. Molecular investigations for Angelman Syndrome, ATRX syndrome, and FG syndrome were negative At this time, hypocalcemia (calcium 6.6 mg/dl, n.v. 8.5-10.5) and high levels of valproic acid
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