Loss of Seizure Control Due to Anticonvulsant-Induced Hypocalcemia

Ali, Fawzi E.; Al-Bustan, Mahmoud; Al-Busairi, Waleed A.; Al-Mulla, Fatema A

doi:10.1345/aph.1d467

Cited by 34 publications

(16 citation statements)

References 12 publications

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“…However, phenytoin can be epileptogenic in presence of hypocalcemia as it increases metabolism of active vitamin D to its inactive form by hepatic enzyme induction resulting in reduced calcium absorption from gut and by causing osteomalacia and reduced calcium mobilization from bones. [15,16] Both these mechanisms lead to worsening of hypocalcemia and seizure control. This possibility must be considered for worsening seizure control in a patient on phenytoin.…”

Section: Discussionmentioning

confidence: 99%

Spectrum of neurological manifestations of idiopathic hypoparathyroidism and pseudohypoparathyroidism

et al. 2011

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We describe clinical, biochemical, radiological profile, and treatment outcome in 97 patients with idiopathic hypoparathyroidism seen over a period of 18 years. Of the 97 patients, 78 (80%) had idiopathic hypoparathyroidism and 19 (20%) had pseudohypoparathyroidism. The mean age±standard deviation (SD) at presentation was 28.7±14.1 years. There were 52 males, the mean lag time from first reported symptom to diagnosis was 5.9±5.2 years and the mean (±SD) follow-up was 1.8±0.4 years. The most common presenting manifestation was carpopedal spasm in 68 (70%) patients, followed by paresthesia and seizures in 52 (54%) patients. The mean (±SD) serum calcium and inorganic phosphate concentrations were 6.1±1.5 mg/dl and 6.3±1.5 mg/dl, respectively. The most common imaging abnormality noted was basal ganglia calcification followed by cerebral cortex and cerebellum calcification. More than one-third of patients were on various antiepileptic drugs including phenytoin. In addition to oral calcium and active vitamin D (calcitriol), twenty-six patients (27%) also required hydrochlorothiazide. The important finding in our study was long lag time from the first reported symptom to diagnosis. Phenytoin was the drug in almost one- third of our patients with seizures. Practicing clinicians should have high index of suspicion of diagnosis hypoparathyroidism in the appropriate clinical states to avoid the morbidity associated with hypoparathyroidism. Phenytoin should be avoided in patients with hypoparathyroidism and seizures.

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Section: Discussionmentioning

confidence: 99%

Spectrum of neurological manifestations of idiopathic hypoparathyroidism and pseudohypoparathyroidism

et al. 2011

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“…However, based on the vitamin D neurosteroid regulation role, a scenario of reverse causation is also plausible and should be considered. Thus, in rachitic children, seizures accompanied by low calcium and 25-OHD 2 concentrations have been observed [52,53] , whereas long-term vitamin D supplementation led to a reduced incidence of these symptoms [54] . Furthermore, a direct antiepileptic effect of 1,25-(OH) 2 D 3 was reported in mice [23,55,56] , suggesting a possible control of the regulation of epileptogenic focuses.…”

Section: Depression and Anxietymentioning

confidence: 99%

Vitamin D and Ageing: Neurological Issues

et al. 2010

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nervous system as a whole, and in particular on the CNS. During cerebral development, vitamin D may act like a neurosteroid hormone in the areas of neurotrans mission, neuroprotection, and neuroimmunomodulation. Moreover, vitamin D deficiency has been associated with neurological and psychiatric disorders. In older adults, hypovitaminosis D has been associated with neuromuscular disorders, dementia, and Parkinson's disease. Thus, vitamin D supplementation might have a protective effect against these neurological disorders. Conclusions: Vitamin D has been associated with many neurological functions and its deficiency with dysfunction. Low serum 25-hydroxyvitamin D concentrations can potentially be reversed. This simple and low-cost correction might contribute to the primo-secondary prevention of various neuropsychiatric disorders.

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“…The effect of anticonvulsants on vitamin D metabolism is well known and has previously been reported in the literature in adult patients [12,13]. Our case report describes an infant with hypoparathyroidism due to an activating mutation in the CaSR, who developed intractable hypocalcaemia despite high doses of 1-AC because of concomitant anticonvulsant therapy.…”

Section: Discussionmentioning

confidence: 66%

“…This resistance in our patient may have been due to the fact that she had been co-prescribed phenobarbitone for the seizures on admission to hospital. Phenobarbitone has been reported to increase the metabolism of vitamin D and its analogues, such as 1-AC, by drug-stimulated increases in hepatic microsomal activity, resulting in hypocalcaemia with secondary seizures and even metabolic bone disease with long-term treatment in adult patients [12,13]. Our patient started to be gradually weaned off phenobarbitone from 4 months of age and was stopped completely by 5 months of age.…”

Section: Case Illustrationmentioning

confidence: 80%

Anticonvulsant Treatment Associated with Intractable Hypocalcaemia in a Female Child with Hypoparathyroidism

et al. 2014

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Background: We report the case of a female infant with hypoparathyroidism due to an activating mutation in the calcium-sensing receptor gene. Case Report: The child presented in the neonatal period with clinical seizures associated with severe hypocalcaemia, hyperphosphataemia, low parathyroid hormone levels and elevated urine calcium:creatinine ratios. She required intravenous calcium and phenobarbitone initially, and then oral 1-alfacalcidol (1-AC) and phenobarbitone were started. The patient had intractable hypocalcaemia in the first 5 months of life despite escalating doses of 1-AC. When the phenobarbitone was stopped at 5 months of age she was admitted soon after with symptomatic hypercalcaemia. We postulate that the phenobarbitone increased the metabolism of 1-AC and thus she needed large doses of 1-AC to treat hypocalcaemia until the phenobarbitone was stopped. Her parents had no biochemical abnormalities on testing. Results: Molecular genetic analysis confirmed that our patient had a de novo missense variant, c.682G>A (p.Glu228Lys) in exon 4 of the calcium-sensing receptor. Conclusion: This case report highlights the importance that clinicians caring for children on vitamin D and its analogues are aware of the interaction with phenobarbitone, which can result in symptomatic hypocalcaemia. 1-AC should be stored at 2-8°C, otherwise it will be rendered inactive.

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Loss of Seizure Control Due to Anticonvulsant-Induced Hypocalcemia

Cited by 34 publications

References 12 publications

Spectrum of neurological manifestations of idiopathic hypoparathyroidism and pseudohypoparathyroidism

Spectrum of neurological manifestations of idiopathic hypoparathyroidism and pseudohypoparathyroidism

Vitamin D and Ageing: Neurological Issues

Anticonvulsant Treatment Associated with Intractable Hypocalcaemia in a Female Child with Hypoparathyroidism

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