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Topiramate and metabolic acidosis in infants and toddlers
Heike Philippi1, Rainer Boor, Bernd Reitter
1Department of Pediatrics, Johannes Gutenberg-University, Mainz, Germany. philippi@kinder.klinik.uni-mainz.de
Insights
Topiramate (TPM) can cause metabolic acidosis in young children. Monitoring acid-base balance is crucial for infants and toddlers treated with TPM, as eight out of nine developed this side effect.
Area of Science:
- Pediatric Neurology
- Clinical Pharmacology
- Biochemistry
Background:
- Topiramate (TPM) is an antiepileptic drug known to inhibit carbonic anhydrase.
- Metabolic acidosis is a potential side effect of TPM, though rarely reported in adults.
- The impact of TPM on acid-base metabolism in pediatric populations is not well-established.
Purpose of the Study:
- To investigate the effects of Topiramate (TPM) on acid-base metabolism in infants and toddlers.
- To determine the incidence and characteristics of metabolic acidosis in young children treated with TPM.
Main Methods:
- A cohort of nine infants and toddlers (aged 5 months to 2.3 years) received TPM.
- TPM was administered at doses ranging from 8.2-26 mg/kg/day, either as monotherapy or adjunct therapy.
- Blood gas parameters were monitored before and during TPM treatment.
Main Results:
- All nine children had normal blood gases prior to TPM treatment.
- Metabolic acidosis developed in eight of the nine children within 8-26 days of TPM initiation.
- Affected children exhibited reduced serum bicarbonate and base excess, with some showing hyperventilation.
Conclusions:
- Metabolic acidosis is a common side effect of Topiramate (TPM) in infants and toddlers.
- Monitoring acid-base metabolism is recommended for young children receiving TPM therapy.
- Early detection and management, including sodium bicarbonate supplementation, can be considered for symptomatic cases.
Purpose:
Topiramate (TPM) inhibits carbonic anhydrase, with metabolic acidosis as a possible side effect, although this has been reported in only two adult cases. We investigated the acid-base metabolism in infants and toddlers treated with TPM.
Methods:
Nine infants and toddlers aged 5 months to 2.3 years (median, 6 months) were treated with TPM at maximal doses of 8.2-26 mg/kg/day (median, 11 mg/kg/day). The maximal TPM dose was achieved after 8-35 days (median, 17 days). TPM was given in addition to other antiepileptic drugs (AEDs) in five cases and as a sole AED in four patients with refractory epilepsy resistant to multiple AEDs. The diagnoses were infantile spasms (n = 5), epilepsia partialis continua (n = 1), infantile epileptic encephalopathy (n = 1), and Lennox-Gastaut syndrome (n = 2).
Results:
The blood gases were normal before treatment with TPM in all nine children. Metabolic acidosis developed in eight children after 8-26 days (median, 14 days) of TPM treatment with a minimum of serum bicarbonate between 15 to 18 mM (median, 17 mM), a minimal base excess between -6.2 and -11.2 mM (median, -7.9 mM), and pH between 7.22 and 7.40 (median, 7.35). Four of nine children showed clinical signs of hyperventilation and received oral sodium bicarbonate (1-2 mmol/kg), while TPM was still effective.
Conclusions:
Because metabolic acidosis developed in eight of the nine infants and toddlers taking TPM, we would suggest that the acid-base metabolism be monitored in young children who receive TPM.