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Related Concept Videos

Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
Drug Toxicity: Risk factors01:24

Drug Toxicity: Risk factors

Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Drug Toxicity: Overview01:00

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Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...
Pharmacokinetics in Pediatric Patients: Drug Excretion01:26

Pharmacokinetics in Pediatric Patients: Drug Excretion

In pediatric medicine, understanding the renal function and drug elimination nuances is crucial for administering safe and effective treatments. Newborns, in particular, display markedly slower renal functions than adults, profoundly affecting how drugs are cleared from their bodies. This slower drug clearance requires clinicians to extend the dosing intervals for many medications to prevent drug accumulation and toxicity while ensuring therapeutic efficacy.One key area where these adjustments...
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...

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Electromagnetic Source Imaging in Presurgical Evaluation of Children with Drug-Resistant Epilepsy
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Published on: September 20, 2024

Simultaneous toxicities in a child on multiple anticonvulsants.

Sarah Isis R Delima1, Laurence E Walsh, Meredith R Golomb

  • 1Division of Pediatric Neurology, Department of Neurology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

Journal of Child Neurology
|March 18, 2008
PubMed
Summary

Simultaneous hepatotoxicity and bone marrow toxicity are rare in children on multiple anticonvulsants. A concurrent viral infection may increase the risk of these adverse events, particularly with valproic acid, lamotrigine, and phenytoin.

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Area of Science:

  • Pediatric Neurology
  • Clinical Toxicology
  • Pharmacology

Background:

  • Anticonvulsant medications are frequently prescribed for pediatric epilepsy.
  • Polypharmacy with multiple anticonvulsants, including valproic acid, lamotrigine, and phenytoin, is common.
  • Simultaneous drug toxicities are uncommon but can be severe.

Observation:

  • A 3.5-year-old child on a regimen of valproic acid, lamotrigine, and phenytoin developed concurrent hepatotoxicity and bone marrow toxicity.
  • The patient experienced a parainfluenza virus type 3 infection during the onset of these toxicities.
  • Seizures were managed with lorazepam while anticonvulsants were discontinued.

Findings:

  • The combination of valproic acid, lamotrigine, and phenytoin may be associated with simultaneous hepatotoxicity and bone marrow toxicity.
  • Concurrent viral infections, such as parainfluenza virus type 3, might potentiate the risk of these adverse drug reactions.
  • Discontinuation of the anticonvulsant regimen led to the resolution of both toxicities.

Implications:

  • Clinicians should be vigilant for rare, simultaneous toxicities in pediatric patients on multiple anticonvulsants.
  • The potential for drug-drug and drug-infection interactions increasing toxicity risk warrants consideration.
  • This case highlights the importance of careful monitoring and prompt management of adverse events in pediatric epilepsy treatment.