Study of Predictors of Response to Anti Epilepsy in Epilepsy

Terminated

• Conditions: Seizure

• Registration Number: NCT02883712
• Lead Sponsor: University Hospital, Lille

Brief Summary

Pharmacoresistant epilepsy remains around 30% despite the development of 25 anti epileptic drugs. Of course, this can be explained by pharmacoresistant epileptic brain diseases, as exemplified by some genetic diseases. However, the lack of specific guidelines for the choice of the anti epileptic drugs (apart from generalized and partial epilepsy) and the very large number of drugs with different and sometimes complex metabolism are challenges for neurologists. Among the 30 % of pharmacoresistant epilepsy, there is a part related to pharmacokinetic drawbacks that could be overcome with a more rigorous approach (i.e. dosage and pharmacogenetics tools). Moreover, the new anti epileptic drugs have metabolism more unrelated with the cytochrome P450 and less generalised adverse events. However, their metabolism could be more complexe (i.e. the less known Uridine 5'-diphospho-glucuronyltransferase (UGT) pathway) and bring more insidious neurological adverse events (i.e. depression, anxiety exacerbation, cognitive disorders worsening) which could largely impede the observance and the quality of life even if the number of seizure is reduced or not. The goal is to determine the predictive and the modulating factors of pharmacoresistance with a global analysis (i.e. whatever the anti epileptic drugs) and with a specific analysis (drug by drug) from a cohort of 1000 patients.

Detailed Description

The goal is to determine the predictive and the modulating factors of pharmacoresistance with a global analysis (i.e. whatever the anti epileptic drugs) and with a specific analysis (drug by drug with their specific metabolism pathways) from a cohort of 1000 patients. The response to the antiepileptic drugs modification will be analyse 3 months after the modification, with the analysis of the number of seizures, the quality of life, the Clinical Global Impression, the adverse events, the systematic dosage of all the molecules (residual concentration just before the taken) and the pharmacogenetic analysis of the main metabolism pathways and the main pharmacodynamic targets.

Study Timeline

• Study Start: 2013-05-21
• Study First Submitted: 2016-08-16
• Study First Submitted QC: 2016-08-24
• Study First Posted: 2016-08-30
• Primary Completion: 2021-01
• Study Completion: 2021-01
• Status Verified: 2021-03
• Last Update Submitted: 2021-03-09
• Last Update Posted: 2021-03-12

Recruitment & Eligibility

• Status: TERMINATED
• Sex: All
• Target Recruitment: 155

Inclusion Criteria

• Epileptic patients who required a treatment adaptation

Exclusion Criteria

• patients unable to give reliable information and without caregiver
• pregnancy
• Severe comorbidity, which would impede interpretation

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
Clinical global impression of the patient	3 months	Clinical global impression assessment

Secondary Outcome Measures

Name	Time	Method
Pharmacogenetics of the uridine 5'-diphosphate glucuronosyltransférases (UGT1A1, UGT2B7, UGT1A4)	3 months	the metabolism pathways of the drug
Pharmacogenetics of the Cytochrome P450 (2D6, 2C9, 2C19)	3 months	the metabolism pathways of the drug
Concentration of the anti epileptic drug	3 months	plasmatic drug concentration will be systematically
Depression inventory for epilepsy	3 months	Neurological Disorders Depression Inventory for Epilepsy
Quality of life	3 months	Analyse with the Quality Of Life In Epilepsy Questionnaire
Adverse events	3 months	reported by the patients with a particular attention to attention and concentration worsening on interview
Number of seizure	3 months	recorded on the agenda of patients

Trial Locations

Locations (1)

Hôpital Roger Salengro, CHRU de Lille; 🇫🇷 Lille, France