ENQUETE SUR LES FACTEURS DE RISQUE DE SURDOSAGE EN ANTICOAGULANTS ORAUX ET PLACE DU POLYMORPHISME GENETIQUE DU CYP2C9 (DES PHARMACIE INDUSTRIELLE ET BIOMEDICALE)

CHATENAY M.-PARIS 11-BU Pharma. (920192101) / SudocSudocFranceF

Naltrexone Use in Treating Hypersexuality Induced by Dopamine Replacement Therapy: Impact of OPRM1 A/G Polymorphism on Its Effectiveness

International audienceHypersexuality is a well-known adverse side effect of dopamine replacement therapy (DRT), and anti-craving drugs could be an effective therapeutic option. Our aim was to update the knowledge on this issue, particularly on the influence of an Opioid Receptor Mu 1 (OPRM1) genetic polymorphism. A systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. We also analyzed a case of iatrogenic hypersexuality that occurred in a patient treated with DRT. An analysis of the OPRM1 gene was performed on said patient. Our search identified 597 publications, of which only 7 were included in the final data synthesis. All seven publications involved naltrexone use. Five of them were case reports. None of the publications mentioned DRT side effects, nor did they report genetic data. Regarding our case report, the introduction of naltrexone corresponded with the resolution of the patient's hypersexuality. Moreover, the patient carried the A/G genotype, which has been reported to be associated with a stronger response to naltrexone for patients with an alcohol use disorder. Although studies are inconclusive so far, naltrexone could be an interesting therapeutic option for resistant hypersexuality due to DRT. Carrying the A/G genotype could help explain a good response to treatment

Gaucher disease: french registry cohort of 94 patients treated with eliglustat

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Feg receptor IIIB gene polymorphism is a predictive factor of infectious events under adalimumab in rheumatoid arthritis patients treated in the react study

International audienc

Feg receptor IIIB gene polymorphism is a predictive factor of infectious events under adalimumab in rheumatoid arthritis patients treated in the react study

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Impact of genetic factors (VKORC1, CYP2C9, CYP4F2 and EPHX1) on the anticoagulation response to fluindione.

International audienceWHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * CYP2C9 and VKORC1 genetic variants contribute to differences in patients' responses to anticoagulant coumarin derivatives. Patients carrying the VKORC1 1173TT genotype have a decreased time to the first INR within the therapeutic range and to the first INR >4, and also require lower warfarin maintenance doses. Patients carrying the *2 or *3 CYP2C9 allele have lower maintenance warfarin requirements than those carrying the wild-type allele. The role of CYP2C9 and VKORC1 genetic variants in fluindione response is unknown. WHAT THIS STUDY ADDS * Our results showed that VKORC1 genotype had a significant impact on early anticoagulation (INR value ≥2 after the first two intakes) (P 4 (P= 0.0002) and on the average daily dose of fluindione during the first period of stability (19.8 mg (±5.5) for VKORC1 CC, 14.7 mg (±6.2) for VKORC1 CT and 8.2 mg (±2.5) for VKORC1 TT, P 4 (P= 0.0002). The average daily dose of fluindione during the first period of stability was significantly associated with the VKORC1 genotype: 19.8 mg (±5.5) for VKORC1 CC, 14.7 mg (±6.2) for VKORC1 CT and 8.2 mg (±2.5) for VKORC1 TT (P < 0.0001). CYP2C9, CYP4F2 and EPHX1 genotypes did not significantly influence the response to fluindione. CONCLUSIONS VKORC1 genotype strongly affected anticoagulation induced by fluindione whereas CYP2C9, CYP4F2 and EPHX1 genotypes seemed less determining