L Rietveld1, T van der Hoek2, M H C T van Beek3, A F A Schellekens4. 1. Radboud University Medical Centre, Department of Psychiatry, Nijmegen, the Netherlands. Electronic address: lianne_rietveld@hotmail.com. 2. Radboud University Medical Centre, Department of Psychiatry, Nijmegen, the Netherlands; Mental Health Organization (MHO) GGZ Oost Brabant Land van Cuijk en Noord Limburg, Boxmeer, The Netherlands. 3. Radboud University Medical Centre, Department of Psychiatry, Nijmegen, the Netherlands. 4. Radboud University Medical Centre, Department of Psychiatry, Nijmegen, the Netherlands; Donders Institute for Brain Cognition and Behaviour, Centre for Neuroscience, Nijmegen, The Netherlands.
Abstract
OBJECTIVE: Beta-blockers are commonly used in the treatment of hypertension and cardiac arrhythmias. The incidence of neuropsychiatric side effects is generally low. This case report shows the potential familial liability of a metoprolol-induced psychosis. METHOD: We report a case of metoprolol-induced psychosis. Potential pharmocogenetic factors mediating this familial metoprolol-induced psychosis are discussed. RESULTS: A middle-aged man developed psychosis after starting metoprolol, which diminished after ceasing the medication. Two of his family members experienced similar symptoms after using metoprolol. All family members were genotyped as CYP2D6*4 allele carriers indicating reduced CYP2D6 enzyme activity. CONCLUSION: The case presented here suggests a potential familial liability for metoprolol- induced psychosis. Pharmacokinetic mechanisms are hypothesized to mediate this familial liability through genetic variation in the CYP2D6 genotype. A family history of psychotic symptoms after treatment with beta-blockers should be taken into account, when prescribing this beta-blocker.
OBJECTIVE: Beta-blockers are commonly used in the treatment of hypertension and cardiac arrhythmias. The incidence of neuropsychiatric side effects is generally low. This case report shows the potential familial liability of a metoprolol-induced psychosis. METHOD: We report a case of metoprolol-induced psychosis. Potential pharmocogenetic factors mediating this familial metoprolol-induced psychosis are discussed. RESULTS: A middle-aged man developed psychosis after starting metoprolol, which diminished after ceasing the medication. Two of his family members experienced similar symptoms after using metoprolol. All family members were genotyped as CYP2D6*4 allele carriers indicating reduced CYP2D6 enzyme activity. CONCLUSION: The case presented here suggests a potential familial liability for metoprolol- induced psychosis. Pharmacokinetic mechanisms are hypothesized to mediate this familial liability through genetic variation in the CYP2D6 genotype. A family history of psychotic symptoms after treatment with beta-blockers should be taken into account, when prescribing this beta-blocker.