Selective acquired long QT syndrome (saLQTS) upon risperidone treatment
1 Division of General Psychiatry, University Hospitals of Geneva and Faculty of Medicine of the University of Geneva, 1202 Geneva, Switzerland
2 Division of Old Age Psychiatry, Hospices-CHUV, 1008, Prilly, Switzerland
3 Laboratoire de Génétique Moléculaire, Service de Génétique Médicale, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
Citation and License
BMC Psychiatry 2012, 12:220 doi:10.1186/1471-244X-12-220Published: 5 December 2012
Numerous structurally unrelated drugs, including antipsychotics, can prolong QT interval and trigger the acquired long QT syndrome (aLQTS). All of them are thought to act at the level of KCNH2, a subunit of the potassium channel. Although the QT-prolonging drugs are proscribed in the subjects with aLQTS, the individual response to diverse QT-prolonging drugs may vary substantially.
We report here a case of aLQTS in response to small doses of risperidone that was confirmed at three independent drug challenges in the absence of other QT-prolonging drugs. On the other hand, the patient did not respond with QT prolongation to some other antipsychotics. In particular, the administration of clozapine, known to be associated with higher QT-prolongation risk than risperidone, had no effect on QT-length. A detailed genetic analysis revealed no mutations or polymorphisms in KCNH2, KCNE1, KCNE2, SCN5A and KCNQ1 genes.
Our observation suggests that some patients may display a selective aLQTS to a single antipsychotic, without a potassium channel-related genetic substrate. Contrasting with the idea of a common target of the aLQTS-triggerring drugs, our data suggests existence of an alternative target protein, which unlike the KCNH2 would be drug-selective.