Venous thromboembolism has been associated with antipsychotic drugs, but the underlying mechanisms are largely unknown. Hypotheses that have been made include body weight gain, sedation, enhanced platelet aggregation, increased levels of antiphospholipid antibodies, hyperhomocysteinemia, whereas hyperprolactinemia has recently attracted attention as a potential contributing factor. The highest risk has been demonstrated for clozapine, olanzapine, and low-potency first-generation antipsychotics; however, presently there is no data for amisulpride. In the present paper we describe a case of pulmonary embolism in a female bipolar patient, receiving treatment with amisulpride, aripiprazole, and paroxetine. Although a contribution of aripiprazole and paroxetine cannot completely be ruled out, the most probable factor underlying the thromboembolic event seems to be hyperprolactinemia, which was caused by amisulpride treatment. Increased plasma levels of prolactin should probably be taken into account during the monitoring of antipsychotic treatment as well as in future research concerning venous thromboembolism in psychiatric settings. 1. Introduction Venous thromboembolism (VTE) is a common condition, with an annual incidence of more than 1 per 1000 persons [1]. Deep vein thrombosis (DVT) and pulmonary embolism (PE) are two clinical expressions of VTE, the latter of which, if untreated, is associated with a mortality rate of 30% [2]. Risk factors can be divided in to congenital, such as hereditary thrombophilia, and acquired, including advanced age, obesity, surgery, malignancies, and estrogen therapy [3]. Recent research has focused on increased risk for VTE in psychiatric settings [4]. Psychiatric conditions which have been found dangerous in this regard are physical restraint [5], catatonia [6, 7], and neuroleptic malignant syndrome [8]. Possible underlying mechanisms are immobilization and dehydration in all three conditions, plus vessel injury in the situation of physical restraint, due to heavy resistance of the patient, or fever and rhabdomyolysis in the case of neuroleptic malignant syndrome [4]. Higher risk for VTE has also been demonstrated for specific classes of psychotropic drugs, most consistently for antipsychotics [9–15]. Exact mechanisms have not been elucidated yet, and only recently increased prolactin has been implicated as a potential contributing factor [16]. In the present paper we describe a case of PE most probably related to amisulpride treatment. Amisulpride is a Second Generation Antipsychotic (SGA) with no affinity for serotonin
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