Key result
Amisulpride treatment is linked to pulmonary embolism, likely driven by hyperprolactinemia.
Case Report (n=1)
Amisulpride treatment may be associated with an increased risk of venous thromboembolism, potentially mediated by hyperprolactinemia.
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Amisulpride may warrant VTE vigilance in bipolar patients; single case leaves open hyperprolactinemia-mediated risk.
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.
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Σκώκου et al. (2013) conducted a case report in Bipolar disorder (n=1). Amisulpride was evaluated on Pulmonary embolism. Amisulpride treatment was associated with a case of pulmonary embolism in a female bipolar patient, likely driven by hyperprolactinemia.
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