Delusion of pregnancy – Is there a role of prolactin?

To the Editor

Delusion of pregnancy (DOP) is a fixed false belief that one is pregnant, despite evidence to the contrary. Recently, there have been several reports linking DOP with antipsychotic-induced hyperprolactinaemia (Ahuja et al., 2008; Ali et al., 2003).

Ms S is a 36-year-old woman with a 6-year history of schizoaffective disorder. Her symptoms have been stable on paliperidone depot 75 mg monthly for the last 2 years.

Ms S was admitted to a drug and alcohol rehabilitation facility for cocaine and alcohol detoxification, but was evicted after 2 weeks due to ‘disruptive behaviour’. At the time, Ms S was speaking in an American accent, declaring she was a ‘pregnant 14-year-old girl from the USA’. After 2 weeks, Ms S presented to the emergency department with abdominal pains related to her DOP. She reported amenorrhoea, and physical examination revealed a markedly swollen abdomen, but her beta-human chorionic gonadotropin (β-hCG) and abdominal ultrasound were negative for pregnancy. Ms S insisted she was pregnant, stating she could hear her unborn child’s voice. She was assessed as having a manic episode with psychotic features. On admission, her prolactin was 2038 mIU/L (59–619). On day 3, paliperidone 3 mg oral daily was initiated to supplement her depot paliperidone, with auditory hallucinations ceasing on day 5. On day 7, her DOP resolved, despite her prolactin levels remaining elevated (2700 mIU/L). Paliperidone was subsequently swapped to aripiprazole depot 400 mg monthly, amid concerns about hyperprolactinaemia and its contribution to DOP. However, shortly after discharge, Ms S had another psychotic relapse requiring admission, but without DOP. Her prolactin had normalised by this point (277 mIU/L), following the transition to aripiprazole.

This case contrasts with other reports that link the resolution of DOP with normalisation of prolactin levels (Ahuja et al., 2008; Ali et al., 2003; Hu et al., 2015). The hyperprolactinaemia was likely instrumental in her amenorrhoea and abdominal distention, which may have contributed to her phenomenology of DOP. However, it is unlikely to have been solely causative of her psychotic episode because the normalisation of prolactin levels was not contingent to the resolution of her DOP. Indeed, the swap to a prolactin-sparing agent (aripiprazole) in this patient precipitated a relapse. This provides evidence for the need to see hyper-prolactinaemia as a component factor rather than sole explanatory model for DOP. In summary, clinicians should be aware of the links between hyperprolactinaemia and DOP, but exercise caution in changing previously effective treatment regimens on this basis alone.