810 – Zolpidem-induced galactorrhea via gabaergic inhibition of dopamine: a case report

Abstract

Objective To discuss a case of zolpidem-induced galactorrhea. Introduction The prevalence of insomnia can be as high as 32 to 33%. Non-benzodiazepines (such as zolpidem) have become more commonly used to treat insomnia. Case report The patient is a 29-year-old woman with a history of (PTSD) who presented with PTSD associated insomnia. She was started on zolpidem 5 mg po qhs. Two months after the initiation of zolpidem treatment, the patient presented with breast tenderness and galactorrhea. Zolpidem was discontinued and the galactorrhea resolved after two weeks. A serum prolactin level drawn shortly after discontinuation of zolpidem was 15.67 mg/ml. Discussion Zolpidem has a high affinity at the α1 containing GABAA receptors, with reduced affinity for those containing the α2- and α3- GABAA receptor subunits and minimal affinity for α5 receptor subunit. Psychotropic drugs have been well recognized to produce hyperprolactinemia. However, there has been no reported case of zolpidem-induced hyperprolactinemia. Specifically, zolpidem has been noted to activate GABAergic neurons within the ventral tegmental area (VTA), where there is a sizable population of GABAergic neurons. These GABAergic neurons regulate the firing of dopaminergic counterparts, also located in the VTA, which send projections throughout the brain. This inhibition results in a decrease in the dopaminergic inhibitory influence on prolactin and an increase in prolactin releasing factors which act on the anterior pituitary, leading to hyperprolactinemia and thus galactorrhea. Conclusion Pharmacologically induced hyperprolactinemia may be a problem of underestimated prevalence due to the lack of externally visible symptoms.