Why does D2 (dopamine receptor 2) antagonism lead to hyperprolactinemia?

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From the Guidelines

D2 antagonism leads to hyperprolactinemia because dopamine normally inhibits prolactin secretion from the pituitary gland, and blocking dopamine D2 receptors removes this inhibitory control, resulting in excessive prolactin release into the bloodstream. This mechanism is supported by the fact that dopamine agonists, such as cabergoline, are used to reduce serum prolactin concentrations and induce tumour shrinkage in patients with prolactinoma, as recommended by the consensus guideline for the diagnosis and management of pituitary adenomas in childhood and adolescence 1. When medications block dopamine D2 receptors in the tuberoinfundibular pathway, they remove this inhibitory control, resulting in excessive prolactin release into the bloodstream. The degree of hyperprolactinemia typically correlates with the medication's D2 receptor binding affinity. Patients taking these medications may experience symptoms such as galactorrhea (inappropriate milk production), amenorrhea, sexual dysfunction, and gynecomastia.

Some studies have shown that antipsychotic polypharmacy, which often involves the use of multiple D2 antagonists, is associated with an increased risk of hyperprolactinemia 1. However, the most recent and highest quality study on this topic is not directly related to the question of why D2 antagonism leads to hyperprolactinemia. Therefore, the focus should be on the underlying mechanism of D2 antagonism and its effects on prolactin secretion, rather than the specific effects of antipsychotic polypharmacy.

Key points to consider when managing patients on D2 antagonists include:

  • Monitoring prolactin levels, especially when symptoms develop
  • Being aware of the potential for hyperprolactinemia and its associated symptoms
  • Considering medication adjustments if clinically significant hyperprolactinemia occurs
  • Using dopamine agonists, such as cabergoline, to reduce serum prolactin concentrations and induce tumour shrinkage in patients with prolactinoma, as recommended by the consensus guideline 1.

From the FDA Drug Label

As with other drugs that antagonize dopamine D2 receptors, RISPERIDONE elevates prolactin levels and the elevation persists during chronic administration. Hyperprolactinemia may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotropin secretion This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients.

D2 antagonism leads to hyperprolactinemia because it suppresses the hypothalamic secretion of Gonadotropin-Releasing Hormone (GnRH), resulting in reduced pituitary gonadotropin secretion. This is due to the elevation of prolactin levels caused by D2 receptor antagonism, which impairs gonadal steroidogenesis in both female and male patients 2.

From the Research

Mechanism of D2 Antagonism Leading to Hyperprolactinaemia

  • D2 antagonism leads to hyperprolactinaemia because dopamine normally inhibits the secretion of prolactin from the anterior pituitary gland by binding to D2 receptors on lactotroph cells 3, 4.
  • When D2 receptors are blocked by antipsychotic drugs, the inhibitory effect of dopamine on prolactin secretion is removed, resulting in an increase in prolactin levels 3, 4.
  • The degree of hyperprolactinaemia caused by antipsychotic drugs depends on their affinity for D2 receptors and their ability to cross the blood-brain barrier 3, 4.

Factors Influencing the Degree of Hyperprolactinaemia

  • The faster an antipsychotic drug dissociates from D2 receptors, the lesser the increase in prolactin levels 3.
  • Antipsychotic drugs with a higher peripheral-to-central dopamine receptor potency are more likely to cause hyperprolactinaemia 4.
  • Sex and hormonal contraception can also influence the degree of hyperprolactinaemia, with women being more susceptible to hyperprolactinaemia than men, especially those using hormonal contraception 5.

Clinical Consequences of Hyperprolactinaemia

  • Hyperprolactinaemia can lead to sexual dysfunction, infertility, amenorrhea, gynecomastia, and galactorrhoea 3, 6.
  • Long-term hyperprolactinaemia can result in premature bone loss in both men and women 3, 6.
  • Hyperprolactinaemia may also be involved in the development of breast cancer, although its role is unclear for prostate cancer 3.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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