PATHOPHYSIOLOGY OF HYPERPROLACTINEMIA: THE ROLE OF DOPAMINERGIC DISINHIBITION AND PITUITARY HYPERSECRETION

Authors

  • Vitor de Castro Silva Author
  • Pedro Paulo Nunes Costa Author
  • Paula Guimarães Oliveira Author
  • Ana Luiza Modesto Bezerra de Souza Author
  • Vanessa Marcolina Author
  • Nilson Hitoshi Yoshimoto Author
  • Ana Clara da Costa Souza Author
  • Felipe Lessa dos Reis Author
  • Vanessa Oliveira dos Reis Author

DOI:

https://doi.org/10.56238/arev8n3-057

Keywords:

Hyperprolactinemia, Prolactin, Dopamine, Pituitary Neoplasms, Dopamine Agonists

Abstract

Hyperprolactinemia (HPRL) is one of the most recurrent endocrine disorders in clinical practice and can interfere with reproductive, metabolic, and bone formation processes. Regarding the hormone that generates this condition, prolactin, it is known that its secretion is predominantly regulated by inhibitory dopaminergic control through the action of the hypothalamus on the lactotrophs of the anterior pituitary gland. That is, when there is any alteration in this mechanism, it can lead to an elevation of hormone levels. In this context, two pathophysiological mechanisms stand out: autonomous hypersecretion of prolactin, found mainly in prolactinomas, and dopaminergic disinhibition, commonly associated with the use of D2 receptor antagonist drugs. The present study aimed to review the main pathophysiological mechanisms involved in hyperprolactinemia, with emphasis on dopaminergic disinhibition and pituitary hypersecretion. This is a narrative literature review conducted in the PubMed database, using the descriptors "Hyperprolactinemia," "Diagnosis," and "Treatment," combined with Boolean operators. Studies published in the last five years, in Portuguese or English, available in full text, and related to the pathophysiology, diagnosis, and clinical management of HPL were included. The analyzed studies showed that drug-induced hyperprolactinemia, especially antipsychotic D2 receptor antagonists, represents one of the most prevalent causes of the condition. Furthermore, prolactinomas constitute the main tumorous cause, characterized by the autonomous secretion of prolactin. Thus, treatment is mainly based on the use of dopaminergic agonists, such as cabergoline and quinagolide, which show great efficacy in hormonal regulation and tumor reduction. It is concluded, therefore, that understanding the pathophysiological mechanisms of hyperprolactinemia is essential for accurate diagnosis and for defining more effective therapeutic strategies in the management of hyperprolactinemia.

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References

BENETTI-PINTO, C. L. et al. Hyperprolactinemia in women: treatment. Revista Brasileira de Ginecologia e Obstetrícia, v. 46, p. e-FPS05, 2024.

JIANG, Q. et al. Treatment of antipsychotic-induced hyperprolactinemia: an umbrella review of systematic reviews and meta-analyses. Frontiers in Psychiatry, v. 15, p. 1337274, 2024.

LAGUNA, C. et al. Treatment of hyperprolactinemia in women: A Position Statement from the Brazilian Federation of Gynecology and Obstetrics Associations (Febrasgo) and the Brazilian Society of Endocrinology and Metabolism (SBEM). Archives of Endocrinology and Metabolism, v. 68, p. 1-12, 2024.

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RUSGIS, M. M. et al. Guidance on the treatment of antipsychotic-induced hyperprolactinemia when switching the antipsychotic is not an option. American Society of Health-System Pharmacists, p. 1-10, 2021.

ZENG, Y. et al. The efficacy and safety of quinagolide in hyperprolactinemia treatment: A systematic review and meta-analysis. Frontiers in Endocrinology, v. 14, p. 1027905, 2023.

Published

2026-03-13

Issue

Section

Articles

How to Cite

SILVA, Vitor de Castro; COSTA, Pedro Paulo Nunes; OLIVEIRA, Paula Guimarães; DE SOUZA, Ana Luiza Modesto Bezerra; MARCOLINA, Vanessa; YOSHIMOTO, Nilson Hitoshi; SOUZA, Ana Clara da Costa; DOS REIS, Felipe Lessa; DOS REIS, Vanessa Oliveira. PATHOPHYSIOLOGY OF HYPERPROLACTINEMIA: THE ROLE OF DOPAMINERGIC DISINHIBITION AND PITUITARY HYPERSECRETION. ARACÊ , [S. l.], v. 8, n. 3, p. e12506 , 2026. DOI: 10.56238/arev8n3-057. Disponível em: https://periodicos.newsciencepubl.com/arace/article/view/12506. Acesso em: 14 mar. 2026.