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This review examines the mechanisms of valvulopathy in prolactinoma patients treated with cabergoline, suggesting monitoring improvements.
Prolactinomas are the most prevalent neuroendocrine tumors in the cranial cavity and the primary cause of hyperprolactinemia. Dopamine receptor agonists, especially cabergoline, effectively reduce prolactin levels and tumor volume and are thus first-line treatments for prolactinomas. However, long-term use of cabergoline may bring about some serious side effects, which seriously affects patients' health. Cabergoline-associated valvular disease (CAV) is a disease with an unknown mechanism that mainly affects the mitral valve, tricuspid valve and aortic valve. In prolactin-pituitary adenomas, there is still some controversy over whether the use of cabergoline leads to related heart valve diseases and the mechanism of CAV. This review examines the current understanding of CAV and discusses its potential molecular mechanisms, which include cabergoline’s interactions with catecholaminergic, serotonergic, and TGF-β-related signaling pathways, and inflammatory responses. This effort is intended to enhance the understanding of cabergoline’s side effects, specifically the occurrence and pathogenic mechanisms of CAV, and to encourage enhanced clinical surveillance for the safety of patients with prolactinomas using this medication.
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Tan et al. (2026) studied this question.
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