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Is prolactin involved in the evolution of atherothrombotic disease?
Anne Q Reuwer1,2, Menno Hoekstra3, Philippe Touraine4,5,6
1a Department of Vascular Medicine, Academic Medical Center, 1105 AZ Amsterdam, The Netherlands.
Insights
Elevated prolactin levels may contribute to cardiovascular diseases (CVDs) by promoting atherothrombosis. Prolactin-lowering treatments could be a future therapy for patients with high prolactin and vascular disease.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Pathophysiology
Background:
- Cardiovascular diseases (CVDs) are a leading cause of global mortality, with atherothrombosis being a primary driver.
- Endocrine disorders are increasingly linked to cardiovascular pathology.
- Prolactin, a pituitary hormone, is emerging as a potential factor in CVD development.
Purpose of the Study:
- To explore the potential role of prolactin in the development of atherothrombosis and cardiovascular diseases.
- To investigate whether reducing prolactin levels could be a therapeutic strategy for CVD.
Main Methods:
- Review of recent clinical and experimental studies linking prolactin to cardiovascular health.
- Speculative analysis of prolactin's mechanisms in atherothrombosis.
- Consideration of therapeutic implications for patients with hyperprolactinemia.
Main Results:
- Prolactin may influence CVD through direct effects on atherosclerotic plaques and systemic metabolic risk factors.
- The exact role of prolactin in CVD pathogenesis requires further elucidation.
- Elevated prolactin levels are associated with increased risk of atherothrombotic vascular disease.
Conclusions:
- Prolactin-lowering therapy is a potential future treatment for patients with elevated prolactin and existing or high risk of vascular disease.
- These findings may influence clinical management strategies for conditions like prolactinomas.
Abstract:
Cardiovascular diseases (CVDs) account for approximately 30% of all deaths globally. The most important cause of CVD is atherothrombosis, in other words, narrowing of the arteries as a result of the deposition of cholesterol and other lipoid substances within the arterial wall. Several endocrine disorders have been linked to this pathological state. Recent clinical and experimental studies have suggested that prolactin, a pleiotropic pituitary hormone, may potentially contribute to CVD, either through direct modulation of local cellular processes within atherosclerotic plaques/thrombi and/or through influencing conventional cardiovascular metabolic risk factors. However, the precise role of prolactin in the pathology of CVD remains largely unknown. Here, the authors speculate whether prolactin-lowering treatment may become a future therapeutic approach in patients with elevated prolactin levels and concomitantly presenting with coexisting vascular disease or a significantly elevated risk for premature atherothrombotic vascular disease. Awareness of these new developments may also change our clinical opinions about therapeutic strategies in patients with prolactinomas.
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