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New insights into human prolactin pathophysiology: genomics and beyond
Sydney Chang1,2, Alan B Copperman1,2
1Department of OBGYN and Reproductive Science, Icahn School of Medicine at Mount Sinai, Klingenstein Pavilion, New York City.
Current Opinion in Obstetrics & Gynecology
|May 3, 2019
Summary
Recent findings reveal kisspeptin mediates infertility in hyperprolactinemia, challenging previous understanding. New research also highlights genetic factors in prolactinomas and potential therapies for hyperprolactinemia.
Area of Science:
- Endocrinology
- Reproductive Medicine
- Molecular Biology
Background:
- Hyperprolactinemia was traditionally thought to cause infertility by directly inhibiting gonadotropin-releasing hormone (GnRH) neurons.
- Prolactin's role in reproductive function and the pathophysiology of prolactin-secreting tumors are areas of ongoing research.
Purpose of the Study:
- To summarize current knowledge on hyperprolactinemia and prolactinomas.
- To review recent advancements in understanding the mechanisms and potential treatments for these conditions.
Main Methods:
- Review of molecular and genetic studies on prolactin and its receptors.
- Analysis of the role of kisspeptin in endocrine signaling.
- Examination of new therapeutic targets for hyperprolactinemia.
Main Results:
- Kisspeptin is identified as a key mediator of hyperprolactinemia-induced infertility, acting upstream of GnRH neurons.
- Macroprolactin, previously considered inactive, may be associated with reproductive issues and sexual dysfunction.
- Genetic mutations and polymorphisms in the prolactin receptor offer insights into familial hyperprolactinemia and prolactinomas.
Conclusions:
- New molecular and genetic insights are clarifying the pathophysiology of hyperprolactinemia and its reproductive effects.
- Kisspeptin and tyrosine kinase inhibitors represent promising therapeutic avenues for hyperprolactinemia and dopamine-resistant prolactinomas.
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