Hyperprolactinemia is the most common endocrine disorder of the hypothalamic pituitary axis, being an important cause of subfertility and infertility in both sexes. Prolactin is synthesized by the anterior pituitary lactotrophs, and is influenced by multiple factors, the main inhibitory factor being dopamine. There are multiple etiologies of hyperprolactinemia, and an appropriate diagnosis is essential for a correct treatment. There are physiologic and pathological causes, use of medications, presence of prolactin isoforms with high molecular weight (macroprolactin), and genetic alterations. Moreover, some illicit drugs can cause hyperprolactinemia. Lastly, idiopathic hyperprolactinemia is diagnosed when no cause is identified.
There are several challenges not only in the broad causes of hyperprolactinemia, but also in reaching the correct diagnosis. The magnitude of prolactin elevation may suggest the etiology, given that prolactin levels of >200-250 are highly suggestive of prolactinomas. However, these levels can be found in other causes. In addition, macroprolactin can be a cause of high prolactin, mostly in asymptomatic patients.
The hook effect can cause an incorrect diagnosis and an unnecessary surgery in prolactinomas. This effect consists of falsely low prolactin levels, an assay artifact produced by very high levels of prolactin. It can be seen in large pituitary adenomas with normal prolactin or moderately increased levels (<200 ng/ml). The hook effect can be revealed by 1:100 serum prolactin sample dilution. When there is discordance between the clinic and prolactin levels heterophilic or human anti-mouse antibodies should be taken into account as they may affect prolactin levels in sandwich immunoassays.
For the accurate diagnosis of hyperprolactinemia, it is essential to utilize a thorough medical history, a physical exam, coupled with laboratory evaluation and imaging as needed. Prolactinomas are the most common pituitary adenomas and the main cause of pathological hyperprolactinemia. First line treatment of prolactinomas is dopamine agonists, mainly cabergoline, and the search for alternative treatments for resistant/aggressive prolactinomas not responding to dopamine agonists are a current challenge. Consequently, the opportunity to compile information about new insights, current challenges, recent advances, and future perspectives in the field is of particular interest.
In this Research Topic the authors should focus on the broad etiologies of hyperprolactinemia, including but not limited to the following aspects:
• Molecular mechanisms and pathways,
• Pitfalls and challenges in pursuing the correct etiology,
• Its association to infertility,
• Prolactinomas and their current treatment,
• And the correct algorithm of diagnosis.
We welcome original research articles, reviews, mini reviews, clinical studies, and perspectives related to the field.
Hyperprolactinemia is the most common endocrine disorder of the hypothalamic pituitary axis, being an important cause of subfertility and infertility in both sexes. Prolactin is synthesized by the anterior pituitary lactotrophs, and is influenced by multiple factors, the main inhibitory factor being dopamine. There are multiple etiologies of hyperprolactinemia, and an appropriate diagnosis is essential for a correct treatment. There are physiologic and pathological causes, use of medications, presence of prolactin isoforms with high molecular weight (macroprolactin), and genetic alterations. Moreover, some illicit drugs can cause hyperprolactinemia. Lastly, idiopathic hyperprolactinemia is diagnosed when no cause is identified.
There are several challenges not only in the broad causes of hyperprolactinemia, but also in reaching the correct diagnosis. The magnitude of prolactin elevation may suggest the etiology, given that prolactin levels of >200-250 are highly suggestive of prolactinomas. However, these levels can be found in other causes. In addition, macroprolactin can be a cause of high prolactin, mostly in asymptomatic patients.
The hook effect can cause an incorrect diagnosis and an unnecessary surgery in prolactinomas. This effect consists of falsely low prolactin levels, an assay artifact produced by very high levels of prolactin. It can be seen in large pituitary adenomas with normal prolactin or moderately increased levels (<200 ng/ml). The hook effect can be revealed by 1:100 serum prolactin sample dilution. When there is discordance between the clinic and prolactin levels heterophilic or human anti-mouse antibodies should be taken into account as they may affect prolactin levels in sandwich immunoassays.
For the accurate diagnosis of hyperprolactinemia, it is essential to utilize a thorough medical history, a physical exam, coupled with laboratory evaluation and imaging as needed. Prolactinomas are the most common pituitary adenomas and the main cause of pathological hyperprolactinemia. First line treatment of prolactinomas is dopamine agonists, mainly cabergoline, and the search for alternative treatments for resistant/aggressive prolactinomas not responding to dopamine agonists are a current challenge. Consequently, the opportunity to compile information about new insights, current challenges, recent advances, and future perspectives in the field is of particular interest.
In this Research Topic the authors should focus on the broad etiologies of hyperprolactinemia, including but not limited to the following aspects:
• Molecular mechanisms and pathways,
• Pitfalls and challenges in pursuing the correct etiology,
• Its association to infertility,
• Prolactinomas and their current treatment,
• And the correct algorithm of diagnosis.
We welcome original research articles, reviews, mini reviews, clinical studies, and perspectives related to the field.
