Hcer Dx diferencial. Valoración general: Antecedentes del edo. menstrual, embarazos, fertilidad, así como uso de fármacos y otros síntomas. La hiperprolactinemia es un motivo de consulta frecuente en la práctica diaria. frecuentes son la oligomenorrea/amenorrea, la galactorrea y la infertilidad. A hiperprolactinemia causa hipogonadismo, irregularidade menstrual ou menstrual irregularities or amenorrhea in women, low serum testosterone levels in colecistoquinina, bombesina, neurotensina, neuropeptídeo Y. Outros fatores .

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Prolactin PRL is an anterior pituitary hormone which has its principle physiological action in initiation and hiperprolactinemai of lactation. In human reproduction, pathological hyperprolactinemia most commonly presents as an ovulatory disorder and is often associated with secondary amenorrhea ameorrea oligomenorrhea.

Galactorrhea, a typical symptom of hyperprolactinemia, occurs in less than half the cases. In women with hyperprolactinemic amenorrhea one important consequence of estrogen deficiency is osteoporosis, which deserves specific therapeutic consideration. This hipedprolactinemia explain many cases of very high prolactin levels sometimes found in normally ovulating women and do not require hiperprolactinekia treatment.

Dopamine agonist is the mainstay of treatment. However, presence of a pituitary macroadenoma may require surgical or radiological management. Prolactin PRL plays a central role in a variety of reproductive functions.

Initially, even though this hormone was recognized in relation to lactation in women, lately immense interest has been focused on prolactin with respect to its effect on reproduction. Hyperprolactinemia is a condition of elevated prolactin levels in blood which could be physiological, pathological, or hipeprrolactinemia in origin.

Similarly elevated prolactin levels could be associated with severe clinical manifestations on one side of the spectrum or be completely asymptomatic on the other side. Unlike other tropic hormones secreted by the anterior pituitary gland, prolactin secretion is controlled primarily by inhibition from the hypothalamus and it is not subject to negative feedback directly or indirectly by peripheral hormones.

It exercises self-inhibition by a counter-current flow in the hypophyseal pituitary portal system which initiates secretion of hypothalamic dopamine, as well as causes inhibition of pulsatile secretion of gonadotropin releasing hormone GnRH.

This negatively modulates the secretion of pituitary hormones responsible for gonadal function. It is a common endocrine disorder of the hypothalamic-pituitary axis.

It occurs more commonly in women. The prevalence of hyperprolactinemia ranges from 0. Prolactin is a 23 kDa polypeptide hormone amino acid synthesized in the lactotroph cells of the anterior pituitary gland. Its secretion hiperptolactinemia pulsatile and increases with sleep, stress, food ingestion, pregnancy, chest wall stimulation, and trauma.

Even though monomeric 23 kDa form is the predominant form, prolactin is also present in different molecular forms on which the bioactivity of the hormone depends. Such forms are rarely physiologically active but may register in most prolactin assays. Many commercial assays do not detect macroprolactin. Polyethylene glycol precipitation is an amenorrrea way to detect the presence of macroprolactin in the serum.

The main biological action of prolactin is inducing and maintaining lactation. However, it also exerts metabolic effects, takes part in reproductive mammary development[ 8 ] and stimulates immune responsiveness. Actual serum prolactin level is the hperprolactinemia of a complex balance between positive and negative stimuli derived from both external and endogenous environments. Plenty of mediators of central, pituitary, and peripheral origin take part in regulating prolactin secretion through a direct or indirect effect on lactotroph cells.

Prolactin secretion is under dual regulation by hypothalamic hormones. The predominant signal is tonic inhibitory control of hypothalamic dopamine which traverses the portal venous system to act upon pituitary lactotroph D2 receptors.

Other prolactin inhibiting factors include gamma amino butyric acid GABAsomatostatin, acetylcholine, and norepinephrine. The hiperprolwctinemia signal is stimulatory which is hioerprolactinemia by the hypothalamic peptides, thyrotropin releasing hiperprolacttinemia TRHvasoactive intestinal peptide VIPepidermal growth factor EGFand dopamine receptor antagonists.


Serotonin physiologically mediates nocturnal surges and suckling-induced prolactin rises and is a potent modulator of prolactin secretion. Histamine has a predominantly stimulatory effect due to the inhibition of the dopaminergic system. Estrogen stimulates the proliferation of pituitary lactotroph cells especially during pregnancy.

However, lactation is inhibited by the high levels of estrogen and progesterone during pregnancy.

The rapid decline of estrogen hiprrprolactinemia progesterone in the postpartum period allows lactation to commence. During lactation and breastfeeding, ovulation may be suppressed due to the suppression of gonadotropins by prolactin, but may resume before menstruation resumes.

Hyperprolactinemia hiperporlactinemia be physiological or pathological. Some of the common causes are listed in Figure 1. Etiology of hyperprolactinemia[ 11 ]. Physiological hyperprolactinemia is usually mild or moderate.

Pathological hyperprolactinemia can be caused by both hypothalamic-pituitary hiprrprolactinemia prolactinomas as well as non-hypothalamic-pituitary disease.

Raised prolactin hpierprolactinemia can also be caused by pituitary adenomas cosecreting prolactin hormone. Lesions affecting the hypothalamus and pituitary stalk such as nonfunctioning adenomas, gliomas, and craniopharyngiomas also results in prolactin elevation. Many patients with acromegaly have prolactin cosecreted with growth hormone. The predominant physiologic consequence of hyperprolactinemia is hypogonadotropic hypogonadism HH which is due to suppression of pulsatile GnRH.

The clinical manifestations of conditions vary significantly depending on the age and the sex of the patient and hiperprolactinemua magnitude of the prolactin excess. Clinical presentation in women is more obvious and occurs earlier than in men. Women can present with symptoms of oligomenorrhea, amenorrhea, galactorrhea, decreased libido, infertility, and decreased bone mass. It is worth noting amenorreea many premenopausal women with hyperprolactinemia do not have galactorrhea, and many with galactorrhea do not have hyperprolactinemia.

This is because galactorrhea requires adequate estrogenic or progesterone priming of breast. Conversely, isolated galactorrhea with normal prolactin levels occurs due to increased sensitivity of the breast to the lactotrophic stimulus. Prolonged hypoestrogenism secondary to hyperprolactinemia may result in osteopenia. Men with hyperprolactinemia may present with erectile dysfunction, decreased libido, infertility, gynecomastia, decreased maenorrea mass, but rarely galactorrhea.

Over time, the patient may have diminished energy, reduced muscle mass, and increased risk of osteopenia. Macroprolactinomas usually present with neurological symptoms caused by mass effects of the tumor. Symptoms include headaches, visual field losses, cranial neuropathies, hypopituitarism, seizures, and cerebrospinal fluid rhinorrhea. Unless the prolactin levels are markedly elevated, the investigation should be repeated before labeling the patient as hyperprolactinemic.

Even one normal value should be considered as normal and an isolated raised one should be discarded as spurious. Other common conditions which must be excluded when considering hipdrprolactinemia prolactin levels are non-fasting sample, excessive exercise, history of drug intake, chest wall surgery or trauma, renal disease, cirrhosis, and seizure within hours. Hyperprolactinemia without an identified cause requires imaging of the hypothalamic-pituitary area. A mildly elevated serum prolactin level may be due to a nonfunctioning pituitary hiperlrolactinemia or craniopharyngioma compressing the pituitary stalk, but high prolactin levels are commonly associated with a prolactin secreting prolactinoma.

For management purpose, hyperprolatinemics can be broadly divided into three groups [ Figure 3 ].

Dopamine agonist is the mainstay of management if fertility is desired or there are symptoms of estrogen deprivation or galactorrhea. Bromocriptine is the first option for this condition and has now been used for the longest period of time.

Best way is to give it is as continuous therapy and prolactin levels reduce in about a week; ovulation and menstruation resumes in weeks. Weekly assessment of progesterone is the most popular method to confirm resumption of ovulatory function in oligo or amennorrhic women.


In the remaining women, exogenous gonadotropin stimulation can be added along with dopamine agonist to achieve ovulation. Medical management can be undertaken for a period ranging from 18 months to 6 or more years.

No treatment is required in asymptomatic and very slow growing tumors which do not metastasize. Follow-up is mandatory with yearly estimation of prolactin levels, MRI, and visual fields. However, hormone replacement therapy HRT to replenish estrogen deficit should be given to all patients with amenorrhea.

Dopamine agonists have been in clinical use for many years and remain the cornerstone for therapy of prolactinomas. Initially it was thought that patients would require lifelong dopamine agonist therapy but the current use has evolved into a dynamic process depending on the patient’s requirement.

Most commonly used dopamine agonists are bromocriptine and cabergoline. Others are lisuride, pergolide, quinagolide, terguride, and metergoline. Patients who are intolerant hiperprolactinemiz fail to respond to one agent may do well with another. Side effects associated with amenogrea drugs are nausea, vomiting, headache, constipation, dizziness, faintness, depression, postural hypotension, digital vasospasm, and nasal stuffiness.

These symptoms are most likely amenkrrea occur with initiation of treatment or when the dose is increased. One rare but notable side effect is neuropsychiatric symptoms which present as auditory hallucinations, delusion, and mood changes. This may be due to hydrolysis of the lysergic acid part of the molecule. It quickly resolves with discontinuation of the drug.


Bromocriptine is a lysergic acid derivative with a bromine substitute at position 2. It decreases prolactin synthesis, DNA synthesis, cell multiplication, and overall size of prolactinoma. It has a short half-life and so it requires twice daily administration to maintain optimal suppression of prolactin levels. Intolerance to bromocriptine amenorreaa common and it is the main indication of using an alternative drug.

Tolerance is better when one starts with the lowest possible dose of 1. Another alternative to oral administration is vaginal usage of the same drug which is well tolerated. Vaginal absorption is nearly complete and avoidance of the liver first pass metabolism allows lower therapeutic dosing. Cabergoline shares many characteristics and amenirrea effects of bromocriptine but has a hiperprolactinemla long half-life allowing weekly dosing.

This is more effective in suppressing prolactin and reducing tumour size. It can also be given vaginally if nausea occurs when taken orally.


Maximum dose that can be given is 1 mg twice a week. Though both amdnorrea have been found to be safe in pregnancy, the number of reports studying bromocriptine in pregnancy far exceeds that of cabergoline. Kisspeptin, when administered exogenously, has the ability to reverse the hypogonadotropic effects of hyperprolactinemia and can also restore pulsatile LH secretion.

The aim of the treatment is reduction in tumor mass along with the correction of the biochemical consequences of the hormonal excess including restoration of fertility, prevention of bone loss, and suppression of galactorrhea. Dopamine agonists are the first line of treatment with surgery and radiotherapy reserved for refractory and medication intolerant patients.

Some show prompt shrinkage with low doses while others may require prolonged treatment with higher dosage. Reduction in tumor size can take place in several days to weeks.