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The aim was to formulate practice guidelines for the diagnosis and treatment of hyperprolactinemia. Participants: The Task Force consisted of Endocrine Society-appointed experts, a methodologist, and a medical writer. Evidence: This evidence-based guideline was developed using the Grading of Recommendations, Assessment, Development, and Evaluation GRADE system to describe both the strength of recommendations and the quality of evidence.
Consensus Process: One group meeting, several conference calls, and e-mail communications enabled consensus. Conclusions: Practice guidelines are presented for diagnosis and treatment of patients with elevated prolactin levels. These include evidence-based approaches to assessing the cause of hyperprolactinemia, treating drug-induced hyperprolactinemia, and managing prolactinomas in nonpregnant and pregnant subjects. Indications and side effects of therapeutic agents for treating prolactinomas are also presented.
The Task Force followed the approach recommended by the Grading of Recommendations, Assessment, Development, and Evaluation GRADE group, an international group with expertise in development and implementation of evidence-based guidelines 1.
A detailed description of the grading scheme has been published elsewhere 2. The Task Force used the best available research evidence to develop some of the recommendations. The Task Force also used consistent language and graphical descriptions of both the strength of a recommendation and the quality of evidence. The Task Force has confidence that persons who receive care according to the strong recommendations will derive, on average, more good than harm.
Linked to each recommendation is a description of the evidence and the values that panelists considered in making the recommendation; in some instances, there are remarks, a section in which panelists offer technical suggestions for testing conditions, dosing, and monitoring. These technical comments reflect the best available evidence applied to a typical person being treated.
Often this evidence comes from the unsystematic observations of the panelists and their values and preferences; therefore, these remarks should be considered as suggestions. Introduction and natural history Prolactin synthesis and secretion by pituitary lactotroph cells is tonically suppressed by hypothalamic dopamine traversing the portal venous system to impinge on lactotroph D2 receptors 3.
Factors inducing prolactin synthesis and secretion include estrogen, thyrotropin-releasing hormone, epidermal growth factor, and dopamine receptor antagonists. The isolation of human prolactin in permitted development of RIAs 4 , 5 , which enabled identification of hyperprolactinemia as a distinct clinical entity and resulted in distinguishing prolactin-secreting tumors from nonfunctioning adenomas 6. Prolactin acts to induce and maintain lactation of the primed breast.
Hyperprolactinemia may also develop due to pharmacological or pathological interruption of hypothalamic-pituitary dopaminergic pathways and is sometimes idiopathic.
Regardless of etiology, hyperprolactinemia may result in hypogonadism, infertility, and galactorrhea, or it may remain asymptomatic 7 — 9. Bone loss occurs secondary to hyperprolactinemia-mediated sex steroid attenuation. The reported population prevalence of clinically apparent prolactinomas ranges from 6—10 per , to approximately 50 per , 12 , In an analysis of patients with medically treated hyperprolactinemia, the calculated mean prevalence was approximately 10 per , in men and approximately 30 per , in women, with a peak prevalence for women aged 25—34 yr However, the prevalence of ever-treated hyperprolactinemia was approximately 20 per , male patients and approximately 90 per , female patients.
In women aged 25—34 yr, the annual incidence of hyperprolactinemia was reported to be Prolactinomas may rarely present in childhood or adolescence. In girls, disturbances in menstrual function and galactorrhea may be seen, whereas in boys, delayed pubertal development and hypogonadism are often present.
The treatment options are the same as in adult patients. Testing for hyperprolactinemia is straightforward, owing to the ease of ordering a serum prolactin measurement. Accordingly, an evidence-based, cost-effective approach to management of this relatively common endocrine disorder is required. Diagnosis of Hyperprolactinemia Recommendation 1. To establish the diagnosis of hyperprolactinemia, we recommend a single measurement of serum prolactin; a level above the upper limit of normal confirms the diagnosis as long as the serum sample was obtained without excessive venipuncture stress.
Evidence Serum prolactin is assessed with the use of assays that yield accurate values, and assessment usually presents no challenges in the clinical setting. Dynamic tests of prolactin secretion using TRH, L-dopa, nomifensine, and domperidone are not superior to measuring a single serum prolactin sample for the diagnosis of hyperprolactinemia 15 , Even minimal prolactin elevations may be consistent with the presence of a prolactinoma, but a non-prolactin-secreting mass should first be considered.
However, substantial prolactin elevations can also occur with microadenomas. Remarks The initial determination of serum prolactin should avoid excessive venipuncture stress and can be drawn at any time of the day. A single determination is usually sufficient to establish the diagnosis, but when in doubt, sampling can be repeated on a different day at to min intervals to account for possible prolactin pulsatility 15 , Recommendation 1.
Antiprolactin autoantibodies may also be associated with macroprolactinemia Larger prolactin forms macroprolactin are less bioactive, and macroprolactinemia should be suspected when typical symptoms of hyperprolactinemia are absent 20 , Many commercial assays do not detect macroprolactin. Polyethylene glycol precipitation is an inexpensive way to detect the presence of macroprolactin in the serum. Because macroprolactinemia is a common cause of hyperprolactinemia, routine screening for macroprolactin could eliminate unnecessary diagnostic testing and treatment Because true hyperprolactinemia and macroprolactinemia cannot be reliably distinguished on clinical criteria alone, we suggest screening for macroprolactin in investigation of asymptomatic hyperprolactinemic subjects.
This association between serum prolactin levels and tumor size is not always consistent, and tumor mass and prolactin levels may be dissociated 15 , One potential reason for the discrepancy is the hook effect, an assay artifact that may be observed when high serum prolactin concentrations saturate antibodies in the two-site immunoradiometric assay.
The second signaling antibody binds directly to the excess prolactin remaining in the solution and, therefore, is less available to the prolactin already bound to the first coupling antibody. Therefore, artifactually low results are obtained. We recommend that when prolactin values are not as high as expected, the assay should be repeated after a serum sample dilution to overcome a potential hook effect.
Alternatively, after prolactin binding to the first antibody, a washout could be performed to eliminate excess unbound prolactin before adding the second antibody. Modestly elevated prolactin may occur in patients with large nonfunctioning adenomas due to decreased dopamine, which inhibits prolactin secretion from normal lactotrophs because of hypothalamic stalk dysfunction.
When prolactin values are not as high as expected in a patient with a large macroadenoma, the assay should be repeated after a serum sample dilution. This step will overcome a potential hook effect and will distinguish between a large prolactinoma and a large nonfunctioning adenoma.
We recommend that this artifact be excluded in patients who have pituitary macroadenomas and apparently normal or mildly elevated prolactin levels 25 , Newer assays may obviate this problem, and alternative reference laboratories may be used Causes of hyperprolactinemia Recommendation 2. Evidence A number of physiological states including pregnancy, breast-feeding, stress, exercise, and sleep can cause prolactin elevation, as can medications Table 1 Patients with renal insufficiency may have moderate hyperprolactinemia caused by impaired renal degradation of prolactin and altered central prolactin regulation 29 , In about one third of patients with kidney disease, hyperprolactinemia develops because of decreased clearance and enhanced production of the hormone 30 , Dialysis does not alter serum levels, but prolactin levels normalize after renal transplantation.
Hyperprolactinemia may contribute to hypogonadal symptoms that accompany chronic kidney disease, and menses may return after bromocriptine therapy.
Some patients with primary hypothyroidism have moderate hyperprolactinemia 6 , 32 , Long-term or inadequately treated primary hypothyroidism can cause pituitary hyperplasia that may mimic a pituitary tumor. Hyperprolactinemia and enlargement of the pituitary gland due to thyroid failure can be reversed by treatment with L-thyroxine 34 , 35 , which may also decrease TRH drive.
Because prolactin secretion is tonically inhibited by hypothalamic dopamine, disruption or compression of the pituitary stalk by a non-prolactin-secreting pituitary tumor or other parasellar mass will lead to hyperprolactinemia. Table 1.
Prolactina alta: Tratamiento para combatirla
Si la hormona prolactina elevada ...
Hiperprolactinemia: revisión y aspectos relevantes