Diagnosis of the syndrome of persistent galactorrhea-amenorrhea
Last reviewed: 23.04.2024
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If the diagnosis of the typical forms of the syndrome of persistent galactorrhea-amenorrhea today seems to be quite simple, the differential diagnosis of "erased", "incomplete" forms from the symptomatic forms of the syndrome of persistent galactorrhea-amenorrhea, as well as various vaguely outlined and poorly studied clinical syndromes in which galactorrhea develops against the background of normal serum prolactin level and its correction does not change the course of the underlying disease and does not alleviate the patient's condition, it is very complicated.
The laboratory and instrumental examination necessary to confirm the presence of the syndrome of persistent galactorrhea-amenorrhea consists of 4 stages:
- confirmation of the presence of hyperprolactinaemia by determining the serum level of prolactin;
- exclusion of symptomatic forms of the syndrome of persistent galactorrhea-amenorrhea (definition of the functional state of the thyroid gland, the exclusion of Stein-Levental syndrome, hepatic and renal insufficiency, neuro-reflex and drug effects, etc.);
- clarification of the condition of adenohypophysis and hypothalamus (radiography of the skull, computer or magnetic resonance imaging of the head, if necessary with additional contrast), carotid angiography;
- clarification of the condition of various organs and systems against the background of chronic hyperprolactinaemia (determination of the level of gonadotropins, estrogens, DEA-sulfate, study of the state of carbohydrate and fat metabolism, bone system, etc.).
When evaluating the prolactin content in the case of small deviations from the norm, it is advisable to carry out three to fivefold studies in order to avoid erroneous conclusions, since the very manipulation of blood sampling is often the reason for moderate hyperprolactinaemia.
In a special group it is necessary to isolate patients with galactorrhea against the background of the normal ovulatory and menstrual cycle, which have clinical manifestations of asthenoneurotic syndrome, sometimes with elements of carcinophobia that constantly check the presence of breast reflexes that are separated from the mammary glands and this self-palpation reflexively supporting the galactorrhea. In these patients, unlike patients with the syndrome of persistent galactorrhea-amenorrhea with a high prolactin level, galactorrhea is the main complaint persistently presented to the doctor in combination with other neurasthenic complaints. Termination of self-palpation in many of these patients contributes to the elimination of galactorrhea.
Determination of serum prolactin level is not only diagnostic, but also differential-diagnostic value. Moderate increase is more common in "idiopathic" forms, the level of the hormone is significantly increased with prolactinomas. It is generally accepted that prolactinemia more than 200 μg / l reliably indicates the presence of prolactinoma even with an X-ray-intact Turkish saddle. To identify the "hidden", "transient", hyperprolactinemia use the dynamic definition of prolactin during the day and in different phases of the menstrual cycle. Typical "exaggerated", hyperergic nighttime prolactin level rise, exceeding the normal maximum, as well as periovulatory hyperprolactinemia.
Until recently, experts were puzzled by the discrepancy in a number of patients between sufficiently high serum prolactin levels and extremely poorly presented clinical symptoms of GH, in combination with the resistance to ongoing therapy with dopamine agonists. The work of recent years, aimed at studying isoforms of prolactin, allowed to find the answer to this question. As it turned out, the total pool of immunoreactive prolactin includes forms with different molecular masses. In patients with classical GH symptoms, prolactin with a molecular mass of 23 kDa is detected in the study of blood serum by gel filtration, whereas in women without a typical symptom complex of persistent amarantoritis galactorrhea, the predominant form (80-90% of the total pool) is prolactin with molecular mass of more than 100 kD (big-big-prolactin), which has a low biological activity (the phenomenon of macro-prolactinemia). It is assumed that the origin of high molecular weight prolactin is heterogeneous. This form of hormone can result from the aggregation of monomeric prolactin or its association with other proteins, for example, immunoglobulin. It is possible that big-big-prolactin can directly represent a specific immunoglobulin, which manifests in the immunochemical analysis systems the ability to simulate the presence of prolactin. Macroproprolinaemia accounts for up to 20% of all cases of hyperprolactinaemia.
A number of tests have been proposed that allow studying the secretion of prolactin under stimulation conditions (with thyreoliberin, chlorpromazine, insulin, sulpiride, cerul-cal, cimetidine, domperidone). For micro- and macro-prolactin, a typical decrease in the response to stimulating effects that directly correlate in most patients with adenoma size. However, the probability of a false-positive or false-negative conclusion about the form of the disease on the basis of the results of stimulation samples in each individual patient is up to 20%.
The level of other hormones in the syndrome of persistent galactorrhea-amenorrhea is quite typical: unchanged or decreased levels of LH and FSH with a good response to lyuliberin, a decrease in the level of estrogens and progesterone, an increase in the level of dehydroepiandrosterone (DEA) sulfate.
Specific for the syndrome of persistent galactorrhea-amenorrhea biochemical changes, despite numerous experimental data on the effect of prolactin on various types of metabolism, is not revealed. Often there are only signs of a violation of fat metabolism, an increase in the level of NEFIC and triglycerides.
The level of electrolytes in the serum is usually normal. On the ECG, there may be signs of myocardial dystrophy: a negative or biphasic T wave in the pectoral leads. The samples with hyperventilation, orthostatic and with potassium or obzidan load reveal the non-coronary nature of these disorders. Chronic, uncorrectable hyperprolactinemia leads to the development of osteoporosis. The leading role in the pathogenesis of osteoporosis in the syndrome of persistent galactorrhea-amenorrhea belongs to the slowing down of bone formation, which is confirmed by a decrease in the level of osteocalcin in the blood.
Patients with this syndrome have an increased serum insulin level. Given the normal level of glucose, it is commonly believed that they have some insulin resistance.
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