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Endocrinology

Giperprolaktinemiya

Table of contents
Giperprolaktinemiya
Giperprolaktinemiya reasons
Anamnesis of a giperprolaktinemiya
Physical inspection
Diagnostic testings
Assessment

Close concepts: an amenorrhea syndrome — a galactorrhoea, the increased content of prolactin in plasma

According to MKB-10 the giperprolaktinemiya belongs to the class:
Diseases of endocrine system, disorder of food and disbolism
Block:
Disturbances of other closed glands
Code:
E22.1

Giperprolaktinemiya is characterized by increase of concentration of hormone of prolactin in blood. Though prolactin is considered as independent hormone long ago, its value in pathology of the person remained not clear till 1971 when prolactin was emitted in pure form and the specific radio immunological method of its definition was developed.

In studying of physiology and a pathophysiology of pituitary prolactin the last decade became especially fruitful.

PROLACTIN

Human pituitary prolactin (PRL) represents the polypeptide consisting approximately of 200 amino-acid remains which is biologically excellent, but is structurally close to the growth hormone (GH) and placental lactogen of the person (PL). It cosecretes lactotropic cells of a front share of a hypophysis. Secretion of PRL is regulated by a hypothalamus which produces a prolaktiningibiruyushchy factor (mutual fund). The mutual fund initially possesses dopaminergic properties, and is not excluded that it represents actually a dopamine. Thus, normal the mutual fund comes to a front share of a hypophysis and to lactotropic cells through the portal blood circulatory system of a hypophysis and suppresses release of prolactin. Most likely, the main control of release of prolactin in a lobby of a share of a hypophysis happens at the expense of dopaminergic inhibition of secretion of PRL though it is known that such hormones of a hypothalamus as the thyrotropin-rileasing-hormone (TR) and the gonadotrophin-rileasing-hormone (GR), are quite powerful secretagogues of PRL in a front share of a hypophysis.

Prolactin can be produced not only tissues of a hypophysis. In particular, its local secretion is possible in a decidual endometria, a large number it can be also synthesized by a decidua during pregnancy and come to amniotic liquid. At nonpregnant women secretion of PRL an endometria is insignificant and cannot be taken into consideration by search of the reasons of a giperprolaktinemiya. Prolactin secretion cases are described by malignant tumors (for example, an ovsyanokletochny cancer of a lung), but the probability of it is low and prolactin cannot be considered as a reliable marker of a tumor.

In fauna of PRL has diverse functions. At the person the only thing which is not raising doubts physiological effect of PRL is "start" of a lactation. So, during pregnancy together with other hormones (estrogen, progesterone, cortisol, insulin, thyroxine, etc.) PRL participates in preparation of mammary glands for a lactation; in a puerperal period it plays a crucial role in initiation of a lactation. During pregnancy the maintenance of PRL in plasma considerably increases (to 200 ng/ml in comparison with less than 30 ng/ml before pregnancy). It is explained by the direct stimulating influence of high level of the estrogen emitted by a placenta. Despite such high content of PRL, the lactation during pregnancy does not arise. Assume that she is oppressed by estrogen (and it is possible, progesterone), which blocks effect of prolactin directly at the level of mammary glands. At childbirth the placenta separates and, thus, the cause of high content of steroids is removed; during 24 h the content of estrogen after the delivery becomes lowered. Though after the delivery the incentives increasing secretion of PRL a hypophysis disappear at once, the PRL level in plasma decreases to initial only in 3 — 4 weeks. During this short period when the hypoestrogenemia and a giperprolaktinemiya is observed, the active lactation begins. The lactation can proceed indefinitely at continuous suction or irritation of a mammary gland that stimulates the increased emission of PRL.
Other impacts of PRL on a human body are less studied. Believe that PRL participates also in forming of chest glands during puberty (mammotrofichesky effect). In spite of the fact that receptors of PRL are found in ovaries, the question of influence of PRL on functions of female gonads demands further research.

Giperprolaktinemiya

Prolactin level in plasma can be determined by means of radio immunoassay. Tests usually select in the morning. Normal content of prolactin in plasma makes from 5 to 25 ng/ml at persons of both sexes. Though sometimes at a hypopituitarism, a hypothalamic gonadotropic amenorrhea, neurogenic anorexia and in a climacteric the PRL level less than 5 ng/ml is found, the specific syndrome of a gipoprolaktinemiya is not allocated. If the content of prolactin exceeds 30 ng/ml, the state is regarded as a giperprolaktinemiya.

Experienced clinical physicians were able to distinguish many giperprolaktinemichesky diseases and when there was no reliable way of measurement of level of prolactin. These syndromes, as a rule, shown a galactorrhoea and an amenorrhea, include Forbes's syndrome — Albright (a galactorrhoea, an amenorrhea and a tumor of a hypophysis); Kiari's syndrome — Frommelya (the galactorrhoea which is not stopping after the child's birth and an amenorrhea), and also Agumad's syndrome — Del-Castillo (Argonts — Del-Castillo) (the galactorrhoea and an amenorrhea which are not connected with pregnancy). Presently the states proceeding with an amenorrhea and a galactorrhoea classify by the giperprolaktinemiya reasons, and traditional names of these syndromes are of mostly historical interest.

Usually giperprolaktinemichesky states are combined with the hypophysis lowered by allocation of FSG and LG. There are many hypotheses concerning the nature of communication of the increased PRL level with reduced secretion of FSG and LG. Theoretically high level of the circulating PRL can exert impact on effects of gonadotrophins at the level of ovaries, however clinical value of such peripheral mechanism remains not clear. Introduction of gonadotrophins from the outside (human FSG and LG, pergonal) effectively stimulates ovaries and causes an ovulation in patients with the high content of prolactin. Other possible explanation of reduced allocation of gonadotrophins is the assumption that the high content of PRL slows down secretion of gonadotrophins at the level of a hypophysis; however it is not enough proofs of it. The third mechanism — disturbance of formation of GRG at the level of a hypothalamus — is most probable. This disturbance can be explained with one general defect causing deficit of GRG and mutual fund that conducts to a giperprolaktinemiya and decrease in level of gonadotrophins. To the contrary, increase of the PRL level can cause on a feedback mechanism deficit of GRG at the level of a hypothalamus. Usually, if the maintenance of PRL becomes normal or almost normal, gonadotropic function is recovered.



 
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