Screening for Macroprolactinemia Is Indispensable for Proper Treatment of Hyperprolactinemia Microadenoma

BACKGROUND: Macroprolactin microadenoma is a combination of non-functional microadenomas with macroprolactinemia. This study aimed to explore the significance of macroprolactinemia screening for the antidiastole of prolactin microadenoma and macroprolactin microadenoma.METHODS: Retrospective analysis of patients with pituitary microadenoma and screening for macroprolactinemia in patients with hyperprolactinemia was conducted. Based on the prolactin content and screening results, patients were divided into non-functional microadenoma, prolactin microadenoma, and macroprolactin microadenoma groups. The existing forms of prolactin in serum samples were analyzed by gel filtration chromatography and a luminescence immunoassay analyzer. The clinical course of patients and treatment were retrospectively reviewed.RESULTS: The results of gel filtration chromatography confirmed that prolactin in patients with macroprolactin microadenoma was mainly in the form of macromolecules, and the small molecular prolactin was within the normal range. Among 84 patients with hyperprolactin microadenomas, 9 (10.7 %) were diagnosed with macroprolactin microadenoma, and 5 (55.6 %) were treated with bromocriptine. The prolactin content (55.9 ~ 81.0 ng/mL) in the macroprolactin microadenoma group was elevated before the screening and significantly decreased (11.2 ~ 21.2 ng/mL) after screening. The incidence of clinical manifestations was the same as that of the non-functional microadenoma group, but the rate of drug use was higher, which was similar to that of the prolactin microadenoma group.CONCLUSION: Macroprolactinemia screening can effectively identify prolactin microadenomas and macroprolactin microadenomas, which prevent misdiagnosis and mistreatment of macroprolactin microadenomas.

The stress hormones effect on the progression of vaginal bacterial dysbiosis

Annotation. The stress objective marker is the neuro-hormonal stress-implementing system stress and the increase the cortisol and prolactin levels in the blood, leading to the “distress syndrome” formation. Aim – to establish the stress effect, revealed according to the level of stress- implementing hormones, in particular cortisol and prolactin, on the progression of vaginal bacterial dysbiosis and the bacterial vaginosis (BV) development. During the study there were used the data taken from 298 women, who were divided into the following groups according to the Opportunistic pathogenic microflora index (OPMI) and normobiota index (NBI): normocenosis (n=53), dysbiosis I (n=128) and II degree (n=117) among the latter 83 patients with NBI>1 lg GE/sample were identified, in which BV was established. Molecular genetic studies of the epithelium scraping from the vagina posterolateral wall were carried out by Polymerase chain reaction (“DNK-Technologiia” LLC, RF). Facultative and obligate anaerobes, myco- and ureplasmas, and yeast-like fungi were quantified. The cortisol and prolactin blood levels were identified. For statistical analysis, the Statistica 10 software (StatSoft, Inc., USA) was used. Catch out that the blood cortisol content with dysbiosis progression compared with the normocenosis has changed in two-phase: it was increased with I degree dysbiosis (1.2–1.4 times; p<0.01) and decreased with II degree dysbiosis and BV (1.5 times; p<0.001). So, with respect to the classical concept of the General adaptive syndrome of G. Selye, the first dysbiosis development stages can be considered as reaction of “anxiety”, while the development of BV is a reaction of “exhaustion”. The blood prolactin content compared with normocenosis with dysbiosis was increased, which was most expressed in BV (1.5 times; p <0.001). It also reflected the stress response development with increased central nervous system stress. The blood hormones content has relation with BV-associated microbiota indexes: prolactin was positively related with NBI, and cortisol was negatively related to the number of Atopobium vaginalis. Thus, according to the data obtained, BV can be attributed to the stress pathology with the "distress syndrome" development and the content of cortisol and prolactin in the blood can be considered as marker factors for hormonal regulation disorder.

A Model for Hypogalactia Treatment Using Electrical Acupoint to Increase Breast Milk Volume and Improve Prolactin Content

Hypogalactia is one of the problems for breastfeeding mothers that accounts for 63%. Nowadays, efforts have been done to prevent hypogalactia pharmacologically. However, this approach often comes with side effects for the mothers. This research proposes the implementation of non-pharmacological electrical acupoint method via activation of neurological, bio-mechanical, and psychological systems. It is aimed at proving the method’s efficacy in improving breast milk volume and prolactin level. The model of electrical acupoint is carried out at 0. 5 watt frequency of scale 3 for 10 minutes at acupoints SI1, ST36 and SP6. Paired t-test statistical test was then conducted to differentiate the effects of electrical acupoint treatment on breastfeeding mothers. Results show significant differences (p<0. 05) after implementation of electrical acupoint. This significant difference is proven from the unpaired t-test which indicated different results of pre-and post-treatment. This means that electrical acupoint improves breast milk volume by an average of 70. 915 mL and prolactin level by around 313. 47 ng/Ml. It can then be inferred that the use of electrical acupoint readily handles the problem of hypogalactia.

Perinatal Glucocorticoid Treatment Disrupts the Hypothalamo-Lactotroph Axis in Adult Female, But Not Male, Rats

This study aimed to test the hypothesis that the tuberoinfundibular dopaminergic neurons of the arcuate nucleus and/or the lactotroph cells of the anterior pituitary gland are key targets for the programming effects of perinatal glucocorticoids (GCs). Dexamethasone was administered noninvasively to fetal or neonatal rats via the mothers’ drinking water (1 μg/ml) on embryonic d 16–19 or neonatal d 1–7, and control animals received normal drinking water. At 68 d of age, the numbers of tyrosine hydroxylase-positive (TH+) cells in the arcuate nucleus and morphometric parameters of pituitary lactotrophs were analyzed. In control animals, striking sex differences in TH+ cell numbers, lactotroph cell size, and pituitary prolactin content were observed. Both pre- and neonatal GC treatment regimens were without effect in adult male rats, but in females, the overriding effect was to abolish the sex differences by reducing arcuate TH+ cell numbers (pre- and neonatal treatments) and reducing lactotroph cell size and pituitary prolactin content (prenatal treatment only) without changing lactotroph cell numbers. Changes in circulating prolactin levels represented a net effect of hypothalamic and pituitary alterations that exhibited independent critical windows of susceptibility to perinatal GC treatments. The dopaminergic neurons of the hypothalamic periventricular nucleus and the pituitary somatotroph populations were not significantly affected by either treatment regimen in either sex. These data show that the adult female hypothalamo-lactotroph axis is profoundly affected by perinatal exposure to GCs, which disrupts the tonic inhibitory tuberoinfundibular dopaminergic pathway and changes lactotroph morphology and prolactin levels in the pituitary and circulation. These findings provide new evidence for a long-term disruption in prolactin-dependent homeostasis in females, but not males, after inappropriate GC exposure in perinatal life.

Influence of lactotroph cell density on prolactin secretion in rats

ABSTRACT The relationships between the stimulation of prolactin secretion and proliferation of lactotrophs was studied from a multidisciplinary standpoint in three experimental models. Administration of both oestrogen and sulpiride resulted in a significant increase in prolactin secretion and in the lactotroph population. A single injection of 10 μg oestradiol benzoate (OB) induced a twofold increase in the proliferation of lactotrophs (morphometrically as volume density), which increased further (2·5-fold) after three OB injections. Parallel changes were observed in the net counts made on lactotrophs sectioned through the nucleus to avoid possible distortions in volume density caused by hypertrophic cytoplasms. Comparable results were obtained with the mitotic index in the same groups of rats exposed to treatment with colchicine. The effect of sulpiride on proliferation of lactotrophs was also significant (1·7-fold) but less pronounced than in rats treated with oestrogens. The treatments with oestrogen and sulpiride did not stimulate lactotrophic activity in a similar way, as judged by the levels of serum prolactin and the storage patterns of small and big prolactin in pituitary glands. Serum prolactin (mean ± s.e.m.) in control ovariectomized rats was 4·0±0·9 μg/l and one and three injections of OB raised these levels to 14·4±5·0 and 28·8±4·6 μg/l respectively. The highest levels of serum prolactin were seen in sulpiride-treated rats (467·2±28·7 μg/l). Striking differences occurred in the pituitary contents of big prolactin, the control values increasing from 5·3±0·5 to 10·2±1·3 μg/mg after one OB injection and to 14· 7 ±0·7 μg/mg after three OB injections. In contrast, the concentration of big prolactin in sulpiride-treated rats was very low (1·85 ± 0·2 μg/mg), 2·8-times smaller than the controls. Other changes were also found in the small prolactin content in pituitary tissue with higher values in all the experimental models. These differences could only be detected after differential extraction of big and small molecular forms of prolactin. In ovariectomized rats, treatment with several doses of oestrogen enhanced the proliferation observed in the lactotroph population and increased the number of mitoses. In turn, morphological data could be closely related to the higher levels of prolactin in serum and pituitary glands. A sustained stimulation of lactotrophic secretion was always followed by proliferation of lactotrophs, the number of which fluctuated in parallel with the degree of stimulation. Journal of Endocrinology (1992) 134, 241–246

Concanavalin-A-bound and -unbound prolactin in normal and hyperprolactinaemic rats

ABSTRACT Concanavalin-A (Con-A)-bound and -unbound forms of prolactin were studied in female Wistar–Furth rats, both normal and with hyperprolactinaemia induced by treatment with oestrogen or a prolactinoma graft. In normal rats, Con-A-bound prolactin was the major circulating form (more than 50%) and a minor pituitary component (less than 10%), essentially as 25 kDa prolactin. In oestrogen-treated rats, plasma prolactin levels were 100-fold higher and pituitary weight was fivefold higher than in the controls, but total pituitary prolactin content was unmodified. Under oestrogen, Con-A-bound prolactin represented about one-third of the total hormone levels in the plasma and less than 10% in the pituitary. In the pituitary, bound prolactin was found essentially as 25 kDa and unbound prolactin as 22, 30 and 40–45 kDa. A similar increase in plasma prolactin levels was induced 6 months after the graft of a prolactinoma. Pituitary weights and total pituitary prolactin contents were slightly decreased. Plasma and pituitary Con-A-bound prolactin levels were similar to those observed in oestrogen-treated rats. On the other hand, unbound prolactin was only present as a 22 kDa monomer. In the tumour, Con-A-bound prolactin (essentially as 25 kDa prolactin) represented one-third of the total hormone level and unbound prolactin was composed of the 22 and 45 kDa forms, this latter form being partially transformed into 22 kDa by heating. As Con-A-bound prolactin was previously characterized as glycosylated prolactin, these data suggest that glycosylated prolactin is present in the plasma of the normal rat as a major circulating form, unglycosylated 40–45 kDa is only present when the rate of the prolactin synthesis is high (in the pituitary of oestrogen-treated rats and in the tumour of grafted rats); this result supporting the hypothesis of a precursor product relationship between dimeric and monomeric prolactin. The manners in which prolactin is synthetized are not comparable in normal and tumour cells, percentages of glycosylated prolactin being different in normal pituitary and prolactinoma. Journal of Endocrinology (1992) 134, 27–32

Effect of cysteamine on the lysosomal enzymes of the hyperprolactinaemic rat pituitary

ABSTRACT The effect of cysteamine on the activity of lysosomal enzymes and the prolactin content of isolated hyperprolactinaemic cells has been investigated. In broken cell preparations, cysteamine markedly stimulated acid prolactin protease activity. In intact cells, however, cysteamine inhibited acid prolactin protease activity and β-galactosidase. Moreover, the activities of α-mannosidase, acid phosphatase, β-glucuronidase, total arylsulphatase and hexosaminidase were not changed by the addition of cysteamine. Cysteamine significantly depleted the cells of prolactin, and this action was not compromized by the inclusion of either leupeptin, chloroquine or NH4Cl in the incubation media. Taken together, these results indicate that cysteamine does not promote degradation of prolactin and hence depletion of prolactin from the pituitary through a mechanism involving lysosomal enzyme degradation. Journal of Endocrinology (1990) 125, 75–80