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The authors describe a prospective series of 12 patients with pituitary macroadenomas in whom bromocriptine was only used for 6 weeks before transsphenoidal surgery. As he was administered with high-dose dexamethasone concurrently with the bromocriptine, one patient with size reduction in his tumor was not randomized to either group. All Group A patients had tumours with prolactin granules, according to a pathological examination, although none of Group B tumors had such granules. Two of the five Group A patients discontinued bromocriptine before starting the 6-week course and saw a rapid return of their tumors to pre-treatment size. This finding underscores the fact that bromocriptine's inability to reduce pituitary tumor size in the case of hyperprolactinema does not necessarily indicate a prolactinoma. Pathological changes in responsive prolactinomas during bromocriptine therapy have been demonstrated in this first moderately sized group of patients in whom pathological changes in responsive prolactinomas have been reported.
Source link: https://doi.org/10.3171/jns.1984.60.1.0001
U2713 The possibility that bromocriptine has a selective effect on blood flow in the adenohypophysis was tested in rats. Using the hydrogen clearing method, twenty-four anesthetized male Wistar rats underwent blood flow testing. In both the medial and lateral parts of the adenohypophysis's blood flow was reduced to about 70% of the baseline value after an intravenous injection of 50 g/kg bromocriptine. The course of change in blood flow in the medial and lateral adenohypophysis did not follow the median arterial blood pressure, although blood pressure increased was not equal, although blood pressure changes remained within autoregulation in the adenohypophysis.
Source link: https://doi.org/10.3171/jns.1985.63.1.0120
Two experiments using Spanish Merino ewes were carried out to see if the mysterious prolactin secretion during the sheep oestrous cycle was involved in the patterns of growth and decline of follicle populations. Bromocriptine significantly reduced prolactin secretion, but did not have an effect on FSH levels, the time of the LH preovulatory peak, or LH concentrations in the preovulatory surge, according to the author. Before the preovulatory increase, both doses of bromocriptine resulted in a similar decrease in LH pulse frequency. In conclusion, the effects of bromocriptine on gonadotrophin and prolactin secretion and the follicular dynamics during the sheep oestrous cycle's follicular cycle's follicular cycle suggest that prolactin could have a short-term viability of gonadotrophin-responsive follicles that came shortly after luteolysis.
Source link: https://doi.org/10.1530/reprod/120.1.177
In rat pituitary somatograft somatografe tumor GH3 cells, we investigated the role of the pituitary bone morphogenetic protein system in modulating GH production controlled by a somatostatin analog, octreotide, and a dopamine agonist bromocriptine. BMP-4 and BMP-6; BMP type-1 and type-2 receptors; and Smad signaling molecules were discovered in BMP cells; and Smad signaling proteins. According to cAMP synthesis, Forskolin stimulated GH production in accordance with cAMP synthesis. OCT in combination with BRC had additive effects on lowering GH and cAMP production induced by forskolin. Forskolin's BMP-4 cells' GH secretion and cAMP production was specifically enhanced, as shown by forskolin in GH3 cells. A high percentage of OCT contributes to BRC results by reducing cAMP production and suppressing BMP-4 signaling in GH3 cells together. These results may help to explain the origins of GH reduction in a combination therapy with OCT and BRC for GH-producing pituitary adenomas.
Source link: https://doi.org/10.1677/joe-07-0549
In comparison to bromocriptine therapy, this research investigated the effects of chronic treatment with cabergoline, a new, potent, and long-lived dopamine agonist, on seminal fluid measurements and sexual and gonadal function in hyperprolactinemic males. For six months, seventeenteen males with macroprolactinoma were treated with CAB at a dose of 0. 5 to 1. 5 mg/week, or BRC at a dose of 5-15 mg/day. All patients had a low sperm count with oligosthenospermia, reduced motility, and rapid progression with an abnormal morphology and reduced viability before treatment, as well as a small number of erections. In both groups of patients and were normalized after 6 months. In patients treated with both CAB and BRC, patients with both CAB and BRC were seen with a significant rise in number, total motility, rapid growth, and normal morphology. Following six months, a significant rise in number, total motility, rapid rise, and normal morphology was observed. However, the changes in seminal fluid measurements and sexual function in patients treated with CAB were more apparent and rapid. The number of erections had normalized after six months of CAB therapy for all patients, and in all patients except one treated by BRC, but not one forwarded by BRC. In five patients after BRC administration, mild side-effects were noted at the start of therapy in two patients after CAB and mild-to-moderate side-effects. With CAB normalized PRL levels, improving gonadal and sexual function, and fertility in males with prolactinoma earlier than BRC therapy, providing excellent tolerability and excellent patient compliance to medical care.
Source link: https://doi.org/10.1530/eje.0.1380286
According to the study, resistance to bromocriptine, which is defined as the absence of normalization of prolactin levels after a 15-u201330 mg daily dose of bromocriptine during at least six months, has been present in 56% of the prolactinomas. The recent onset of a potent dopamine agonist, quinagolide, in 28 patients with prolactinomas resistant to bromocriptine in 28 patients. u00b1 185 bcg/l, and decreased to 291 bc/l after a 6u201321 months of bromocriptine therapy. After 1 year of treatment, 12/28 patients of the present series recovered normal gonadal function, with their initial mean baseline PRL of 16 bcg/l approaching 15 bcg/l. A similar good result was maintained in these patients during the three-year follow-up period under quinagolide, with the exception of one man suffering with a secondary rise in PRL under quinagolide. Following two years of quinagolide therapy, three patients recovered, with a second rise in PRL values associated with a new tumor formation in two patients. During the first trimester, however, a rapid rise in PRL in two women correlated with tumor formation. In 11/28 patients who were previously resistant to bromocriptine, quinagolide was found in 11/28 patients, retaining normal gonadal function, with a quinagolide daily dose of 300 u03bcg in most of them, and 15/20 women recovered normal gonadal function in the whole population.
Source link: https://doi.org/10.1530/eje.0.1350413
Patients with prolactinoma that is intolerant or resistant to bromocriptine are unable to use dopamine agonist cabergoline. Cabergoline, a new long-acting ergoline derivative used to treat hyperprolactinaemia, is available in ISSN 0804u20134643. No side effect was observed on cabergoline therapy in group I; two patients became pregnant, and normoprolactinaemia was achieved in the five others; no side effect was recorded on cabergoline therapy; no side effects were observed in group I; no one affected was observed on cabergoline therapy; two patients became pregnant and normoprolactinaemia was achieved in the five others. In two out of the three patients, cabergoline was present and well tolerated; in another patient normoprolactinaemia was restored and decreased by 60%; in the third patient cabergoline was stopped due to side effects and inefficacy.
Source link: https://doi.org/10.1530/eje.0.1340454
In acromegaly, otide, but not bromocriptine, raises circulating insulin-like growth factor 1-binding protein 1 levels. After placebo or single doses of octreotide or bromocriptine, twenty-three patients with active acromegaly underwent serum testing for growth hormone, insulin, and insulin-like growth factor binding protein 1. After octreotide and 49% after bromocriptine, integrated 24-h serum GH levels dropped by 90% after bromocriptine and 49%. After octreotide and bromocriptine, a statistically significant relationship was found between the course of GH levels. Bromocriptine produced a non-significant rise in integrated 24-h serum IGFBP-1 levels in acromegaly, despite a direct regulatory effect of GH on IGFBP-1 production in acromegaly. When compared to treatment directed at the pituitary level, the alleged inhibitory effect of IGF-I on the biological effects of IGF-I might result in an additional clinical benefit in acromegalic patients.
Source link: https://doi.org/10.1530/eje.0.1330195
In a clonal strain of rat pituitary adenoma cells, the effects of the dopamine agonist bromocriptine on prolactin release, electrical membrane stability, and transmembrane Ca 2 + fluxes have been investigated. The normal biphasic membrane response to TRH and the depolarizing effect of elevated K+ levels were not affected by bromocriptine, whereas the Ca 2+ spikes in a Na + -free environment were suppressed by the drug. We therefore recommend that bromocriptine blocks the voltage sensitive Ca 2+ channels of GH 3 cells.
Source link: https://doi.org/10.1530/acta.0.1110185
In a small group of hyperprolactinaemic women, the effect of long-term bromocriptine therapy on TSH dynamics was also examined. After the TRH administration of Fifty-two hyperprolactinaemic patients with no other signs of pituitary or thyroid dysfunction had significantly higher mean TSH serum concentrations and mean TSH peak values following the TRH treatment than 75 healthy controls. In both daily cycling women and patients with hyperprolactinaea, low-dose DA infusion reduced TSH responses to TRH. Long-term bromocriptine therapy not only normalized serum Prl levels, but also reduced the TSH response to TRH in 7 hyperprolactinaemic women who had exaggerated TSH levels to the basal TRH test. Both low-dose DA infusion and long-term bromocriptine treatment effectively reduced TSH levels in hyperprolactinaemic patients, rather than elevated, in pathological hyperprolactinaemia.
Source link: https://doi.org/10.1530/acta.0.1110154
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