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Treatment of patients with prolactinomas consists primarily of dopamine agonists (DA). Cerebrospinal fluid (CSF) leakage has sporadically been reported in patients with macroprolactinomas treated with short-acting DA such as bromocriptine. Little is known on the incidence of this complication in patients treated with the long-acting D2 specific DA cabergoline. We report three patients with CSF leakage shortly after initiation of cabergoline treatment for macroprolactinoma. All three patients responded rapidly to cabergoline (CAB) by shrinkage of the tumor and release of the optic chiasm compression. The CSF leakage occurred within 10 days after initiation of treatment. CAB treatment was not discontinued. In one patient the CSF leakage ceased spontaneously, with no additional therapy. The second patient had a surgical repair of the CSF fistula, permitting cabergoline to be continued without a recurrence of the CSF leakage. The third patient refused surgical repair of the sellar defect. In this patient the cabergoline dosage was temporarily decreased with no effect on the CSF leakage. Four years later, the CSF leakage is unchanged in this patient, whilst no other complications occurred during the follow-up. No infectious complications occurred in these three patients. In conclusion, patients with large, invasive macroprolactinomas are at risk of CSF leakage during medical treatment with CAB. It is advisable to warn these patients for occurrence of this complication and to monitor them closely especially during the first months of treatment.
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Fourteen women with amenorrhea-galactorrhea were treated with bromo-ergocryptine. Serum prolactin hPRL, hLH, hFSH, estradiol 17-beta (E2), and progesterone values were determined before and during treatment. No consistent pretreatment hormonal pattern was found. During treatment hPRL levels fell in 13 of 14 patients, and E2 rose in 12 of 14 patients. Levels of hLH became normal, and amounts of hFSH did not change. Galactorrhea lessened in all cases and ceased in 11. Menses resumed in 11 patients and 3 women became pregnant. Cessation of galactorrhea and resumption of menses occurred irrespective of initial hPRL or hLH levels. It is suggested that improvement of galactorrhea and resumption of menses in some patients with normal hPRL values are the result of increased serum E2 levels and may be due to a direct action of bromo-ergocryptine on the ovary. Bromo-ergocryptine may also be effective in treatment of amenorrhea, unassociated with galactorrhea or elevated hPRL levels.
Neuroleptic malignant syndrome (NMS) continues to be an unpredictable and rare, but potentially fatal complication of antipsychotic medications. Presumptively linked to dopamine blockade, it nonetheless occurs in patients receiving newer atypical antipsychotics. The features of NMS, its pathophysiology, differential diagnosis, clinical course, risk factors, and morbidity and mortality are reviewed. Nonpharmacologic management centers on aggressive supportive care including vigilant nursing, physical therapy, cooling, rehydration, anticoagulation. Pharmacologic interventions include immediate discontinuation of antipsychotics, judicious use of anticholinergics, and adjunctive benzodiazepines. The utility of specific agents in actively treating NMS is reviewed. Bromocriptine and other dopaminergic drugs and dantrolene sodium have alternatively been considered without merit or efficacious. Guidelines for using these agents are presented. Electroconvulsive therapy, also somewhat controversial, is identified as a second line of treatment. Finally, management of the post-NMS patient is also reviewed.
The inhibitory effects of dopamine and various ergot alkaloids on prolactin secretion were studied using continuously perfused columns of dispersed rat anterior pituitary cells. Bromocriptine (5 nmol/l) and lisuride hydrogen maleate (5 nmol/l) both inhibited prolactin secretion, the effects persisting for more than 3 h after the end of the administration of the drugs. A similar although less long-lasting effect was observed with lergotrile (50 nmol/l) and the new ergoline derivative, pergolide (5 nmol/l). These effects contrasted with the rapid disappearance of the action of dopamine. The potency estimates of the ergots relative to that of dopamine were: lergotrile, 2.3; bromocriptine, 13; lisuride, 15; pergolide, 23. Ther dopamine-receptor blocking drugs, metoclopramide and haloperidol, antagonized the prolactin release-inhibiting activity of the compounds; bromocriptine and lisuride showed the highest resistance to this dopaminergic blockade. The results suggested that the direct effect of the ergot derivatives on dispersed pituitary cells was mediated through dopamine receptors and emphasized the long-lasting action of bromocriptine and lisuride in vitro.
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We conducted an open label investigation of bromocriptine treatment in 7 patients with active non-life threatening SLE. Patients received bromocriptine daily during the treatment phase of 6 to 9 months and were followed for 5 months after bromocriptine was discontinued. Disease activity was assessed by determination of the SLE activity Measure (SLAM) and the Toronto SLE Disease Activity Index (SLEDAI). Serum prolactin concentrations and a battery of serologic and urine tests were obtained at baseline and at monthly intervals during and after bromocriptine treatment.
Four beagle bitches were treated orally, twice daily with 250 micrograms bromocryptine, an inhibitor of prolactin secretion, from D1-D5 (D1 is defined as the first day of the luteal period) until the onset of the next prooestrus (n = 2) or the end of the luteal period (n = 2) of the following cycle. The mean interoestrous interval in the experimental group (123.3 +/- 23.1 day; n = 4) was significantly (p less than 0.001) shorter than the average of the mean values of the interoestrous interval (245.9 +/- 8.8 day; n = 36) of 10 control bitches. This shortening is mainly a consequence of a reduction to 35% of the anoestrous period of normally cyclic dogs. The luteal period of the first cycle was shortened to 78% compared with the luteal period of control dogs and this is also a contributing factor.
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A 49-yr-old woman presented with an extensive prolactinoma (serum PRL > 10,000 mU/L, normal range < 450 mU/L). Over a 5-yr period following transsphenoidal surgery and pituitary irradiation, she became increasingly resistant to high doses of bromocriptine and underwent transfrontal surgery followed by stereotactic radiotherapy. In spite of these treatments, serum prolactin estimations rose progressively to > 100,000 mU/L. Magnetic resonance imaging scanning demonstrated a massive cystic tumor invading the temporal lobes, extending into the cervical and thoracic spine, with metastases to cervical lymph nodes. High-dose cabergoline administration resulted in a 30% decrease in serum PRL. Octreotide was administered as a continuous sc infusion with a profound analgesic effect on facial pain but with no effect on tumor progression. She was treated with a course of chemotherapy consisting of carboplatin and etoposide without any noticeable effect. The patient died 6 months following chemotherapy. Immunocytochemical analysis demonstrated positive nuclear staining for WAF-1, Rb protein, c-myc, and p53 both in the original and metastatic tumors. The metastases but not the primary tumor stained for c-jun. Metastatic prolactinoma remains a therapeutic challenge. It is associated with a variable proto-oncogene expression, which may be coincidental or causal. Cabergoline had no advantage over bromocriptine. Octreotide relieved facial pain but did not alter tumor progression. An effective therapy for metastatic prolactinoma remains to be identified.
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Normal aging brings with it changes in dopaminergic and memory functions. However, little is known about how these 2 changes are related. In this study, we identify a link between dopamine, episodic memory networks, and aging, using pharmacological functional magnetic resonance imaging. Young and older adults received a D2-like agonist (Bromocriptine, 1.25 mg), a D2-like antagonist (Sulpiride, 400 mg), and Placebo, in a double-blind crossover procedure. We observed group differences, during memory encoding, in medial temporal, frontal, and striatal regions and moreover, these regions were differentially sensitive across groups to dopaminergic perturbation. These findings suggest that brain systems underlying memory show age-related changes and that dopaminergic function may be key in understanding these changes. That these changes have behavioral consequences was suggested by the observation that drug modulations were most pronounced in older subjects with poorer recognition memory. Our findings provide direct evidence linking ageing, memory, and dopaminergic change.
Monoaminergic neuronal systems have been implicated in the mechanisms of action of most ergot derivatives (including those that are clinically useful and those that are "hallucinogenic"). Among the various assays that have been useful in determining the extent of such involvement is drug discrimination. In this procedure, animals are trained to respond in one way (e.g., press the right lever) following saline and to respond differently (e.g., press the left lever) after either a particular ergot or a neurotransmitter agonist, and are subsequently tested with other ergots, transmitter agonists or antagonists (alone or in combination with the training drug). The results to date indicate that: 1) There are similarities in the discriminable effects of lergotrile, lisuride and bromocriptine, which probably involve catecholaminergic neuronal systems (DA or NE). 2) These effects are clearly separable from those of ergonovine and LSD, which may be relatively more serotonergic. More precise delineation of the mechanisms underlying these cues (e.g., D1, D2-selective agonism, antagonism, etc.) awaits further testing with highly specific pharmacological interventions.
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The effects of somatostatin and bromocryptine were examined in patients bilaterally adrenalectomized because of Cushing's disease, in one of whom Nelson's syndrome had developed. Following a 250 microgram (152 nmol) somatostatin bolus, administered i.v., a further 250 microgram *152 nmol) somatostatin was given by infusion over 90 minutes. In all patients the high basal value of the serum ACTH was considerably decreased 60 minutes after the bolus, but after 240 minutes the basic value was almost restored. In the patients without Nelson's syndrome the plasma ACTH decreasing action of oral 2.5 mg (3.38 mumol) bromocryptine exceeded 300 minutes. In the Nelson's syndrome patient the early ACTH-decreasing effect of bromocryptine was greater, but after 300 minutes the ACTH level had risen to nearly twice the basic value.
Other clinicians have reported atypical presentations of NMS in patients taking newer neuroleptic agents. Although this patient met diagnostic criteria for NMS, the hallmark symptoms of fever and muscle rigidity were delayed in onset. Also, the patient never remained febrile for more than 24 hours and her maximum temperature was only 38.6 degrees C. An objective causality assessment suggests that this case of NMS was probably related to restarting risperidone.
The medical history of 9 patients interested in childbearing are studied. They all had a high prolactin level, infertility, alteration in the menstrual cycle and in the majority (8/9) breast secretion. The results obtained with the usage of Parlodel (by the oral route) complemented with ovulation induction are evaluated, as well as existing local restrictions to permit fulfilling the various diagnostic procedures, oriented to define the etiology of the above mentioned clinical entity.
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Ten patients with clinical, laboratory and radiographic evidence compatible with the diagnosis of prolactinoma were treated with two dopamine agonists. One group (N = 6) took bromocriptine and the other group (N = 4) used pergolide, a longer-acting agent. Both medications were found to reduce prolactin levels significantly from baseline, but an oscillatory pattern with significant fluctuation was seen in the mean prolactin levels in the patients taking bromocriptine. Three patients did not achieve euprolactinemia on bromocriptine, 2.5 mg qid, the maximum dose used in this study. All of the study group taking pergolide became euprolactinemic rapidly; no more than a single dose of 100 micrograms/day was required. Tumor reduction was noted in two patients taking bromocriptine and two taking pergolide. The duration of side effects was shorter and compliance was improved on pergolide therapy.
During the 13-year period 1970-1983 only 7 cases of multiple endocrine neoplasia type I (MEN I) were seen at Groote Schuur Hospital, suggesting that the associated gene is rare in this area. Only 1 of these patients was black. Endocrine associations were as follows: hyperparathyroidism--6 cases, pituitary hypersecretion--6 cases (3 each involving growth hormone and prolactin), and pancreatic hypersecretion--3 cases (2 of gastrinoma and 1 of insulinoma). The presenting features were predictably diverse and depended on the component which manifested first. There was little difficulty in reaching a diagnosis on routine investigation. All patients with hyperparathyroidism underwent a 3 1/2-gland parathyroidectomy as the first treatment procedure, normocalcaemia being achieved in 5 cases, but persistent hypercalcaemia in the 6th suggested a supernumerary gland. A pituitary adenoma was removed in 4 cases, but persistent prolactinaemia necessitated bromocriptine therapy in 3. Successful distal pancreatectomy was undertaken in a patient with insulinoma and a patient with gastrinoma, and a further patient with gastrinoma awaits surgery. The overall prognosis in cases of MEN I appears to depend on the most aggressive component, often the pancreatic lesion; our patients have run a surprisingly benign course with only 1 late death, from hypertensive heart disease.
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The patient was treated with extensive medical heart failure therapy, and also with bromocriptine for eight weeks. Six months later, left ventricular ejection fraction had significantly improved.
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The secretion of GH in two siblings with clinical dwarfism and high GH plasma levels (the mean of several basal values; 233.83 ng/ml in patient A and 178.16 in patient B has been studied with several dynamic tests. An arginine infusion increased GH levels in both cases (+193.55% for A, +140.27% for B). No significant modifications were obtained with oral glucose tolerance test +18.70% for A, +24.32% for B). A bolus of somatostatin almost completely prevented the rise in GH levels in response to arginine. Pretreatment with bromocryptine clearly increased basal GH plasma levels (A, +58.66%; B, +56.03%) and the response to arginine. As in the case of a normal hypothalamus, the hypothalamus of Laron's syndrome responds to arginine and bromocryptine, with GH elevations. Somatostatin suppresses GH levels. A lack of response to glucose can be considered as a nonspecific effect of the very low biological activity of the stimulus in a hyperstimulated hypothalamus. We suggest that GH secretion by the hypothalmo pituitary system in Laron's syndrome is normal, and that GH hyperproduction may be due to a generalized defect in GH receptors or to the low levels of somatomedin.
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Two cases of TSH-secreting pituitary adenoma were reported. Endocrinological and immunohistochemical features of these cases were described and problems in diagnosis and treatment of the rare disease are discussed. [case 1] A 28 year-old woman suffered from hyperthyroidism with a relatively high value of serum TSH (T3; 350 ng/dl, T4; 10.0 micrograms/dl, TSH; 24.5 microU/ml). She was treated with antithyroid drug and then underwent subtotal thyroidectomy. Although the levels of serum T3 and T4 were lowered to within normal range, the level of serum TSH still remained high. One month later, she developed frontal headache, amenorrhea and bitemporal hemianopsia. A CT scan showed an enhanced mass in the sellar and suprasellar region. Preoperative endocrinological studies showed elevated values of TSH (47 microU/ml) and its alpha-subunit (9.0 ng/ml). The levels of both T3 (190 ng/dl) and T4 (10.0 micrograms/dl) were near the upper normal limit. Serum TSH was suppressed by administration of exogenous T3, but did not respond to exogenous TRH, l-Dopa nor bromocriptine. Under the diagnosis of TSH-secreting pituitary adenoma, the patient was operated on by craniotomy and received local radiation therapy (50 Gy). In 1990, 12 years after the treatment, she is well and endocrinologically normal. Immunohistochemical study revealed that most tumor cells were positive for TSH. [case 2] A 28 year-old woman visited our hospital for examination of hyperthyroidism. Serum level of TSH was detectable (4.5 microU/ml). A CT scan performed at that time disclosed no pituitary tumor. Thyroid function was normalized by antithyroid drug, but the level of TSH was still high and progressively increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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The study was performed in the Clinical Research Center at Leiden University Medical Center.
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The effects of prolactin (PRL) and androgen on the seminal vesicles of immature C3H/HeJ mice were studied. Glands from controls exhibited secretory activity and full differentiation. Glands from castrates were small, markedly atrophic with some stromal hyperplasia and moderate leukocytic infiltration. Testosterone-treated castrates were similar to intact controls. Perphenazine appeared to stimulate the rough endoplasmic reticulum (RER), Golgi, and secretory activity of the epithelium in the intact and castrated mice. Normal secretory granules were not made in the perphenazine-treated castrates, but a flocculent material usually was present in the RER, Golgi, and secretory vacuoles. Bromocriptine reduced cell height and secretory activity in intact mice and promoted anaplasia and epithelial proliferation in castrates. PRL seems to be required for the seminal vesicles to complete and maintain cytological development, but the effect of PRL may be different in the presence or absence of testicular androgens.
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Pituitary adenomas represent the only true adenomas of the cranial cavity. In 1000 asymptomatic pituitary glands examined at autopsy, there was a 22.4 per cent incidence of undetected microadenomas. Advances in diagnostic endocrinology, in radiologic imaging, and in surgical and medical treatments have brought many more patients to the attention of the authors. Over the last 10 years, their treatment approaches have evolved to those presented in this article.
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Symptoms of Parkinsonism, most likely induced by an oral contraceptive, were greatly reduced by combined therapy of nicergoline and bromocriptine. A 38-year-old housewife had taken an oral contraceptive, which contained .05 mg of ethinyl estradiol and .5mg of norgestrel per tablet, for 7 years, when she presented took the following symptoms: she stumbled easily, took short, quick dancing/skating steps without arm movement, and found it increasingly difficult to keep slippers on while walking. In the afternoons she experienced extreme fatigue and rigidity in her lower limbs. After a while, languor spread to other parts of her body as well, and she was examined on April 5, 1991. The patient's face was mask-like, and her body was bent forward with her forearms flexed. She showed frozen gait and lowered initiation in her movement. Muscle rigidity was found in both upper and lower extremities, and especially on the right side. A brain MRI showed lacunar infraction with small patches of high signal intensities in the white matter of the bilateral frontal lobes and high signal intensities in the left periventricular white matter. Urine was normal; blood cholesterol and iron were slightly raised. Hormonal examinations showed lowered LH, FSH, progesterone and 24-hr 17-KGS. CT was normal. She was ordered to stop taking pills and to take nicergoline and bromocriptine, which greatly reduced these symptoms except during the first menstruation following the treatment. When mask-like facial expressions, demarche a petit pas, and languor in her lower extremities did not recur during the next menstruation, bromocriptine treatment was discontinued. Four months later nicergoline therapy was also discontinued.