Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

28 women with amenorrhea-galactorrhea were investigated endocrinologically and treated with bromocryptine 2.5 mg twice daily, ranging from 18 to 150 days. These women were classified into 6 with hypothyroidism, having prolactin (PRL) over 30 ng/ml, thyroid stimulating hormone (TSH) over 8 mcU/ml, luteinizing hormone (LH)6-20 mlU/ml and greater than follicle stimulating hormone (FSH); 8 with radiologically diagnosed pituitary tumors, LH, FSH, and increased PRL; 9 with similar endocrine profiles and suspected pituitary tumors; and 3 with high PRL considered idiopathic. 5 of the hypothyroid group were followed, and achieved ovulation, reduced TSH, PRL, and lactation, and 3 became pregnant. Of the 8 with tumors, 5 menstruated, 4 ovulated, 3 conceived, 3 had reduced lactation, 2 had reduced PRL, and 1 failed to respond clinically; 9 with suspected tumors took bromocryptine for at least 20 days, resulting in 4 pregnancies and 3 with regular menses. The 3 idiopathic cases showed lower PRL and regular ovarian function, 1 pregnancy, yet 1 developed pseudocyesis and recurrent galactorrhea. 2 women had to stop bromocryptine because of vomiting. This drug is longer-acting than L-dopa and safer than estrogen-progestagen combinations in cases of pituitary tumors. Bromocryptine reduces galactorrhea and associated hypothyroidism temporarily.
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PMID:Bromocryptine therapy in cases of amenorrhea-galactorrhea. 57 72

Tne patients with galactorrhea syndrome were treated with two different daily dosages (5 mg and 7.5 mg) of Bromergocryptine. The 5 mg daily dosage often did not produce the desired hormonal and clinical response. Five patients were treated with this regimen for 38 to 90 days, with treatment extending over more than one menstrual cycle. However, the 7.5 mg daily dosage resulted in complete cessation of galactorrhea in all patients, restoration of menstrual cycles in five patients, and pregnancies in four patients. Disappearance of lactation proved to be a very good indicator of the general responsiveness of patients. Nausea, vomiting, and occasional dizziness were side effects of the drug. The case histories and hormonal findings of four typical patients are reported.
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PMID:Clinical and hormonal response of patients with galactorrhea syndrome treated with bromergocryptine. 61 Oct 24

The effects of dihydroergocriptine (DHECP), a dihydrogenated ergot alkaloid with dopaminergic agonistic and alpha-adrenergic antagonistic properties, were studied in 22 women with PRL-secreting microprolactinomas and compared with those recorded in 36 previously studied patients treated with bromocriptine (BRC). After acute administration of 5 mg DHECP, orally, serum PRL decreased by 61 +/- 18% (+/- SD); only 1 patient was unresponsive. The nadir was reached at 300 min. Long term treatment with increasing DHECP doses caused a progressive PRL fall from 125 +/- 142 (+/- SD) to 81 +/- 159 micrograms/L after 1 week of a 3 mg twice daily regimen, to 64 +/- 88 micrograms/L after 1 week of 5 mg twice daily, 46 +/- 57 micrograms/L after 1 week of 10 mg twice daily, and 28 +/- 34 to 33 +/- 45 micrograms/L throughout 9 months of treatment with 10 mg DHECP 3 times daily. Seventy-seven percent of patients had normal serum PRL levels during chronic treatment. All women, including those with supranormal serum PRL levels, resumed regular menses, and 16 had ovulatory cycles; 1 woman became pregnant. Galactorrhea disappeared in all. During treatment the PRL response to TRH, initially absent in all patients, became positive in 10. In 7 patients, after DHECP treatment for 9 months, high definition computed tomographic scan no longer showed the focal lesions initially seen. After drug withdrawal, serum PRL increased again in all except 1 patient. Two patients had regular menses for 6 months, and 3 still had no adenoma imaged by high definition computed tomography. In BRC-treated patients the serum PRL changes and clinical results were very similar to those in the DHECP-treated patients, except for the persistence of normal serum PRL levels in 4 patients after drug withdrawal. On the other hand, side-effects were negligible during DHECP treatment, but remarkable during BRC. Systolic and diastolic blood pressures decreased by only 5.4 and 3.0 mm Hg, respectively, after acute 5 mg DHECP administration, but decreased by 12.8 and 14 mm Hg after acute 2.5 mg BRC administration. Orthostatic hypotension and peripheral vasomotor phenomena occurred in the long term DHECP treated patients except one, but they occurred in 9 and 3 of those treated with BRC, respectively. Gastric discomfort or mild nausea occurred in 12 DHECP-treated patients, while mild or severe nausea or vomiting were observed in 18, 11, and 2 of those taking BRC, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dihydroergocriptine in management of microprolactinomas. 311 32

Lymphoid adenohypophysitis is an autoimmune disorder. Eighteen percent of the multipartums are reported to have autoantibodies to pituitary tissues. The symptoms in lymphoid adenohypophysitis, such as hypopituitarism and sellar tumors, exhibit spontaneous remission. The pituitary is a feasible target organ in other autoimmune diseases of the endocrine system. Of these patients, 19/287 showed a positive immune reaction with pituitary tissue antigens. Our three female patients with sellar and suprasellar mass were clinically diagnosed as having lymphoid adenohypophysitis, because of the spontaneous regression of tumors, or presence of immunologically and endocrinologically abnormal findings. The first case was a 31-year-old woman who had amenorrhea and galactorrhea syndrome for two years after delivery of her second child. CT scan revealed a supraseller enhanced mass lesion. She had concomitant signs of recurrent meningeal irritations. The number of cells in the CSF increased, though the protein concentration increased only slightly. During a one-year close observation, the suprasellar mass spontaneously regressed. The second patient was a 66-year-old woman. In 1945, she underwent hysterectomy and oophorectomy for appendicitis followed by adnexitis. She was admitted because of episodes of headache, vomiting and visual field defect in 1983. CT scan also showed a contrast enhanced mass in the suprasellar region. She had two episodes of high fever. After the treatment with antibiotics and anti-inflammatory agents for 4 months, the tumor disappeared. The third case was a 20-year-old female. She had neither neurological nor endocrinological abnormality, except for attacks of vertigo, nausea and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lymphoid adenohypophysitis, with special reference to 2 cases with sellar tumors spontaneously disappearing on the CT]. 377 4

Metoclopramide antagonizes the effect of dopamine in the central nervous system and other organ systems. Metoclopramide's effect on the medullary chemoreceptor trigger zone makes it useful as a routine anti-emetic and in preventing vomiting induced by antineoplastic drugs, particularly cisplatin. Metoclopramide's gastrointestinal smooth muscle stimulatory effects are related to its ability to antagonize the inhibitory neurotransmitter, dopamine; to augment acetylcholine release and sensitize the muscarinic receptors of the gastrointestinal smooth muscle; and to coordinate gastric-pyloric-small intestinal motor function. The indications for which metoclopramide is approved in the United States are reviewed. Adverse effects, which may occur in up to 20% of patients, include drowsiness, lassitude, and akathisia; all are usually mild, transient, and reversible. Tremor, dystonic reactions, and extrapyramidal effects are infrequent; breast enlargement, galactorrhea, and menstrual irregularities are related to prolactin release.
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PMID:Metoclopramide: pharmacology and clinical application. 633 44

The tolerance and prolactin (PRL) release-inhibiting action of the 8 alpha-aminoergoline, mesurlergine, were investigated. In a blind crossover study in six subjects with hyperprolactinemia, 0.5 mg mesulergine induced fewer side effects than did 2.5 mg bromocriptine, while the PRL release-inhibiting effect of the two was of the same order. Six different subjects with suspected PRL-secreting pituitary adenomas who (repeatedly) had to discontinue bromocriptine because of nausea, vomiting, or symptoms of orthostatic hypotension were treated for 20 mo with mesulergine (1 to 2 mg/day). Mesulergine did not induce side effects and its actions resembled those of bromocriptine. Mesulergine induced cessation of galactorrhea and resumption of normal menstrual cycles in five subjects, while in one subject an insufficient luteal phase persisted. No abnormalities in routine blood parameter estimations were observed. In two of three subjects there was shrinkage of a pituitary tumor after 12 to 15 mo on mesulergine. Mesulergine did not directly inhibit PRL release by cultured normal rat pituitary cells and human prolactinoma cells and it antagonized the action of dopamine in a dose-dependent manner. This suggests that the dopaminergic action is carried out by a metabolite of mesulergine, while the parent drug probably prevents the well-known side effects of dopamine-agonistic drugs by its dopamine receptor blocking activity. Because of its acceptability, mesulergine might be important in the treatment of hyperprolactinemia and perhaps also of acromegaly and Parkinson's disease.
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PMID:Mechanism of action and tolerance of mesulergine. 648 83

A 28-year-old woman with bilateral headaches and vomiting was found to have normal prolactin levels despite an eight-year history of intermittent galactorrhea and amenorrhea and the current finding of a pituitary microadenoma. The microadenoma contained hemosiderin. It is concluded that pituitary apoplexy is not confined to large tumors that have outgrown their blood supply, but can occur in microadenomas with regression of a positive endocrinopathy.
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PMID:Apoplexy in a prolactin microadenoma leading to remission of galactorrhea and amenorrhea. 719 10

The clinical effects of CV 205-502, a potent and non-ergot-derived dopamine agonist, were investigated in 24 selected patients with hyperprolactinemia previously treated with standard oral bromocriptine, the slow-release oral form of bromocriptine (BRC-SRO) and/or the long-acting injectable form of bromocriptine (BRC-LAR); 14 were chosen because of their resistance to treatment and ten because they were intolerant of the different forms of bromocriptine. A macroprolactinoma was present in seven patients and a microprolactinoma in ten, whereas seven had no radiological images of a pituitary tumor and were classified as having non-tumoral hyperprolactinemia. All the 24 patients were treated with CV 205-502 at a daily dose of 0.075-0.6 mg for 3-12 months. All the patients had gonadal dysfunction and galactorrhea. Basal serum prolactin values ranged from 70 to 1677 ng/ml. CV 205-502 was effective in 11 of the 14 patients resistant bromocriptine, BRC-SRO and BRC-LAR; serum prolactin levels became normal within 6 months and a tumor shrinkage was obtained in five of the seven macroprolactinomas. In general, the drug was effective and well tolerated. Only three patients (two resistant and one intolerant) manifested nausea, vomiting and postural hypotension. In conclusion, this study shows that CV 205-502 is effective in bromocriptine-resistant hyperprolactinemic patients. Furthermore, CV 205-502 has insignificant and tolerable side-effects in patients intolerant of bromocriptine. CV 205-502 can, therefore, be considered a useful and effective drug, and an interesting therapeutic alternative to the ergot-derived dopamine-agonist drugs in use today.
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PMID:Positive response to compound CV 205-502 in hyperprolactinemic patients resistant to or intolerant of bromocriptine. 784 2

Terguride, a derivative of the ergot alkaloid, was characterized as a new anti-hyperprolactinemic agent in rats and dogs in comparison with bromocriptine. Terguride was found to bind selectively to the pituitary dopamine D2-receptors with a high affinity (Kd = 0.39 nM). In reserpinized rats, terguride at 0.03 mg/kg, p.o. significantly reduced the serum prolactin (PRL) level. The PRL lowering effect and the effective dose were longer lasting and about 30 times lower than those of bromocriptine, respectively. In rats bearing estrogen-induced pituitary prolactinoma, chronic terguride induced shrinkage of the prolactinoma as well as reduction of the high serum PRL level. In lactating rats, terguride (1.0 mg/kg, s.c.) reduced milk production in the mammary gland, whereas bromocriptine showed no significant effect up to 10 mg/kg, s.c. Terguride (10 mg/kg, p.o.) did not induce any stereotypy and hypermotility in reserpinized rats, while bromocriptine induced both stereotypy and hypermotility significantly at 10 mg/kg, p.o. In dogs, terguride, like bromocriptine, reduced the serum PRL level, but did not affect the serum levels of growth hormone and luteinizing hormone. In dogs, bromocriptine induced both emesis and PRL-lowering at almost the same dose, whereas emesis-inducing doses of terguride were about 100 times higher than the PRL-lowering dose. These results suggest that terguride as a dopamine D2-agonist is a potent inhibitor of PRL secretion with less neurotropic side effects compared to bromocriptine, and thus a useful drug for the treatment of galactorrhea and hyperprolactinemia including prolactinoma.
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PMID:Terguride as a new anti-hyperprolactinemic agent: characterization in rats and dogs in comparison with bromocriptine. 790 16

A case of a large empty sella was reported, which was intrasellar herniation of the third ventricle associated with a prolactinoma. The patient was a 46-year-old female admitted due to consciousness disturbance with pyrexia and vomiting. She had amenorrhea, galactorrhea and sterility in her past history. On admission, physical and neurological examinations revealed severe dehydration, systemic edema, systemic hypotension, nuchal rigidity, papilloedema and goiter. A spinal tap was performed and revealed an increase in CSF pressure. Laboratory data indicated CSF lymphocytosis, an increase in CSF protein content, high titers of serum microsome test, a low concentration of anterior pituitary hormones in serum except for PRL, and an unusually high concentration of PRL in serum and CSF (4680 and 222ng/ml, respectively). Plain films of the skull showed destructive enlargement of the sella turcica. The patient was diagnosed as having non-bacterial meningitis, chronic thyroiditis and a prolactinoma with hypopituitarism and was then admitted to our department. Except for amenorrhea she was asymptomatic under the administration of levothyroxine, hydrocortisone and bromocriptine. CT scan, MRI, pneumoencephalography and CT cisternography as further examinations disclosed the intrasellar herniation of cisterns and the third ventricle, which were surrounded by an intrasellar parenchymal layer. This layer was thought to be still viable prolactinoma tissue. We supposed the third ventricle entered the enlarged sellar cavity following the spontaneous degeneration of the large prolactinoma. Although we could find some documented reports of similar cases, the complete herniation of the third ventricle secondary to degeneration of an adenoma might be rare.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Empty sella as an intrasellar herniation of the third ventricle secondary to spontaneous degeneration of a prolactinoma]. 813 65


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