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)

Eight patients with macroprolactinomas were treated with a long-acting injectable form of bromocriptine, depot-bromocriptine (Parlodel LAR). With the exception of one male patient who had partial and short-lasting suppression of PRL levels after two injections and who underwent a second adenomectomy, the patients were given Parlodel LAR injections at 28-day intervals for six months. In all patients, there was a significant fall in serum PRL levels after the first injection. PRL secretion was suppressed to within the normal range in 3 of 7 patients on long-term treatment. PRL was consistently within the normal range in 2 patients from the sixth week and in one, from the 14th week onwards. In the other 4 of 7 patients, a marked suppression of PRL secretion, resumption of menses, and normal libido and potency were recorded. In 3 of 8 patients, no adverse effects were noted. Two patients reported short-lasting nausea, one vomiting, one constipation and in 2 patients, orthostatic dizziness occurred after the first injection. Subsequent injections, however, were well tolerated systematically and locally. Five patients had CT scan evidence of tumour shrinkage. A very large tumour virtually disappeared after the first injection of 50 mg depot-bromocriptine in one patient. The decrease of serum PRL secretion within the first 12 hours after injection did not predict normalization of serum PRL levels during long-term treatment, whereas the fall of serum PRL levels to below 5% of the basal values within the first months of treatment could be a good indicator for the final outcome.
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PMID:Parlodel LAR in the treatment of macroprolactinomas. 231 14

A 68-yr-old man had developed intractable vomiting soon after recovering from a flu-like illness. The use of Compazine as an antiemetic produced classic dystonic manifestations which resolved rapidly after discontinuation and treatment with Artane. However, he later developed a variety of neurobehavioral disturbances which led to his admission to the hospital. Extensive diagnostic procedures failed to identify any gastrointestinal or neurological causes. His condition unceasingly worsened until hypocortisolemia was serendipitously discovered, and all of his symptoms disappeared rapidly and completely with glucocorticoid replacement. Over the course of hospitalization, other than a single episode of orthostatic hypotension, the patient did not manifest any signs of adrenal insufficiency or endocrinopathy. Although detectable, his plasma ACTH level was markedly low in the presence of hypocortisolemia. His adrenal function was subnormal in the cortisol response to ACTH stimulation. His renin-angiotensin-aldosterone system and catecholamine levels were normal. He had normal pituitary responses to GnRH, TRH, and insulin, with rises in plasma levels of LH, FSH, TSH, PRL, and GH, but no stimulation of ACTH. Repeated CRH tests revealed no stimulation of ACTH and cortisol. No circulating anti-ACTH, antiadrenal, or antipituitary antibody was detected. We conclude that this elderly patient had a rare syndrome of selective corticotroph dysfunction which resulted in secondary adrenal failure and exacerbated his mental and neuromuscular abnormalities. To our knowledge, these symptoms, which clearly relate to hypocortisolism, have not been previously reported.
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PMID:Delirium and neuromuscular symptoms in an elderly man with isolated corticotroph-deficiency syndrome completely reversed with glucocorticoid replacement. 255 16

Two male infants with hyperpigmentation, vomiting, lethargy and weight loss were reported. Hypoglycemia, hyponatremia, hypochloremia, hyperkalemia and metabolic acidosis were suggestive diagnosis of salt losing adrenocortical insufficiency. The absence of ambiguous genitalia, low 24 hour urinary 17 KS and pregnanetriol excretion precluded congenital adrenal hyperplasia. Low basal levels of plasma aldosterone and cortisol and low 24 hour urinary 17 OHCS excretion with disability to increase their corticosteroid secretions after ACTH stimulation as well as furosemide and theophylline infusions were supportive for the diagnosis of congenital adrenal hypoplasia. The definitive diagnosis was confirmed by ultrasonogram and computerized tomography. Family histories suggested X-linked recessive inheritance in these reported cases. Evidence of progressive postnatal adrenocortical degeneration was documented by progressive deterioration of adrenocortical functions beginning from mineralocorticoid to total corticosteroid deficiencies. The increased brain serotonin synthesis as the associated pathology of X-linked congenital adrenal hypoplasia was proposed on the basis of elevated basal plasma GH and PRL levels in the reported cases, taken together with an incidence of congenital LH deficiency and persistent ACTH hypersecretion in corticosteroid treated patients reported elsewhere.
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PMID:X-linked congenital adrenal hypoplasia: proposal pathogenesis. 273 38

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

In a double-blind study vs bromocriptine, 30 women who wished to interrupt breast-feeding after a physiological delivery and at least 3 months of nursing were given at random 10 mg dihydroergocristine capsules or 2.5 mg bromocriptine capsules twice a day for 5 days, then 3 times a day for 5 days if treatment had failed to produce an effect. The parameters considered were PRL plasma levels, which were measured at baseline, on the 5th day and, where necessary, on the 10th day of treatment. Milk secretion, breast swelling and pain were recorded at baseline and daily during treatment. The appearance of any side-effect was accurately reported. A prolactin decrease was observed in both groups (p less than 0.01). After 5 days milk secretion was reduced more significantly in the dihydroergocristine group; after 10 days of treatment 6 cases treated with bromocriptine and 1 case treated with dihydroergocristine still revealed a low milk secretion. Breast congestion and pain were absent in both groups. As regards side-effects, a significant decrease in systolic blood pressure (standing position) was reported in the bromocriptine group. Other symptoms, such as nausea, vomiting, insomnia and headache, were reported in 8 patients in the bromocriptine group vs 6 patients in the dihydroergocristine group.
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PMID:Dihydroergocristine in stopping lactation: double-blind study vs bromocriptine. 314 May 92

A 29-year-old woman suffered from frontalgia with vomiting and visual field defects in the 9th month of pregnancy. Two weeks after delivery, a pituitary mass with suprasellar extension was demonstrated on computed tomography (CT). Angiogram revealed elevation of bilateral A1 segments and right persistent primitive trigeminal artery. Repeated CT performed three months after delivery showed that the pituitary mass had undergone a spontaneous regression in size, and her visual impairment improved. The pituitary function tests revealed no response to ACTH, GH and PRL stimulation performed about a year after delivery. Laboratory data showed high titer of antinuclear antibody and low titer of complement. This case suggests that some patients with postpartum hypopituitarism suggestive of lymphocytic adenohypophysitis, and with pituitary mass need not have early surgical intervention but may be closely observed and treated by hormone replacement alone.
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PMID:[A case of pituitary mass suggestive of lymphocytic adenohypophysitis]. 349 79

The effect of a new dopamine agonist, CU 32-085 (8 alpha-amino-ergoline), on pituitary function in acromegaly was evaluated by a controlled, single blind study of 12 acromegalics. The study included a single dose placebo/drug (0.5 mg CU 32-085) trial and a long-term crossover trial with 3 month periods (placebo/CU 32-085 8 mg daily). The patients were evaluated clinically and biochemically (oral glucose tolerance (OGTT), TRH- and LHRH-tests) before and after each 3 month period. Nine patients completed this long-term trial; one died from myocardial infarction during the placebo period, and two dropped out because of side effects. The release of GH, judged from more than 9 h suppression of serum GH following the single dose, and from the response to OGTT after the long-term treatment, was significantly inhibited by CU 32-085. Serum GH reached normal values in 4 of 9 patients. Serum PRL was also markedly suppressed, to subnormal values after the 3 months in all but one hyperprolactinemic patient. Serum TSH, cortisol, FSH and LH were generally unaffected. Glucose tolerance was not significantly altered, although an improvement was found in six of nine patients. A semiquantitative evaluation of subjective symptoms showed a significant improvement following the long-term treatment, while objective signs of acromegaly were unaffected. The blood pressure was slightly lowered, both after a single dose and after 3 months' treatment. Seven patients experienced nausea and dizziness, two of them with vomiting, after a single dose of the drug. Four of these had similar symptoms initially during the long-term treatment, which forced two to interrupt the trial. We conclude that CU 32-085 caused a marked suppression of the release of GH and PRL and an improvement of the major symptoms of acromegaly, a therapeutic effect that is comparable to the previous experience with bromocriptine.
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PMID:The effect of a new ergoline derivative, CU 32-085, in the treatment of acromegaly. A controlled study. 388 7

An 8-yr-old girl is presented who had periodic attacks of vomiting, psychotic depression, drowsiness, and hypertension (160/110 mm Hg) for a period of 16 months after head injury. At the initiation of the attack, serum ACTH and vasopressin levels were prominently increased (610 pg/ml and 41 microunits/ml, respectively), followed by hypercortisolemia, hyponatremia, and hypoosmolality in plasma. Serum PRL also was elevated (91 ng/ml). Responses of GH and cortisol to insulin-induced hypoglycemia and those of TSH to TRH were reduced. Urinary excretion of epinephrine and norepinephrine were increased, while dopamine (DA) excretion was reciprocally decreased, resulting in a marked elevation of the epinephrine plus norepinephrine to DA ratio during the episodes (0.4-4.5); this was normalized on attack-free days (0.08-0.25). During the attack, the concentration of homovanillic acid, a major metabolite of DA in the brain, also was reduced in cerebrospinal fluids from 70 to 23 ng/ml. The administration of methyl-dopa and reserpine effectively suppressed the recurrence of the episode. Although the exact cause of this syndrome is unknown, a periodic metabolic dysfunction of catecholamine in the central nervous system might be postulated.
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PMID:A syndrome of periodic adrenocorticotropin and vasopressin discharge. 627 29

Pergolide mesylate is a synthetic ergoline with dopamine agonist properties. The endocrine profile was studied in a double blind crossover design in six normal males. Circulating PRL, TSH, GH, LH, FSH, and cortisol were measured in the basal state and after TRH (500 micrograms iv) administration at 4.5, 11.5, and 23.5 h after placebo or pergolide (100 micrograms orally). Pergolide caused suppression of basal PRL from 2-8 ng/ml to less than 2 ng/ml commencing 60 min after administration and persisting throughout the 23.5-h study period. For the three TRH tests, a suppression of peak PRL (mean +/- SEM) response to TRH of 54.6 +/- 5.1 vs. 1.9 +/- 0.5, 45.2 +/- 4.1 vs. 4.5 +2- 0.6, and 34.4 +/- 2.9 vs. 6.9 +/- 1.4 ng/ml, respectively, for placebo and pergolide was noted. Basal TSH levels were unaffected by pergolide, but after pergolide the peak TSH response to the first two TRH challenges was blunted (placebo vs. pergolide: 12.3 +/- 1.2 vs. 6.8 +/- 1.0 and 14.8 +/- 2.0 vs. 9.6 +/- 1.0, respectively); however, the third TSH response (9.8 +/- 1.1 vs. 9.3 +/- 1.2) was not blunted after pergolide. GH secretion was stimulated by pergolide with a consistent pulse observed within 60 min of pergolide administration and an enhancement in the number and amplitude of subsequent GH pulses throughout the 24-h period. Cortisol levels rose after pergolide and returned to levels seen on the control day at 16.5 h. FSH levels were unaffected but LH levels were lowered pergolide. Side effects including nausea, vomiting, and hypotension were observed in all subjects. Pergolide is a potent dopamine agonist with the anticipated endocrine profile and clinical effects; its long duration of actions offers promise of single daily dose therapy for hyperprolactinemia.
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PMID:Pergolide mesylate: its effects on circulating anterior pituitary hormones in man. 679 9

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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