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)

Apomorphine, a dopaminergic receptor stimulant, was tested and compared in subemetic doses (0.76 mg subcutaneously) to levodopa (500 mg orally) as a stimulant of growth hormone release in 10 normal volunteer subjects (five male, five female). The administration of levodopa failed to cause a normal increment in serum growth hormone levels (greater than 5 ng/ml from base line) in four patients, produced a borderline normal response in two patients with a normal response in four patients. Apomorphine stimulation produced a borderline normal response in one patient and a normal response in the remaining nine patients. The peak response to apomorphine administration was 26.94 +/- 6.60 ng/ml and to levodopa 9.76 +/- 2.67 ng/ml (p less than 0.025). There was no statistical difference between men and women in whom apomorphine testing was utilized. Side effects (nausea, vomiting) were seen in three patients tested with levodopa and in four patients tested with apomorphine. Such symptoms began within 20 minutes of apomorphine administration, persisted from 30 to 40 minutes and disappeared abruptly. All patients treated with apomorphine noted transient drowsiness.
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PMID:Apomorphine-stimulated growth hormone release. 60 13

Thirty-one patients with Parkinson's disease were treated with the ergot alkaloid bromocriptine, a drug which stimulates dopamine receptors. Bromocriptine had a slight therapeutic effect in patients on no other treatment and an additional effect in patients on levodopa. The mean optimum dosage of bromocriptine, established over a 12 week period, was 26 mg daily. In 20 patients bromocriptine was compared with placebo in a double-blind controlled trial. Active treatment caused a significant (P less than 0.02) reduction in total disability and akinesia scores. The least disabled patients showed the greatest response. Side-effects of bromocriptine--nausea, vomiting, hallucinations, and abnormal involuntary movements--were similar to nature to those of levodopa. In most normal subjects, bromocriptine causes an increase in plasma growth hormone concentration. This was determined in 20 patients with Parkinson's disease after 1-15 mg bromocriptine. Only a single patient showed an obvious increase up to 120 minutes after dosage. Bromocriptine was not effective treatment in two patients who had not previously responded to levodopa and replacement of this drug by bromocriptine in patients with end-of-dose akinesia after chronic levodopa treatment did not totally abolish response swings.
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PMID:Bromocriptine treatment in Parkinson's disease. 77 75

Thirty-seven patients with Parkinsonism were treated with bromocriptine 2.5-300 mg daily. Bromocriptine, alone or combined with levodopa, caused a 20-30% reduction in disability scores in 11 patients treated for one year. Tolerance did not develop during this period. Bromocriptine treatment was not of value in six patients who had previously not responded or who had lost their response to levodopa. However, in four of five patients with response swings on levodopa due to rapid changes in plasma dopa levels, the addition of bromocriptine caused a more stable response. Dose response curves to bromocriptine 12.5, 25, 50, and 100 mg and to levodopa 250, 500, 1000, and 2000 mg were studied in seven patients. Levodopa 2 g had a greater therapeutic effect and caused a greater rise in plasma growth hormone concentration than bromocriptine 100 mg. Levodopa caused emesis more commonly and hallucinations less commonly than bromocriptine. Bromocriptine appears to be a less potent stimulant than dopamine, and has both pre- and post-synaptic effects. Metoclopramide 60 mg oral was given 30 minutes before bromocriptine or levodopa to establish whether this caused dopamine-receptor blockade. Metoclopramide acted as a competitive antagonist to the anti-Parkinsonism and growth hormone effect of both drugs and in individual cases prevented emesis and hallucinations. The fall in blood pressure due to bromocriptine or levodopa was not antagonised by metoclopramide. Central and peripheral vascular dopamine receptors may be different in nature.
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PMID:Bromocriptine in Parkinsonism: long-term treatment, dose response, and comparison with levodopa. 103 99

Ten adolescent and young adults with cystic fibrosis (CF) have had well-documented recurrent attacks of acute pancreatitis. The diagnosis of CF in each patient was delayed because they did not have pancreatic insufficiency. The diagnosis of CF was documented by the typical pulmonary involvement and elevated sweat sodium and chloride levels in all cases and a positive family history in six of the ten patients. Two patients were diagnosed as having acute pancreatitis before the diagnosis of CF was made, thus indicating that acute pancreatitis may be the presenting complaint in the young adult with CF. The diagnosis of acute pancreatitis was based on the presence of severe abdominal pain, usually with vomiting, tenderness in the mid-epigastrium, elevated serum and urinary amylase and serum lipase. Attacks were precipitated by fatty meals, alcohol ingestion; postcholecystectomy and tetracycline administration. In some patients no precipitating event could be elicited. Intravenous secretin-pancreozymin stimulation tests revealed a diminished bicarbonate secretion with little effect on the secretion of the zymogen enzymes. A mild attack of pancreatitis occurred after secretin-pancreozymin stimulation. The endocrine pancreatic function tested in four patients was normal as revealed by the glucose tolerance tests and determinations of serum insulin, growth hormone and free fatty acid. Transduodenal pancreatograms were performed in three patients; one showed a normal pancreatic duct, one showed duct obstruction and in the third patient a beady type of narrowing was found. The selenomethionine Se 75 uptake of the pancreas was noted only in the head of the pancreas. This suggests that loss of function occurs initially to a greater extent in the tail and body of the pancreas. Three patients died and showed characteristic lesions of CF.
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PMID:Recurrent acute pancreatitis in patients with cystic fibrosis with normal pancreatic enzymes. 111 Aug 67

Four men and 4 women with active acromegaly were treated with bromocryptine for 4 to 5 weeks. Serum growth hormone levels response to a glucose load were measured before and in the last weed of treatment. In only 1 patient was the grwotoh hormone response rendered normal by the drug. This patient, but none of the others, also showed an improvement in glucose tolerance and a reductin of the raised serum insulin levels during the glucose load. In three of the 8 patients vomiting was troublesome side effect of treatment.
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PMID:Treatment of acromegaly with bromocryptine. 112 97

The neuroendocrine response to L-5-hydroxytryptophan was compared in 37 prepubertal children who met the Research Diagnostic Criteria for major depressive disorder with that in 23 normal children with no lifetime history of any psychiatric disorder and very low rates of depression in both first- and second-degree relatives. Intravenous L-5-hydroxytryptophan (0.8 mg/kg) was given over a 1-hour interval after preloading with oral carbidopa, an inhibitor of peripheral but not central L-5-hydroxytryptophan metabolism. L-5-Hydroxytryptophan, a precursor of serotonin, increases serotonin turnover in the central nervous system when given after carbidopa. Seven (19%) of the 37 children with major depressive disorder and two (9%) of the 23 normal children had nausea or vomiting and therefore did not complete the full infusion. They were subsequently excluded from data analysis. After this stimulation, prolactin, cortisol, and growth hormone secretion were compared between diagnostic groups. The depressed children secreted significantly less cortisol (effect size, 0.70) and significantly more prolactin (effect size, 0.83). There was a sex-by-diagnosis interaction in prolactin response to L-5-hydroxytryptophan and, on examination, the prolactin hypersecretion was seen in depressed girls but not in depressed boys compared with same-sex controls. There was no significant stimulation of growth hormone in either group. These findings are consistent with dysregulation of central serotonergic systems in childhood major depression.
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PMID:Neuroendocrine response to L-5-hydroxytryptophan challenge in prepubertal major depression. Depressed vs normal children. 144 21

We report a series of 5 representative patients in California who experienced adverse reactions from the illicitly marketed substance gamma-hydroxybutyrate (GHB). The drug is a putative neurotransmitter marketed as a growth hormone releaser for bodybuilders. The most commonly reported symptoms included abrupt drowsiness, dizziness, and a "high". Other effects were headache, nausea, vomiting, myoclonic jerking, and short-term coma. There have been no reported deaths. If product use is discontinued, full recovery with no long-term side effects is universal. No clear dose-response effect was observed; this may be attributable to differences in susceptibility, wide variations in doses taken by the same person, or the coingestion of other substances. Case interviews confirm that, despite being banned by the US Food and Drug Administration, GHB is still widely available in the underground drug market. Athletes and bodybuilders may take drugs for which there are claims of improved performance or body image. Physicians should be alert for signs of GHB poisoning in emergency department and clinic patients.
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PMID:Acute poisoning from gamma-hydroxybutyrate in California. 157 80

Women who are of normal weight and have bulimia nervosa exhibit multiple neuroendocrine disturbances. We hypothesized that bingeing and vomiting behavior could be contributory because food consumption in healthy volunteers increases plasma cortisol and prolactin secretion and suppresses growth hormone secretion. Thus, we investigated the effects of bingeing and vomiting on the circadian pattern (measurements every 20 min for 24 hr) of these hormones in comparison to healthy control women eating normally. Bingeing and vomiting were associated with modest increases in cortisol and prolactin and reductions in growth hormone secretion. However, this bingeing or purging did not alter mean 24-hr pattern of cortisol and growth hormone secretion as values for bulimics were similar to controls. While mean daytime patterns of prolactin secretion were similar in bulimics and controls, bulimic patients had a significant reduction of nocturnal prolactin levels. In summary, bingeing and vomiting does not appear to have a substantial influence on hormonal secretion. However, bulimic women have blunted nocturnal prolactin patterns.
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PMID:Circadian patterns of cortisol, prolactin, and growth hormonal secretion during bingeing and vomiting in normal weight bulimic patients. 189 60

Women who are of normal weight and have bulimia nervosa have multiple neuroendocrine disturbances. The reasons for these neuroendocrine abnormalities are not known, but there are reasons to suspect that bingeing and vomiting behavior could be contributory. It is well known that food consumption in healthy volunteers increases plasma insulin, cortisol, and prolactin secretion and suppresses growth hormone secretion, whereas activation of the emetic reflex increases plasma arginine vasopressin (AVP) secretion. The purpose of this study was to investigate the effects of bingeing and vomiting on these hormones. In comparison with healthy control women consuming a large meal, bulimic patients, when bingeing and vomiting, had an exaggerated secretion of either the amount and/or the duration of insulin, cortisol, and prolactin. Vasopressin secretion was not increased during or after bingeing and vomiting, probably because bulimic subjects do not become nauseated. In addition, bulimic patients had significantly reduced baseline plasma prolactin and possibly elevated baseline cortisol compared with controls. In summary, this study supports the presence of neuroendocrine disturbances in bulimia and raises a question as to whether or not excessive and prolonged food consumption (and/or vomiting) are contributory.
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PMID:The effect of bingeing and vomiting on hormonal secretion. 264 57

Over a period of 4 years, 20 patients suffering from severe forms of psoriasis (erythrodermic, sub-erythrodermic, resistant generalized forms and/or forms associated with acute arthropathy) were treated with 96 h of continuous i.v. infusion of somatostatin (Stilamin, Serono) diluted in D5W at 250 micrograms/h. In addition to the usual blood chemistry parameters, circadian levels of growth hormone (GH) and epidermal growth factor (EGF) were measured before, during, and after therapy. Approximately 2-3 weeks after termination of therapy, erythrodermic and suberythrodermic symptoms had disappeared. In some patients, a few lesions of psoriasis vulgaris remained, although they were much less severe. Remission of acute arthropathy was impressive. Blood chemistry parameters were unchanged after therapy. Circadian levels of GH and EGF, normal before therapy, were significantly decreased after therapy. The infusion was well-tolerated. Infusion rates of greater than 250 micrograms/h caused only some complaints of abdominal pain, nausea, and vomiting. During the 4 years, erythrodermic symptoms reappeared only in seven patients, three of whom were also arthropathic. After 6-8 months, they underwent a second course of somatostatin therapy with good results. The other patients are still able to control their disease with tar-based products alone or with low-dose 8-methoxypsoralen + UVA (PUVA) or UV therapy. The arthropathic patients control their symptoms with periodic low-dose nonsteroidal antiinflammatory drug therapy.
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PMID:Treatment of severe psoriasis with somatostatin: four years of experience. 290 Jun 24


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