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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this pilot clinical trial conducted in 10 postmenopausal women with advanced breast cancer, we evaluated the endocrine effects and toxicity of combined somatostatin analog and dopaminergic therapy in the attempt to suppress both growth hormone (GH) and prolactin (PRL) secretion. The patients' mean age was 63 years (range: 54-77) and the average number of previous treatments was 4.8 +/- 2 (SD). All patients were treated with the somatostatin analog SMS 201-995 (100-200 micrograms s.c. in a.m. and h.s.) and bromocriptine (2.5 mg orally twice a day). During treatment, GH levels following provocative testing (either L-DOPA or insulin-induced hypoglycemia) were suppressed in 7/9 patients. Basal somatomedin-S (Sm-C) levels declined in 6/9 women. Both GH and Sm-C levels decreased in 4 patients, while in the remaining 5 only one of the two parameters was lowered on treatment. PRL secretion (during provocative TRH testing) was almost totally abolished in 8/9 patients. The treatment did not affect circulating levels of FSH, LH, E1, E2, E1-S, T4, T3RU, or cortisol. Seven patients experienced no side effects. Nausea occurred in 3, but was severe enough in only one to require discontinuation of therapy. One patient experienced disease stabilization consisting of less than 50% regression of skin nodules and pleural effusion, a decline in CEA titer, and an improved performance status lasting 7 months. We conclude that combined SMS 201-995 and bromocriptine therapy is safe and frequently suppresses GH and PRL secretion. Its role in the treatment of metastatic breast cancer should be tested in patients with less advanced disease.
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PMID:Endocrine effects of combined somatostatin analog and bromocriptine therapy in women with advanced breast cancer. 257 6

Octreotide is an analogue of somatostatin. Like endogenous somatostatin, it exerts a potent inhibitory effect on the release of anterior pituitary growth hormone and thyroid-stimulating hormone, and peptides of the gastroenteropancreatic endocrine system, while overcoming some of the shortcomings of exogenously administered somatostatin, namely a short duration of action, a need for intravenous administration and postinfusion rebound hypersecretion of hormone. Clinical studies have shown that octreotide is effective in the treatment of acromegaly and thyrotrophinomas. In comparative trials octreotide was significantly superior to bromocriptine in patients with acromegaly. Octreotide also appears to provide a significant advantage over existing therapies in the management of the carcinoid syndrome and offers considerable therapeutic potential in reversing carcinoid crises which may be life-threatening. Trials in patients with tumours producing vasoactive intestinal peptide demonstrated that octreotide may be an effective first-line choice for this condition, which has usually metastasised and become refractory to traditional symptomatic therapy. In limited studies in patients with high-output secretory diarrhoea, including cryptosporidium-related diarrhoea associated with AIDS and in patients with small bowel fistulas, octreotide has been shown to be effective in reducing stool/fistula output. However, well-designed clinical trials are still required to confirm its long term usefulness in these disorders. Similarly, although the use of octreotide in other conditions such as neonatal hypoglycaemia caused by nesidioblastosis, reactive pancreatitis, insulin-dependent diabetes mellitus, postprandial hypotension and the dumping syndrome has provided encouraging preliminary results, more studies are needed to clarify the place of octreotide in their treatment. Overall, octreotide appears to be well tolerated with the most frequently reported reactions being pain at the site of injection and gastrointestinal symptoms such as abdominal cramps, nausea, bloating, flatulence, diarrhoea and steatorrhoea. These adverse effects usually abate with time. Additionally, octreotide, like endogenous somatostatin, may also result in cholelithiasis, presumably by altering fat absorption and possibly by decreasing motility of the gallbladder. Thus, octreotide represents a new departure from traditional therapies in the treatment of various pathophysiological states associated with excessive peptide production and secretion. It offers a significant advantage over existing therapies in the medical management of patients with acromegaly, thyrotrophinomas, the carcinoid syndrome, tumours producing vasoactive intestinal peptide and severe secretory diarrhoea in whom conventional management options have either become exhausted or have provided suboptimal symptomatic relief.
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PMID:Octreotide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in conditions associated with excessive peptide secretion. 268 36

With the development of sensitive and specific radio-immunoassays to measure the low circulating concentrations of vasopressin there has been a quantum leap in our understanding of the physiological processes involved in the regulation of its secretion. The results of Verney's pioneering studies in dogs led to the concept of 'osmoreceptors'. It is now appreciated that osmoregulation of vasopressin release is of principal importance in the maintenance of water balance. Functional characteristics of the osmoregulatory system have been defined clearly by independent laboratories, and more recently the physiological influences that can subtly alter this very finely controlled system have been described. Non-osmotic factors that release vasopressin have been recognized for many years. Secretion of vasopressin in response to haemodynamic influences has been characterized, and significant hypotension and/or hypovolaemia are potent stimuli to hormone release. Other non-osmotic factors--nausea/emesis, hypoglycaemia--may play important roles in disturbances of water balance. Vasopressin should not, however, be regarded as a stress hormone, since recent careful studies in a variety of species indicate that secretion is not enhanced following a series of different noxious stimuli.
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PMID:Regulation of vasopressin secretion. 269 40

A 37 year old black female presented with congestive cardiac failure, 2 months postpartum. She developed spontaneous hypoglycaemia and symptoms of acute adrenal crisis (hypotension, nausea, abdominal pain and tachycardia with small thready pulse), which responded to i.v. dextrose, sodium chloride and hydrocortisone. Biochemical investigations revealed low serum cortisol and plasma adrenocorticotrophic hormone (ACTH) levels. The patient initially showed an impaired cortisol response to intramuscular aqueous tetracosactrin, but an exuberant response after priming with intramuscular tetracosactrin depot. These findings, together with the normal remaining pituitary function, led us to conclude that this patient had isolated ACTH deficiency associated with congestive cardiac failure and acute adrenal crisis.
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PMID:Isolated adrenocorticotrophic hormone (ACTH) deficiency associated with acute adrenal crisis. 299 71

A 39 year old woman was admitted to a maternity unit at 34 weeks' gestation with nausea, vomiting, and jaundice. Her condition deteriorated, and she was transferred to hospital, deeply unconscious and hypotensive. The diagnosis of acute fatty liver of pregnancy was initially suggested by the typical history of prodromal malaise and vomiting and the rapid onset of hepatic encephalopathy with profound hypoglycaemia and only small increases in transaminase activities. Computed tomography was performed: there was no enlargement of the liver or spleen, but the attenuation value over the liver indicated appreciable fatty infiltration of the liver, establishing the diagnosis of acute fatty liver of pregnancy. Computed tomography is of value in the diagnosis of liver disease of late pregnancy, and this technique may become the method of choice for the investigation of acute fatty liver of pregnancy.
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PMID:Acute fatty liver of pregnancy and diagnosis by computed tomography. 308 Jan 42

Hypoglycaemia (blood glucose 1.3-2.5 mmol/l) was induced in thirty diabetic children by reduction of their morning meal. Glucagon, 10 or 20 micrograms/kg was then given by intramuscular or subcutaneous injection. Ten min later, all signs of hypoglycaemia had disappeared and blood glucose concentrations increased by 0.7-3.3 mmol/l. Glucagon plasma concentrations at glucose nadir were low, 23 +/- 8 pmol/l, rose to 300 +/- 42 ten min after the injection and reached peak values after another ten min. Later, a slow decrease was noted. No significant difference of blood glucose or plasma glucagon concentrations were found after subcutaneous or intramuscular injections of 20 micrograms/kg. After 10 micrograms/kg, slightly lower increase of blood glucose was seen, but the clinical effect was equally good. Nausea occurred in four children given 20 micrograms/kg. The rise of blood glucose did not correlate to the peak glucagon concentration obtained after the injection but showed significant correlations to the lowest glucose concentration and, inversely, to the concentration of free insulin in blood at glucose nadir. It is concluded that glucagon injections are effective in hypoglycaemia in insulin-treated diabetic children and that the injection of 10-20 micrograms/kg gives long-standing supraphysiological concentrations which make repeated injections unnecessary.
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PMID:Hypoglycaemia in childhood diabetes. II. Effect of subcutaneous or intramuscular injection of different doses of glucagon. 339 8

Eating related difficulties and symptoms and postprandial serum glucose levels were studied in 11 patients (44 to 70 years old) five to 48 months after total gastrectomy and Roux-en-Y reconstruction for carcinoma of the stomach with no signs of metastasis or residual tumor. Three tests were used. The first contained 150 milliliters of 50 per cent glucose alone, the second had 150 milliliters of 50 per cent glucose with 5 grams of guar gum (viscose dietary fiber) and the third was a vegetable meal containing 75 grams of glucose. All of the patients with total gastrectomy had eating related symptoms, such as dumping and difficulties with the large volume of a meal. They had to eat small meals and the most usually experienced postprandial symptoms were abdominal pain, nausea and faintness. The postprandial serum glucose level was highest after drinking glucose alone and the lowest after eating the vegetable meal (as the highest 9.4 +/- 2.0 and 6.2 +/- 1.6 millimole per liter, respectively, 50 minutes postprandially, p less than 0.01). Hyperglycemia was associated with nausea, sweating, faintness, reduction of blood pressure and increase of pulse rate. The large volume of the vegetable meal produced difficulties (dysphagia and abdominal distension) in eating for everyone except one patient. Guar gum eaten with glucose reduced the postprandial hyperglycemia near to the level found after the vegetable meal. Also, the symptoms experienced after glucose with guar gum reduced from that after glucose alone, five patients became symptomless. Four of these five patients have supplemented guar gum regularly for several months into their daily meals with the result of reduction of the postprandial subjective symptoms. The dose has been adjusted individually from 2 to 7 grams of guar gum three times daily. Loose stools and diarrhea may occur at the beginning. These are avoided by a gradual increase of the dose during an adaptation period of two weeks. Sometimes glucose with guar gum may result in hypoglycemia with prolonged symptoms after immediate hyperglycemia. It is concluded that guar gum gives a possibility to avoid the symptoms related to a large volume of a meal and to reduce those produced by a high glucose content of a meal in patients after total gastrectomy. Guar gum also works in practical prolonged use when the dose is estimated from postprandial symptoms.
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PMID:Postprandial hyperglycemia after different carbohydrates in patients with total gastrectomy. 358 24

The response of plasma growth hormone and cortisol to the intramuscular injection of 1 mg glucagon was used to assess anterior pituitary function in a group of 97 normal subjects (23 men, 74 women). Ninety-three subjects (96%) responded with a peak GH of at least 8 ng/mL, and 89 (92%) had either a peak cortisol of at least 500 nmol/L (18 micrograms/dL) or a maximal increment in plasma cortisol of at least 250 nmol/L (9 micrograms/dL) above the baseline. In 12 subjects, a second test showed that the responses were reproducible. A greater proportion of subjects over the age of 50 failed to achieve a peak GH of 10 ng/mL (7 of 20, 35%) compared to those who were either under 30 (1 of 37, 2.7%) or between 30 and 50 (4 of 40, 10%) (chi 2 = 12.85, P less than .005). GH responses were not affected by sex or elevation of the basal level of GH. In contrast, cortisol responses were smaller in men and in individuals with high basal cortisol levels but were not affected by age. Mild nausea in approximately 30% of subjects (29 of 97), and transient vomiting and retching in approximately 10% (10 of 97) were the only side effects that were noted. Glucagon is therefore a safe and reliable alternative to insulin-induced hypoglycemia for the assessment of both somatotrophic and corticotrophic function.
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PMID:Intramuscular glucagon as a provocative stimulus for the assessment of pituitary function: growth hormone and cortisol responses. 360 Feb 80

Pentamidine, recently released for clinical use, is effective in therapy for the hemolymphatic stage of Gambian trypanosomiasis, antimony-resistant leishmaniasis, and Pneumocystis carinii pneumonia. The mechanism of action is unclear and may differ for different organisms. Trypanosomes actively transport pentamidine intracellularly, and the drug may then interfere with DNA biosynthetics. However, pentamidine appears to kill nonreplicating P. carinii. The mechanism of killing is unexplained. The pharmacokinetics of pentamidine has been incompletely studied in humans. The estimated volume of distribution is 3 liters/kg. Levels in plasma of pentamidine range from 0.3-1.4 microgram/ml after standard 4 mg/kg dosing, with no appreciable increase in drug levels on successive dosing and no correlation between levels and creatinine clearance or adverse reactions. The drug appears to be concentrated in the kidney and excreted in the urine, with levels detectable six to eight weeks after cessation of therapy. Immediate adverse reactions have included hypotension, nausea, and vomiting. Local pain or abscess formation at an injection site, mild azotemia, leukopenia, abnormal findings from liver function tests, and hypoglycemia may also occur.
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PMID:Pentamidine: a review. 390 42

A case of central pontine myelinolysis (CPM) following rapid correction of hyponatremia was reported and literatures were reviewed. The case was 61-year-old nonalcoholic female who had taken an operation of craniopharyngioma 23 years ago. Fifteen years later, she received re-operation for the recurrent tumor, followed by replacement therapy of corticosteroid and clofibrate. She was otherwise well until two weeks before entry, when she noticed abrupt onset of high grade fever, nausea, vomiting and general malaise. She was admitted to an emergency hospital because of weakness, disorientation and a slight impairment of consciousness, but she was able to speak and to take some food per os. Laboratory studies disclosed urinary tract infection and showed a serum sodium level of 117 mEq/l, potassium 2.9 mEq/l, a serum osmolarity 232 mO sm/l and urine osmolarity 141 mEq/l. She was diagnosed to have an exacerbation of adrenal insufficiency with hyponatremia and hypotonic dehydration triggered by urinary tract infection. Intravenous administration of vitamin B complex, electrolytes including KCL, 5% glucose solution and physiological saline with a large amount of corticosteroid was performed aggressively. Serum sodium concentration was raised to 161 mEq/l in two days, and the increased level had been maintained more than five days, resulting in coma and flaccid quadriplegia. During this period, there was no episode of hypotension, hypoglycemia, hypoxia nor hepatic failure which could have caused brain damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central pontine and extrapontine myelinolysis following rapid correction of hyponatremia--report of an autopsy case]. 646 6


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