Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies have shown that, in patients with threatened premature labor, fenoterol and ritodrine are effective agents for delaying its onset. However, the side-effects of these drugs can be a problem. Among 133 patients studied, the intravenous administration of either agent caused marked tachycardia (but no changes in blood pressure) and a high incidence of palpitations, trembling, and nausea. During oral therapy, subjective symptoms were less frequent. The addition of the calcium antagonist, iproveratril, to the therapeutic regimen did not influence the effectiveness of the 2 agents or the incidence of their adverse side-effects.
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PMID:The treatment of threatened premature labor by betamimetic drugs: a comparison of fenoterol and ritodrine. 3 2

Various reports have associated intravenous prostaglandins with gastrointestinal side effects. It is possible that prostaglandins may also cause contraction of the human gallbladder and precipitate side effects in patients with gallbladder disease. To find out, the authors studied the effects of prostaglandin E2 (PGE2) on the radiological size of the gallbladder during oral cholecystography with 16 g. of Solu-Biloptin (calcium ipodate). PGE2 was slowly injected, under fluoroscopic observation of the gallbladder, in 12 patients (8 female and 4 male) who had no signs of gallbladder disease in films taken before a fatty meal was given. The PG was given in doses of 20 mcg, 50 mcg, and 75 mcg (4 patients in each dose group). New films were taken 15 minutes and 30 minutes after PG injection. An ordinary fatty meal (200 ml of cream) and a 4th set of films was taken 30 minutes later. Previously described radiography and measurement of gallbladder volume were undertaken, and spontaneously reported side effects recorded. Intravenous PGE2, regardless of dose, did not change the form or size of the gallbladder. After the fatty meal, gallbladder contraction was the same as in untreated patients. The 50 mcg dosage resulted in temporary distress in 1 patient, while the 75 mcg dosage caused dizziness, nausea, and collapse in 3 patients. There was no reported side effects after the fatty meal. It was concluded that clinical doses of PGE do not cause gallbladder contraction, nor do they interfere with normal response of the gallbladder to a fatty meal.
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PMID:Letter: Intravenous prostaglandin and the gallbladder. 4 17

Using a 12-hour infusion of salmon synthetic calcitonin (S-CT), distinct and sustained inhibition of gastric acid and pepsin secretion has been demonstrated in 4 normal subjects, 3 patients with peptic ulcer disease and 3 high risk patients. In 3 patients with Zollinger-Ellison syndrome, treated in the same way, elevated serum gastrin was reduced by about 50% and acid secretion by more than 90%. In healthy volunteers oral administration of human synthetic CT (H-CT) led to reduction in basal and pentagastrin-stimulated acid and pepsin secretion by about 50%, lasting for more than 2 hours after the instillation of CT. In 4 subjects receiving CT intravenously, slight nausea and headache were registered, while there were no side effects after the oral route. Serum calcium did not change after i.v. or oral administration of CT. Wheras therapeutical applications of CT, given by i.v. route, seem to be restricted to selected cases, i.e. acute gastric ulcerations with imminent or existent bleeding, the eventual benefit or orally administered CT in peptic ulcer disease should be evaluated in controlled long-term trials.
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PMID:Long-term effects of calcitonin on gastric secretion in normals, peptic ulcer and high risk patients. 6 56

In the acute experiment six healthy volunteers were given orally two doses of lithium chloride, 16 and 32 mmol, and placebo sodium chloride 32 mmol in a double-blind standardized procedure, with a 1-week interval between treatments. Compared to sodium, lithium produced a decrease in subjective well-being, decrease of skin conductance fluctuations, and increase in plasma calcium concentrations. Dose-related effects were maximal at the first hour after ingestion, decreasing or disappearing at 3--5 h. Most effects did not correlate with plasma or erythrocyte lithium concentrations, but drug effects and feelings of nausea were highly correlated. Accordingly, most acute effects seemed due to peripheral drug effects. In the chronic experiment six healthy volunteers were given orally 16 mmol of lithium chloride or sodium chloride (placebo) twice a day for 1 week in a double-blind standardized procedure with a 2-week interval between treatment weeks. Compared to placebo, lithium produced feelings of subjective impairment, an increase in EEG slow waves and of auditory evoked response variability, a deficit in long-term memory, and an increase in plasma magnesium concentrations. Most lithium effects did not correlate with plasma or erythrocyte lithium concentrations.
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PMID:Acute and chronic effects of lithium chloride on physiological and psychological measures in normals. 9 11

Five male patients, aged between 31 and 58 years, presented with anginal chest pain with nausea and sweating after the interruption of exercise. Prinzmetal variant angina was observed during the recovery phase of exercise tolerance testing. Coronary arteriography and selective left ventricular angiography were normal in all cases. Ergonovine, used in one case, induced coronary artery spasm. The angina was eased by Nifedipine in three patients and passed off with time in the other two patients. In one case attack occurred with amiodarone therapy and in another with glyceril trinitrate, after normal exercise tolerance tests. Vagotonia, all the more pronounced when sympathetic tonus is increased, and hyperventilation seem to be the causative factors of what probably results from coronary artery spasm. Nifedipine, a calcium-blocking agent would appear to be the treatment of choice.
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PMID:[Prinzmetal's angina initiated by interruption of exercise. 5 cases with normal coronary radiograms]. 11 38

The findings of 152 patients with proven primary hyperparathyroidism are reportedmthe purpose of the analysis was to find difference between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups, Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in an atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck; The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The sucess of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There ist still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are reposible for the different action on bone and kidney is discussed; In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting, abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in over 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcenia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparthyroidism. Analysis of 152 patients with special reference to acute life threatening complications (acute hyperparathyroidism)]. 20 39

Effect of ethanol on adenosine 3', 5' cyclic monophosphate (cAMP), calcium (Ca) and magnesium (Mg) excretion was studied in controlled clinical conditions in man. Seven male volunteers served as their own controls. In 5 subjects cAMP excretion was primarily suppressed by ethanol. Ethanol appeared to have a biphasic effect on Ca excretion, an initial stimulation followed by a conservation phase. Mg excretion was stimulated by ethanol in 5 subjects. Subjects having nausea and vomitus and the most severe hangover symptoms had the lowest urinary Ca excretion and the lowest imitial cAMP excretion. Ca and Mg metabolism and the susceptibility of the body to the toxic effects of ethanol appeared to be interrelated.
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PMID:Adenosine 3',5' cyclic monophosphate, calcium and magnesium excretion in ethanol intoxication and hangover. 23 65

The current state of knowledge in regard to nutritional requirements for pregnant and lactating women and for women who are taking oral contraceptives is reviewed. During pregnancy caloric intake should be moderately increased, and the consumption of 30-60 mg of iron and 800-1200 mg of calcium is recommended. Phosphorus intake should also be increased, but this increase should be balanced by a corresponding increase in calcium intake. Consumption of vitamins A and D should be increased but excessive increases should be avoided. Vitamin E should be slightly increased. The desirability of increasing vitamin K is till a matter of dispute. Pregnant women have a slightly increased need for most water soluble vitamins. Research has adequately demonstrated the need to increase folic acid and B6 consumption. There is some evidence that iodine, chromium, and zinc deficiencies may be teratogenic. Some care should be taken not to overconsume sodium, but the need for stringest restriction is unwarranted. Heavy consumption of alcohol and caffeine should definitely be discouraged during pregnancy. Certain problems experienced by pregnant women, such as nausea, may be managed through nutritional modification. The increased nutritional needs for lactating women can, in most cases, be met by increasing milk consumption by 3-3 1/2 cup/day and by consuming a well balanced diet. The content of maternal milk may to some extent be altered by the consumption patterns of the mothers. Ingestion of certain drugs and chemicals may also alter maternal milk. The use of oral contraceptives apparently affects metabolism, but the consequences of these effects are largely unknown. Oral contraceptive usage generally increases the serum levels of triglycerides, iron, copper, and vitamin A and reduces levels of some B vitamins of vitamin C and of zinc and albumin. These effects vary from woman to woman and at the present time there is no agreement on the need for dietary supplementation. The effects of a variety of drugs on lactating women and the effects of oral contraceptive usage on nutritional status are presented in tabular form.
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PMID:Nutrition during pregnancy, lactation, and oral contraception. 25 28

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

The effects of synthetic salmon CT, administered subcutaneously and intermittently (1 MRC U/kg/day for 15 days/month over 6 months) were investigated in 15 uremic patients on regular dialysis treatment (RDT), all presenting various degrees of osteodystrophy. Clinically, osteoarticular pain disappeared in 8 out of 10 cases; 1 patient with rib fractures had a rapid calcification of the bone fracture repair tissue. No significant changes were found in serum calcium and PTH levels. Phosphotemia showed a significant decrease within the first 20 days. The varying individual hypophosphatemic response proved to be related to the initial level of phosphatemia. The alkaline phosphatase, when increased, showed a decrease to the normal range. A significant decrease in osteoclastic hyperactivity (active resorption surface, osteoclast index) and a slight increase in osteoblastic pool (active osteoid surface) were documented. No change was noted when osteomalacia predominated. Side effects included: anorexia, nausea, vomiting, face flushing. Our data suggest that salmon CT may be usefully employed in chronic uremic patients on RDT, when secondary hyperparathyroidism predominates.
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PMID:Effect of calcitonin on bone lesions in chronic dialysis patients. 49 16


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