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)

This randomized double-blind placebo-controlled study was designed to evaluate the effects on postoperative pain of the local anesthetic, 0.5% bupivacaine with epinephrine, sprayed hepatodiaphragmatically under the surgeon's direct view during laparoscopic cholecystectomy. Metabolic endocrine responses to surgery (glucose and cortisol) and nonsteroidal anti-inflammatory drug requirements were investigated, as well as the presence of nausea, vomiting, and sweating. Local anesthetics or placebo solutions were given as follows. Immediately following the creation of a pneumoperitoneum, surgeons sprayed the first 20 mL of solution (S1), and an additional 20 mL of solution (S2) was sprayed at the end of the operation. Patients were classified into three groups (14 patients per group). Group A received 20 mL of saline during both S1 and S2, group B received 20 mL of saline during S1 and 20 mL of bupivacaine during S2, and group C received 20 mL of bupivacaine during both S1 and S2. The degree of postoperative pain was assessed using the visual analogue scale (VAS) and the verbal rating scale (VRS) on arrival in the recovery room and subsequently at time intervals of 4 h, 8 h, 12 h, and 24 h. The results of this study indicate a significant decrease of postoperative pain in patients treated with local anesthetic. VAS and VRS pain scores, as well as respiratory rate and analgesic requirements, were significantly lower in group C. The postoperative plasma cortisol level in group C was significantly lower than in groups A and B.
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PMID:The effects of intraperitoneal local anesthetic on analgesic requirements and endocrine response after laparoscopic cholecystectomy: a randomized double-blind controlled study. 884 11

Suspected postprandial (reactive or idiopathic) hypoglycemia is characterized by predominantly adrenergic symptoms appearing after meals rich in carbohydrates and by their rare association with low blood glucose level (< 2.77 mmol/L). We studied heart rate, blood pressure, plasma insulin, C-peptide, and catecholamine responses during a 5-h oral glucose tolerance test in eight patients with suspected postprandial hypoglycemia and eight age-, sex-, and body mass index-matched healthy controls. We also evaluated beta-adrenergic sensitivity by using the isoproterenol sensitivity test. Psychological profile was assessed by the Symptom Checklist (SCL-90R) self-report symptom inventory. Patients with suspected postprandial hypoglycemia had higher beta-adrenergic sensitivity (defined as the dose of isoproterenol required to increase the resting heart rate by 25 beats/min) than controls (mean +/- SEM, 0.8 +/- 0.13 vs. 1.86 +/- 0.25 microgram isoproterenol; P = 0.002). After administration of glucose (75 g) blood glucose, plasma C-peptide, plasma epinephrine, and plasma norepinephrine responses were identical in the two groups, but plasma insulin was higher in the patients (group effect, P = 0.02; group by time interaction, P = 0.0001). Both heart rate and systolic blood pressure were significantly higher (but remained in the normal range) after glucose administration in patients with suspected postprandial hypoglycemia than in controls (group by time interactions, P = 0.004 and 0.0007, respectively). After glucose intake, seven patients had symptoms (palpitations, headache, tremor, generalized sweating, hunger, dizziness, sweating of the palms, flush, nausea, and fatigue), whereas in the control group, one subject reported flush and another palpitations, tremor, and hunger. Analysis of the SCL-90R questionnaire revealed that patients had emotional distress and significantly higher anxiety, somatization, depression, and obsessive-compulsive scores than controls. We may conclude that patients with suspected postprandial hypoglycemia have normal glucose tolerance, increased beta-adrenergic sensitivity, and emotional distress.
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PMID:Suspected postprandial hypoglycemia is associated with beta-adrenergic hypersensitivity and emotional distress. 796 39

Cisapride induces acetylcholine release in cells of the myenteric plexus, thus promoting gastrointestinal motility. We studied the effects of cisapride on 11 patients with idiopathic gastroparesis. All had negative gastrointestinal endoscopy, normal glucose, and took no drugs capable of influencing motility. Most (9/11) were prior metoclopramide treatment failures. Patients' symptoms were scored (0-60) for pain, satiety, bloating, nausea, vomiting, and heartburn. All underwent a solid gastric emptying study using a Technetium-99-labeled egg meal and received placebo prior to cisapride. There were 10 females and one male with a mean (+/- SE) age of 37.8 +/- 2.6 years. Disease duration was 7.9 +/- 2.8 years. The dose of cisapride was 30-60 mg/day and the duration of therapy was 12.6 +/- 2.6 months (range 2.5-25 months). The symptom score improved on cisapride from 30.9 +/- 3.6 to 14.4 +/- 2.7 (P < 0.002 signed rank test). Emptying half-time improved from 113 +/- 4 min to 94 +/- 6 min, and 46.9 +/- 2.4% food remaining at 120 min decreased to 35.5 +/- 3.6% (both P < 0.05). Emptying half-time in normals was 68 +/- 5 min with 16.9 +/- 2.9% remaining at 120 min. Nine of 11 patients gained weight, with a mean increase of 6.7 +/- 1.6 lb (range 2-12 lb). We conclude that cisapride significantly reduces gastrointestinal symptoms and promotes weight gain in patients with idiopathic gastroparesis and is associated with improvement in solid gastric emptying. The drug is useful in patients who previously failed metoclopramide.
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PMID:Open label study of long-term effectiveness of cisapride in patients with idiopathic gastroparesis. 802 48

The effects of preexercise hyperinsulinemia on exercising plasma glucose, plasma insulin, and metabolic responses were assessed during 50 min cycling at 62% VO2max. Subjects were fed a 6% sucrose/glucose solution (LCHO) or a 20% maltodextrin/glucose solution (HCHO) to induce changes in plasma insulin. During exercise, subjects assessed perceived nauseousness and light-headedness. By the start of exercise, plasma glucose and plasma insulin had increased. In the LCHO trial, plasma glucose values significantly decreased below the baseline value at 30 min of exercise. However, by 40 min, exercise plasma glucose and insulin values were similar to the baseline value. Exercise plasma glucose and insulin did not differ from baseline values in the HCHO trial. Ingestion of LCHO or HCHO was not associated with nausea or lightheadedness. It was concluded that the hyperinsulinemia induced by preexercise feedings of CHO did not result in frank hypoglycemia or adversely affect sensory or physiological responses during 50 min of moderate-intensity cycling.
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PMID:Glycemic and insulinemic response to preexercise carbohydrate feedings. 816 54

Responses to glucose of spontaneously active neurons were investigated by extracellular recording in the rat area postrema slice preparations (in vitro). Among 67 spontaneously active neurons, 16 neurons displayed a marked increase or decrease in discharge rate in response to increases or decreases of the glucose concentration in perfusate. These results confirm the existence of glucose-responsive neurons within the area postrema suggested in prior in vivo experiments. Response to CCK or dopamine was also examined on the isolated area postrema slices. The neuron that showed a marked increase in discharge rate responding to glucose elicited a marked increase of discharge rate in response to 2.1 microM CCK, suggesting that glucose and CCK affect the same neurons. Some neurons showed a marked increase or decrease in the discharge rate in response to 20 microM dopamine, but these neurons showed neither response to CCK nor to glucose. It is likely that different neuronal networks in the area postrema contribute to control of ingestion and to initiation of nausea.
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PMID:Glucose-responsive neurons exist within the area postrema of the rat: in vitro study on the isolated slice preparation. 822 Nov 48

The aim of the present study was to compare intra-nasal glucagon with subcutaneous glucagon as a treatment of insulin-induced hypoglycaemia in 11 children, 7-12 years old, with Type 1 (insulin-dependent) diabetes mellitus. Hypoglycaemia (1.6 +/- 0.1 vs 1.8 +/- 0.2 mmol/l) was induced twice in each child by continuous insulin and variable glucose infusions. One milligram of intranasal glucagon or 0.5 mg of subcutaneous glucagon was given in a randomized order. At 15 min after the administrations of either intranasal or subcutaneous glucagon, the blood glucose concentration increased by 1.5 +/- 0.2 mmol/l or 1.7 +/- 0.2 mmol/l above the glucose nadir, respectively. After nasal administration, the maximal rise in blood glucose was seen after 25 min. Subcutaneous injections induced higher and more sustained plasma glucagon concentrations but the children suffered more often from nausea than when they were treated intranasally. In conclusion, treatment with intranasal glucagon seems to be efficient and results in a rapid correction of insulin-induced hypoglycaemia with few side-effects.
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PMID:Intranasal glucagon treatment relieves hypoglycaemia in children with type 1 (insulin-dependent) diabetes mellitus. 824 72

One-hundred-and-thirty-eight women suffering from hypothalamic or hyperandrogenic ovarian failure were treated with daily doses of 25-150 mg of the opiate antagonist naltrexone for 4-100 weeks. In patients with hypothalamic ovarian failure, treatment with naltrexone alone was followed by an increase of gonadotrophins and by normalization of the menstrual cycle in approximately 70% of patients. Eight of 10 patients who did not respond to naltrexone and had not previously ovulated in response to clomiphene administration exhibited ovulatory cycles when both compounds were administered. Twenty-four pregnancies were achieved in 22 women, corresponding to an overall pregnancy rate of 26%, with a cumulative pregnancy rate closely resembling that of a normal population. In contrast, in hyperandrogenic insulin-resistant patients, the pattern of gonadotrophin secretion did not seem to change dramatically during naltrexone treatment. However, the rise of insulin in plasma following an oral load of glucose (oGTT) was blunted considerably, resulting in normalization of previously elevated circulating insulin levels. Since the time course of plasma glucose after oGTT did not appear to be affected by treatment, this indicates an increase in insulin sensitivity (or a decrease in insulin resistance) during naltrexone therapy. Side-effects of naltrexone treatment were negligible in patients with hypothalamic ovarian failure. Hyperandrogenic patients, however, did experience more intense and prolonged side-effects, such as nausea and dizziness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Opiate antagonist treatment of ovarian failure. 827 53

Recombinant human insulin-like growth factor-1 (rhIGF-1) is currently used experimentally to treat patients with insulin-resistant diabetes mellitus, impaired growth, protein malnutrition, and osteoporosis. We report here the case of a marked transient alteration in consciousness in a healthy 22-year-old man who was given an IV infusion of a relatively low dose of rhIGF-1 for 1 hour. This individual developed the sudden onset of dizziness, nausea, coldness, air hunger, and pallor. He became unresponsive to simple questions and experienced diaphoresis, a feeling of warmth, and paresthesias. Although there was a mild fall in heart rate and blood pressure, these hemodynamic effects did not appear sufficient to cause the altered mentation. There were no changes in serum glucose, phosphorus, or potassium that could seem to account for these events. This individual recovered completely several minutes after stopping the rhIGF-1 infusion.
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PMID:Altered mental function during intravenous infusion of recombinant human insulin-like growth factor 1. 855 53

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin--lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although these agents have been proven safe in clinical trials, like any drug, they carry the risk for adverse effects. The bile-acid sequestrants may cause constipation, reflux oesophagitis, and dyspepsia, and may bind coadministered medications such as digitalis glycosides, beta blockers, warfarin, and exogenous thyroid hormone. Nicotinic acid use is commonly associated with flushing and pruritus and may also cause non-specific gastrointestinal complaints, hepatotoxicity (hepatic necrosis, hepatitis, or elevated liver enzymes), gout, myolysis, decreased glucose tolerance and increased fasting glucose levels, and ophthalmological complications including decreased visual acuity, toxic amblyopia, and cystic maculopathy. The HMG-CoA reductase inhibitors may produce liver enzyme elevations, creatine kinase elevations and rhabdomyolysis. The combination of a reductase inhibitor and a fibrate increases the risk for rhabdomyolysis. Possible adverse effects of the fibric-acid derivatives include abdominal discomfort, nausea, flatulence, increased lithogenicity of bile, liver enzyme elevations and creatine kinase elevations. Probucol may increase the QTc interval and may cause non-specific gastrointestinal complaints.
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PMID:Currently available hypolipidaemic drugs and future therapeutic developments. 859 27

I.v. pentamidine is well known to cause severe multiorgan adverse effects and is usually given to hospitalized patients under close monitoring. The primary purpose of this retrospective quality assurance study is to assess the safety of administering i.v. pentamidine in the medical daycare unit (MDCU) for outpatients. Thirty-five outpatients infected with the HIV made 306 visits to the MDCU from January 1991 to December 1993. They received i.v. pentamidine in a dosage of either 300 mg once a month for prophylaxis or 4 mg/kg/d 5 days a week for treatment of Pneumocystis carinii pneumonia (PCP). BP was monitored every 15 to 30 min over 3 to 4 h and clinical side effects were noted. CBC count, BUN, creatinine, amylase, and blood glucose values were taken twice a week. The records were reviewed retrospectively and analyzed for clinical and biochemical derangement. GI side effects occurred in 59 of 306 (19%) visits; 43 (73%) of the side effects were nausea. Routine normal saline solution boluses before and after pentamidine infusion prevented the drop in BP and actually significantly elevated BP after i.v. pentamidine. The most common biochemical derangement was elevated BUN level in eight patients and creatinine in nine patients, but they were mild and required no intervention. Significant neutropenia occurred in three, anemia in two, hyponatremia in two, hyperamylasemia in two, and hyperglycemia in two patients. No palpitation or irregular pulse was encountered. No death was associated with the administration of i.v. pentamidine. Three patients required hospital admission. Only one hospital admission was definitely related to adverse drug effects. In conclusion, the side effects of i.v. pentamidine are common but minor. We conclude that it is safe to administer i.v. pentamidine in carefully selected patients with appropriate monitoring in an ambulatory setting. This has a major health economic implication, because ambulatory i.v. pentamidine can result in significant cost savings and can also enhance quality of life. Further studies regarding the feasibility of home administration of i.v. pentamidine is warranted as even further cost savings and improvement in the quality of life of HIV-infected patients may be achieved.
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PMID:The safety of i.v. pentamidine administered in an ambulatory setting. 868 17


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