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)

Although deleterious events following abrupt withdrawal of antihypertensive treatment are relatively uncommon, considerable attention has recently been focused on this problem. A withdrawal syndrome may occur after termination of almost all types of antihypertensive drugs, but most experience has been with the centrally acting agents and with beta-adrenoreceptor blockers. Abrupt discontinuation of high doses of centrally acting drugs such as alpha-methyldopa, clonidine, and guanabenz can produce a syndrome of sympathetic overactivity that includes agitation, headache, sweating, and nausea and less commonly can provoke rapid upswings in blood pressure. If beta blockers are suddenly stopped, a similar pattern can occur that may be related to excessive activity of thyroid hormones as well as sympathetic factors. Additionally, patients with ischemic heart disease may be susceptible to an acute exacerbation of their cardiac disease when beta-blocker treatment is stopped. It seems likely that discontinuation events can be particularly severe when combinations of different types of antihypertensive medications are sud-disease when betablocker treatment is denly stopped. This problem can be dealt with by educating patients to avoid sudden drug cessation and when elective discontinuation is planned, by gradual dose reduction.
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PMID:The abrupt discontinuation of antihypertensive treatment. 3 49

Deprenyl is a synthetic, selective inhibitor of the monoamine oxidase-B enzyme system. The mechanism of its beneficial effect in early and advanced Parkinson's disease is not settled. Increased striatal dopamine accumulation, sensitization of surviving dopamine neurons with increased dopamine production and reduced nigro-striatal toxicity may all contribute. The standard daily dose of deprenyl is 10 mg. Selectivity may be lost at higher doses. Deprenyl is especially indicated in untreated patients, improving up to 50 percent of patients with mild motor fluctuations. Major symptomatic benefit also occurs in occasional levodopa treated patients. Adverse effects are common, however. Increase dyskinesias, confusion and hallucinations, nausea and postural hypotension may necessitate drug withdrawal or the use of low dose regimens. Caution should be exercised with older patients, those with ulcer disease, which may be worsened by deprenyl, and individuals with active ischemic heart disease where the safety of this drug is not yet clear.
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PMID:Deprenyl in Parkinson's disease: mechanisms, neuroprotective effect, indications and adverse effects. 157 60

Safety information was pooled from 4,859 patients, mainly treated in controlled clinical trials with a dispersible tablet of sumatriptan or by a subcutaneous injection, and from 1,164 patients who received placebo by these routes. Safety monitoring involved collection of all adverse events, regardless of their relationship to treatment, and included routine laboratory screening tests and some special investigations. Individuals experienced several groups of symptoms that might be considered to be features of migraine itself or of the post-migraine period or due to treatment. The commonest complaints were an unpleasant taste or pain on injection. After oral sumatriptan (100-300 mg), some events (nausea, malaise) were characteristic of migraine and others (fatigue, sedation, weakness) were characteristic of the recovery period. With subcutaneous sumatriptan (4-8 mg) similar events were observed, but certain distinctive symptoms variously described as heaviness, pressure sensation, tingling, feelings of heat or warmth, were more common and affected various parts of the body. Their early onset and transient nature suggests some pharmacological mechanism, as yet not identified. Despite the mixed picture of symptoms recorded after treatment, they were not serious, they were transient and they were accepted by patients. Close patient monitoring allowed detailed evaluation of any possible cardiovascular side-effects as seen with other anti-migraine agents, particularly ergotamine. The evidence is reassuring but, since experience in patients with symptomatic ischaemic heart disease is limited, it is recommended that they should initially be treated with sumatriptan under medical supervision for their first two or three attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The safety and tolerability of sumatriptan: an overview. 165 42

Fifty-one patients with symptomatic ventricular tachycardia who failed control on current anti-arrhythmics were studied. Seventy-four percent had ischemic heart disease and 81% had congestive heart failure. Patients underwent serial 24 Holter recordings and radionuclide ventriculography before, during dose titration and during long-term mexiletine therapy. Twenty-eight patients (55%) were successfully controlled. Of these, 17 (33%) remained controlled greater than or equal to 1 year. Early and late side effects were common but benign and included mostly gastric pain and nausea. Twenty-eight patients underwent radionuclide ventriculography before and during mexiletine therapy: there was no significant difference in heart rate, blood pressure, left ventricular ejection fraction, stroke volume and end-diastolic volumes before and during mexiletine. Left ventricular ejection fraction was 21.4 +/- 2.2%, (SD) and 21.3 +/- 2.2% (SD) before and during mexiletine respectively. Digoxin blood levels measured in 15 patients were not significantly changed by mexiletine. In conclusion, mexiletine is effective and safe in many patients with intractable ventricular tachycardia. It has no significant hemodynamic effects even in patients with congestive heart failure nor does it affect digoxin blood levels. Its usefulness is limited by a high incidence of gastric intolerance.
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PMID:Mexiletine: long-term efficacy and hemodynamic actions in patients with ventricular arrhythmia. 241 74

Nausea and vomiting occurring during myocardial ischemia is believed to be associated with inferior wall infarction. However, data supporting such an association are limited, and an alternative hypothesis that cardiac vomiting is related to infarct size has also been advanced. The 2 hypotheses were tested in a cross-sectional study of 265 patients consecutively admitted to the coronary care unit. Nausea or vomiting was a good predictor of myocardial infarction (p less than 0.0001). The odds of having an infarction was 3.14 times greater for patients with nausea or vomiting than for those without these symptoms. Nausea was not a good predictor for inferior wall infarction (p = 0.14): 51% of patients with inferior infarcts had nausea or vomiting and 66% with anterior infarcts had these symptoms. Using peak serum creatine kinase level as an index of infarct size, nausea or vomiting was a good predictor of larger infarction. While 55% of all patients with infarction had nausea or vomiting, for patients with infarctions that produced a peak creatine kinase level of more 1,000 IU/liters, 78% had nausea or vomiting. Sex was a marginally important variable. After adjusting for sex, the presence of nausea or vomiting still predicted infarct size (p less than 0.001). Thus, cardiogenic nausea and vomiting are associated with larger myocardial infarctions but do not suggest infarcts in a particular location.
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PMID:Nausea and vomiting during acute myocardial infarction and its relation to infarct size and location. 360 39

Although the exposure of human subjects to prostacyclin (PGI2) infusion has been broad, no systematic approaches have been made in order to investigate the dose-related side effects in patients with angina pectoris and coronary artery disease (CAD). We studied 25 patients with typical chest pain and overt CAD. All patients underwent a cycloergometer stress testing (25 W increments at 2-min intervals). PGI2 was infused in scalar doses up to 10 ng/kg/min. During the infusion 25 patients (100%) had facial flushing, 7 (28%) moderate headache and one (4%) had nausea. In addition, 4 patients experienced the typical chest pain and had significant (greater than or equal to 0.1 mV) ST segment depression at 8.10 ng/kg/min infusion rates. These patients had lower tolerance to exercise (6.7 +/- 1.7 vs. 8.8 +/- 1.9 min; p less than 0.05) and coronary artery lesions more severe than those observed in patients without drug-induced angina pectoris. Our data therefore indicate that PGI2 at therapeutic doses may induce myocardial ischemia in patients with angina pectoris, low tolerance to exercise and severe CAD. In patients with mild to moderate degree of CAD, PGI2 was found to be well tolerated. These findings suggest that patients with angina pectoris and low tolerance to exercise should be excluded from clinical studies directed at elucidating the effectiveness of PGI2 in cardiovascular disorders.
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PMID:Side effects of prostacyclin in patients with angina pectoris and coronary artery disease. 390 57

A review of the available literature concerning sudden withdrawal of antihypertensive drugs shows that withdrawal syndromes after cessation of such agents have occurred with beta-blockers, methyldopa, clonidine hydrochloride, guanabenz, and bethanidine sulfate. Most commonly, these syndromes are limited to nervousness, tachycardia, headache, and nausea 36 to 72 hours after cessation of the drug. In rare cases, serious exacerbation of myocardial ischemia (beta-blockers) or hypertension (clonidine, methyldopa) may occur in the posttreatment period. The withdrawal syndromes generally respond promptly to reinstitution of antihypertensive therapy. The infrequent occurrence of withdrawal syndromes should not discourage use of these efficacious agents.
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PMID:Withdrawal syndromes and the cessation of antihypertensive therapy. 611 20

In a randomized double-blind study with flexible dosage, morphine, nicomorphine and pethidine were compared with regard to analgetic effect, dose requirements, dose intervals and adverse reactions. A total of 275 patients were included, and 28 patients were excluded due to adverse reactions (n = 16) and for practical reasons, etc. Acute myocardial infarction (AMI) was diagnosed in about 60% of the patients, and about 30% had ischemic heart disease without AMI. All three analgesics provided equally efficient pain relief in relative doses of morphine 10, nicomorphine 10 and pethidine 75 mg/ml. Severe adverse reactions were few (allergy 3 cases, respiratory insufficiency 4, severe bradycardia 4), whereas nausea was recorded in 20-30%, vomiting in 5-15% and dizziness in 10-30% of the patients, with no difference between the three drugs. Significant blood pressure drop (greater than 30 mmHg) was seen in 3-8% of the patients, with no significant differences between the drugs.
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PMID:Analgetic treatment in acute myocardial infarction. A controlled clinical comparison of morphine, nicomorphine and pethidine. 637 74

Sumatriptan is a potent and selective agonist at a vascular serotonin1 (5-hydroxytryptamine1; 5-HT1) receptor subtype (similar to 5-HT1D) and is used in acute treatment of migraine and cluster headache. Following administration of sumatriptan 100mg orally, relief of migraine headache (at 2 hours) was achieved in 50 to 67% of patients compared with 10 to 31% with placebo in controlled clinical trials. In a comparative study, oral administration of sumatriptan 100mg consistently achieved significantly greater response rates than a fixed combination of ergotamine 2mg plus caffeine 200mg during 3 consecutive migraine attacks (66 vs 48% for first attack). Oral sumatriptan 100mg was also more effective than aspirin 900mg plus metoclopramide 10mg orally in a similar study. In the majority of controlled clinical trials, headache relief (at 1 hour after administration) was achieved in 70 to 80% of patients with migraine receiving sumatriptan 6mg subcutaneously compared with 18 to 26% of placebo recipients. Approximately 40% of patients who initially responded to oral or subcutaneous sumatriptan experienced recurrence of their headache, usually within 24 hours, but the majority of these patients responded well to a further dose of sumatriptan. Patients with cluster headache were treated for acute attacks with sumatriptan 6mg subcutaneously or placebo in 2 crossover trials. Headache relief was achieved within 15 minutes in 74 and 75% of patients receiving sumatriptan in these studies compared with 26 and 35%, respectively, with placebo. Patients receiving sumatriptan 12mg had a similar response rate as those receiving 6mg, but the higher dose was associated with an increased incidence of adverse events. Based on extensive safety data pooled from controlled clinical trials, sumatriptan is generally well tolerated and most adverse events are transient. The most frequently reported adverse events following oral administration include nausea, vomiting, malaise, fatigue and dizziness. Injection site reactions (minor pain and redness of brief duration) occur in approximately 40% of patients receiving subcutaneous sumatriptan, although the incidence appears to be markedly reduced when patients self-administer the drug with an auto-injector. Chest symptoms (mainly tightness and pressure) occur in 3 to 5% of sumatriptan recipients, but have not been associated with myocardial ischaemia except in a few isolated cases. Sumatriptan is contraindicated in patients with ischaemic heart disease, angina pectoris including Prinzmetal (variant) angina, previous myocardial infarction and uncontrolled hypertension, but is not contraindicated in patients with migraine and asthma. Data from long term studies in acute treatment of migraine and cluster headache suggest that sumatriptan remains effective and well tolerated over several months.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sumatriptan. A reappraisal of its pharmacology and therapeutic efficacy in the acute treatment of migraine and cluster headache. 751 61

BW12C79 stabilizes the oxyhemoglobin molecule resulting in a reversible left-shift of the oxygen saturation curve. The activity of a number of bioreductive anticancer drugs, such as mitomycin C, may be enhanced under hypoxic conditions. Twenty-four patients with various malignancies received BW12C79 and mitomycin C. BW12C79 was administered i.v. with a loading dose (20-50 mg/kg) over 1 h followed by a maintenance infusion of 4 mg/kg/h for 5 h. Percentage modification of the oxyhemoglobin (degree of left-shift) was dose related with maximum modification of 56% and was maintained for the duration of maintenance infusion of BW12C79. Hemoglobin electrophoresis showed a fast moving band consistent with the BW12C79-oxyhemoglobin complex. Side effects at the top dose level comprised headache, nausea/vomiting, vein irritation, and myocardial ischemia. One other patient suffered from an acute encephalopathy of unknown etiology a few days following BW12C79. 31P magnetic resonance spectroscopy of exercising calf muscles showed increased breakdown of high energy phosphate stores and a greater reduction in pH. Recovery of the high energy phosphate stores after exercise was slow. These results were consistent with reduced oxygen supply due to either a left shift of the oxygen saturation curve and/or reduced muscle blood flow. BW12C79 did not interfere with the pharmacokinetics of mitomycin C. In conclusion, this phase I study demonstrates the feasibility of achieving a significant left shift in the oxygen saturation curve in cancer patients which is maintained for at least 5 h with acceptable toxicity. The maximum tolerated dose of BW12C79 was 50 mg/kg loading infusion followed by a maintenance infusion of 4 mg/kg/h. Magnetic resonance spectroscopy results were consistent with reduced supply of oxygen to exercising skeletal muscle. BW12C79 may be of potential benefit as an adjunct to bioreductive drugs in the treatment of solid tumors.
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PMID:A phase I study of the left-shifting agent BW12C79 plus mitomycin C and the effect on the skeletal muscle metabolism using 31P magnetic resonance spectroscopy. 824 19


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