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)

Eighteen evaluable children who relapsed with acute lymphocytic leukemia (ALL) were treated with intermittent, high-dose actinomycin D. Objective responses occurred in four of 11 children who had relapsed with chemotherapy which did not contain an anthracycline. The major toxic effects included thrombocytopenia and granulocytopenia. Minor toxic effects included nausea, vomiting, skin rash, and stomatitis. The onset of the maculopapular skin rash coincided with the platelet count nadir. These data suggested that actinomycin D is active in ALL.
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PMID:Actinomycin D in childhood acute lymphocytic leukemia. 27 97

Since July 1976, 19 patients with carcinoma of the bladder have been treated with adriamycin, 5-fluorouracil, and levamisole combined with radiotherapy (60 Gy [6000 radsA1/24 fractions/6 weeks). Chemotherapy and radiotherapy were initiated simultaneously, with the entire treatment lasting 7--8 months. Three months after the completion of radiotherapy, 14 of the 18 patients in whom cystoscopy was performed were found to be in complete remission. Overall, 17 of the 19 patients have responded to the treatment and 15 patients have at some time shown complete remission. The toxic effects seen were myelosuppression, nausea, vomiting, diarrhea, loss of weight, and alopecia. Thirteen patients received the entire treatment as outpatients while six patients had to be hospitalized for a period of 8--14 days because of severe side effects, especially in Weeks 3--8. Serious complications such as bowel perforation were not seen, but one patient died with septicemia as a result of agranulocytosis, which was attributed to the treatment with levamisole.
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PMID:Phase II study of adriamycin, 5-fluorouracil, levamisole, and irradiation in carcinoma of the bladder. 44 95

Aprindine hydrochloride is an antiarrhythmic drug now under investigation. The drug is most effective in prophylaxis of ventricular dysrhythmias. Previously recognized toxic effects include neurological side effects, nausea, vomiting, as well as a reported association with agranulocytosis. To our knowledge, this is the first report of agranulocytosis associated with documented elevated serum concentrations of aprindine. Further correlation of drug levels with toxic reactions may help in establishing the mechanism of bone marrow suppression.
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PMID:Agranulocytosis associated with aprindine therapy. 48 54

Fifteen patients were treated in a Phase I study of intracarotid carboplatin (200-400 mg/m2) in 5% dextrose and water infused over 15 to 30 minutes through a transfemoral catheter with a 0.2-micron inline filter. This study was done because intravenous carboplatin has less neurotoxicity than cisplatin and is active against brain tumors. Eleven men and four women ranging in age from 37 to 72 years (median, 59 years) were treated. The Eastern Cooperative Oncology Group performance status was 1 in 3, 2 in 4, and 3-4 in 8 patients. Eight patients had one to three previous chemotherapy regimens; previous radiotherapy had failed in 13 patients. The response of patients in the Phase I study follows: glioblastoma, 6 failed; not evaluated because of early death from pulmonary embolus, 1; recurrent Grade II and III glioma, 1 stable (minor response with neurologic improvement) and 2 failed; malignant oligodendroglioma, 1 failed; brain metastases from nonsmall cell lung cancer, 1 partial remission, 1 stable (minor response), and 1 failed; brain metastases from unknown primary, 1 stable (minor response with neurological improvement). Median survival was 9 weeks. Nausea was mild to moderate. One patient had granulocytopenia, and 2 had thrombocytopenia (mild). At 200 mg/m2 (2 patients), 1 had a focal seizure. At 300 mg/m2 (9 patients), 2 with abnormally small arteries had severe pain early in the treatment and posttreatment ipsilateral conjunctival edema, decreased vision, and cerebral edema (with partially reversible increased hemiparesis); 1 other had mild decrease in ipsilateral vision and 1 had transient aphasia on removal of the catheter (possibly the result of a vascular spasm).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I study of intracarotid administration of carboplatin. 131 64

A total of 15 patients with measurable advanced colorectal adenocarcinoma were prospectively treated with fazarabine (Ara-AC), reconstituted in dimethyl sulfoxide, and administered at a starting dose of 48 mg/m2/day as a continuous intravenous infusion for three days. The dose was repeated every 21 days and dose escalations or reductions were made on the basis of toxicities encountered in the preceding course. No patient achieved either a complete or partial response. Major toxicities encountered were granulocytopenia, thrombocytopenia, nausea, vomiting, anemia, and headache. All toxicities were reversible upon discontinuation of the drug and no life-threatening toxicities occurred. These data indicate that further clinical trials in colorectal carcinoma with this agent and schedule of administration are not warranted.
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PMID:Phase II trial of fazarabine in advanced colorectal carcinoma. 137 22

A total of 48 patients with measurable advanced gastric adenocarcinoma (n = 16) or adenocarcinoma of the exocrine pancreas (n = 32) were prospectively treated with iproplatin at a starting dose of 270 mg/m2 intravenously over 2 hours. The dose was repeated every 28 days, and dose escalations or reductions were made on the basis of toxicity in the preceding course. No patient with gastric carcinoma achieved either a complete or partial response. One partial response and two complete responses were seen with pancreatic adenocarcinoma for an overall response rate of 10%. One patient has remained free of disease for more than 2 years. The major toxicities were granulocytopenia, thrombocytopenia, nausea, vomiting, and diarrhea. All toxicities were reversible upon discontinuation of the drug. On the basis of this trial, we conclude that iproplatin has no substantive activity in advanced gastric or pancreatic carcinomas.
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PMID:Phase II evaluation of iproplatin in patients with advanced gastric and pancreatic cancer. 144 17

The activity of amonafide, a benzisoquinoline-1,3-dione, was assessed in 15 patients with advanced or recurrent sarcoma (11 previously treated). Eligible patients had ECOG performance status 0-2, and acceptable renal, hepatic and bone marrow function. Amonafide 300 mg/m2 was given intravenously over one hour daily on five consecutive days, every 3 weeks. Leukopenia and granulocytopenia were the most common and severe toxicities (grade 3 or 4 toxicity in 20% and 27% of patients, respectively). Local irritation and nausea/vomiting, the most common nonhematologic toxicities, were generally mild. No objective responses were seen, though 2 patients had brief stabilization of disease. Amonafide at this dose and schedule has no activity against advanced, recurrent sarcoma.
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PMID:Phase II study of amonafide in advanced and recurrent sarcoma patients. 150 Feb 72

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of ticlopidine are reviewed. Ticlopidine appears to inhibit platelet aggregation induced by adenosine diphosphate. Ticlopidine hydrochloride is rapidly absorbed after oral administration, and maximum antiplatelet effects occur one to three hours after the dose. In multicenter, randomized, double-blind trials, ticlopidine was more effective than aspirin or placebo in preventing stroke, myocardial infarction, or death caused by vascular events. Ticlopidine was more effective than aspirin in preventing recurrent transient ischemic attacks after six months of therapy. Ticlopidine has also been used to prevent occlusion and improve patency of aortocoronary bypass grafts, to prevent ischemic ulcers in patients with chronic arterial occlusive disease, and to slow the progression of diabetic microangiopathy. The most serious adverse effect, neutropenia, occurred in about 1% of patients. The most frequently reported adverse effects are diarrhea, nausea, vomiting, and abdominal cramps. Ticlopidine is indicated for reducing the risk of thrombotic stroke in patients who have experienced a minor stroke, transient ischemic attack, or completed thrombotic stroke. The recommended dosage is 500 mg/day in two divided doses taken with food. Ticlopidine is an alternative agent for the primary and secondary prevention of stroke. Because of the risk of neutropenia and agranulocytosis and the high cost of therapy, ticlopidine should be reserved for patients who are intolerant of or lack benefit from aspirin.
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PMID:Ticlopidine: a new platelet aggregation inhibitor. 161 11

Eleven patients with beta thalassemia major were entered into the trial of the oral chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1). Their ages ranged from 17 to 26 years (mean +/- SD, 22.3 +/- 2.7). Six were male and five were female. L1 was administered at an initial daily dose of 42.5 to 60 mg/kg as a single dose. After 4 weeks, the dose was increased to 85 to 119 (102 +/- 10.7) mg/kg for 191 to 352 days divided into either two or four doses daily, except for one patient who developed agranulocytosis after 11 weeks and was taken off the trial. Initial serum ferritin values in the remaining 10 patients ranged between 1,000 and 9,580 (5,549 +/- 3,333) micrograms/L and at end of the trial their mean serum ferritin was significantly lower (4,126 +/- 2,278; P less than .05 using the paired t-test). Urinary iron excretion at a daily dose of 85 to 119 mg/kg administered as two divided doses ranged between 0.14 and 0.82 (0.44 +/- 0.26) mg/kg/24 h. In three patients, the four doses per day schedule caused substantially more iron excretion than the same total dose divided into two. During the course of the trial, several possible adverse effects have been encountered. One patient (female, aged 20) developed agranulocytosis 11 weeks after starting treatment and 6 weeks after beginning treatment with a daily dose of 105 mg/kg. This patient's neutrophil count recovered spontaneously 7 weeks after the discontinuation of L1. A decrease in serum zinc levels to subnormal levels was observed in four patients with symptoms of dry skin, with an itchy scaly rash in two that was associated with low serum zinc levels that responded to zinc therapy. Urinary zinc levels ranged from 4.7 to 23.4 (13 +/- 5.5) mumol/24 h and were above 9 mumol/24 h (upper limit of normal) in eight patients. Mild nausea occurred in three patients and transient diarrhea in a fourth. Mild musculoskeletal symptoms occurred in three patients but settled without discontinuation of L1 therapy in two and with temporary discontinuation of L1 in the third. A transient increase in serum aspartate transaminase was also noted in five patients, but serum aspartate transaminase levels subsequently decreased in all of them. No cardiovascular, neurologic, renal, or retinal toxicities were demonstrable. These results confirm that L1 is an effective oral iron chelator. Further clinical trials are needed to determine the incidence and severity of adverse effects.
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PMID:Efficacy and possible adverse effects of the oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1) in thalassemia major. 846 82

A phase I trial of fazarabine (ara-AC, 1-beta-D-arabinofuranosyl-5-azacytosine, NSC 281272) administered as a 24-h continuous infusion was performed in 24 adults with solid tumor malignancies. The majority of patients had received prior marrow-suppressive therapy. Level 7 (54.5 mg/m2/h for 24 h) was the maximum tolerated dose since during 6 evaluable first courses, 2 episodes of grade 4 granulocytopenia and 3 episodes of grade 3 occurred. Moderate thrombocytopenia also occurred at level 7 with 3 episodes of grade 1 and 1 episode of grade 4 thrombocytopenia during 6 first course treatments. Minimal myelosuppression, principally leukopenia, was seen prior to level 7. The nadir WBC through 47 courses had a linear relationship with plasma steady-state concentrations of ara-AC. The only other toxicity noted was moderate nausea/vomiting, which did not appear to be dose related. Plasma steady-state concentrations of ara-AC were reached in all patients within 4-6 h and ranged from 1.1 microM (11 mg/m2/h for 24 h) to 7.5 microM (54.5 mg/m2/h for 24 h). The mean total body clearance of ara-AC for 47 courses, levels 1-7, was 592 +/- 147 (SD) ml/min/m2 which is similar to prior pharmacokinetic data from the 24-h and 72-h infusion trials of the Pediatric and Medicine Branches, respectively. There were no objective disease responses during the trial. The recommended adult phase II dose for a 24-h infusion of ara-AC is 45-50 mg/m2/h.
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PMID:Phase I clinical trial of fazarabine as a twenty-four-hour continuous infusion. 170 65


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