Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experience with high-dose cytosine arabinoside (HDAC) in pediatric solid tumors is limited. Sixteen children with solid tumors resistant to conventional therapies were registered in a pilot Pediatric Oncology Group (POG) study that required the administration of HDAC at 3 g/m2 every 12 hours for four doses. There were four cases of rhabdomyosarcoma, two cases of fibrosarcoma, four cases of neuroblastoma, and one case each of germ cell tumor, Wilm's tumor, retinoblastoma, hepatocellular carcinoma, Ewing's sarcoma, and Burkitt's lymphoma. All eligible patients had advanced diseases and had previously received extensive chemotherapy. Thirteen patients received one course of HDAC and three patients received two courses of HDAC. Due to prior treatments, patients had less than normal marrow reserves. Short-term toxicity included nausea, vomiting, suppression of hemopoiesis, drug fever, and increased blood urea nitrogen (BUN), creatinine, and liver enzymes. All evaluable patients recovered from their toxicities. There were no drug-related deaths. None of the patients had neurologic problems, including the only patient with prior irradiation to the skull. With the above schedule, HDAC appears to have manageable toxicity.
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PMID:Toxicity of high-dose cytosine arabinoside in the treatment of advanced childhood tumors resistant to conventional therapy. A Pediatric Oncology Group study. 222 60

Tiazofurin (2-B-D-Ribofuranosylthiazole-4-Carboxamide: NSC 286193) is a nucleoside antimetabolite that acts as a potent inhibitor of IMP dehydrogenase resulting in a guanine nucleotide deprivation. Recent in vivo biochemical observations in rats bearing hepatoma suggested a correlation between depletion of guanine nucleotides and antitumor effect. The present phase I trial utilized a weekly x 3 bolus infusion schedule, repeated every 5 weeks. Biochemical measurements of GTP and dGTP were performed in patients at each dose level. Twelve patients received 16 courses of the drug in doses ranging from 1100 to 2050 mg/m2 weekly x 3. The dose limiting toxicities were pericarditis and clinical symptoms suggestive of a more generalized serositis (chest and abdominal pain). Other toxicities included reversible elevations in CPK (MM band only) and SGOT, nausea, vomiting, and arthralgias. Neurotoxic effects were generally mild, including headaches, anxiety, and malaise. Only 1 of 6 patients evaluated for tiazofurin's biochemical activity showed a sustained depletion of guanine nucleotide pools. No antitumor activity was observed. The maximally tolerated dose of tiazofurin on this intermittent weekly x 3 schedule was 1650 mg/m2. Toxicity and the overall lack of biochemical and biologic effect at clinically achievable doses may preclude further clinical evaluation of this drug on a weekly schedule. The toxicities observed in our study were similar to those reported for phase I investigations using a considerably higher dose intensity with daily x 5 schedules.
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PMID:Phase I trial and biochemical evaluation of tiazofurin administered on a weekly schedule. 234 2

The toxic effects and tissue uptake of both cisplatin and oxaliplatin--[(1R, 2R)-1,2-cyclohexanediamine-N,N'] [oxalato(2-)-O,O']platinum--were previously shown to vary similarly according to dosing time in mice. A 4-hour infusion of cisplatin resulted in fewer side effects and allowed administration of higher doses at 16 hours than at 4 hours in patients with cancer. We hypothesized that the continuous venous infusion of oxaliplatin for 5 days would be less toxic and would deliver a higher dose to the patient if the drug were infused at a circadian rhythm-modulated rate (peak at 16 hr; schedule B) rather than at a constant rate (schedule A). We tested this hypothesis in a randomized phase I trial. We escalated the dose of oxaliplatin to the patient by 25 mg/m2 per course. Courses were repeated every 3 weeks. An external, multichannel, programmable-in-time pump was used for the infusions. Toxicity was assessable for 94 courses in 23 patients (12 patients with breast carcinoma, nine with hepatocellular carcinoma, and two with cholangiocarcinoma). The incidence of neutropenia of World Health Organization grades II-IV and the incidence of distal paresthesias were 10 or more times higher (P less than .05) with schedule A than with schedule B. In addition, vomiting was 55% higher (P = .15) with schedule A than with schedule B. Furthermore, with schedule B, the mean dose of oxaliplatin (P less than .001) and its maximum tolerated dose (P = .06) could be increased by 15% over those doses with schedule A. An objective response was achieved in two of the 12 patients with previously treated breast cancer. We recommend that the dose of oxaliplatin for phase II trials be 175 mg/m2, delivered according to the circadian rhythm-modulated rate.
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PMID:Phase I trial of 5-day continuous venous infusion of oxaliplatin at circadian rhythm-modulated rate compared with constant rate. 234 69

Reported is a case that was treated successfully with a percutaneous intratumoral injection of a CDDP-PC-Lipiodol Suspension (CPLS) of the viable tumor cells of a hepatoma after arterial injection therapy. Although the size of the viable tumor cells remained almost unchanged, a marked reduction in the level of the plasma AFP (484 ng/ml-35 ng/ml) was obtained after the percutaneous injection. No major complication was encountered except for minimal vomiting and mild transient abnormalities of the liver functions.
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PMID:[A case of hepatoma treated successfully with a percutaneous intratumoral injection of CDDP-PC-lipiodol suspension]. 246 10

Twenty-seven patients with unresectable hepatocellular carcinoma (HCC) were treated with Cisplatin-Phosphatidyl-choline-Lipiodol (CPL) suspension. PR was obtained in two of ten cases (20%) by one shot therapy. AFP decreased in 9 of 10 patients by one shot therapy with a 62.1% rate of decrease. In all of 13 patients by TAE, AFP decreased and the rate of decrease was 64.8%. The concentration of CDDP in the peripheral venous blood was lower and continued longer than that of CDDP on the market. Nausea, vomiting and fever were noted in most cases as adverse effects, but they were slight. These results suggest that CPL agents were very chemotherapeutic for unresectable HCC.
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PMID:[Chemotherapy with Cisplatin-Phosphatidyl-choline-Lipiodol (CPL) suspension in unresectable hepatocellular carcinoma]. 247 69

A total of 20 patients with histologically proven primary hepatocellular carcinoma (PHC) received mitoxantrone IV at a dose of 10-16 mg/m2 every 3 weeks. All patients had previous hepatitis B infection. None underwent remission after treatment; 2 had stable disease and 18 progressive disease. The median overall survival was 13 weeks (range, 1-59 weeks). There was no evidence of significant antitumor activity for mitoxantrone in our patients with PHC. Hematotoxicity occurred in 100% of the patients with grades 2-4 leukopenia, 89% of those with grades 1-4 anemia, and 26% of those with grades 2-3 thrombocytopenia. Cardiotoxicity occurred in 20% of the patients after 14-30 mg/m2 mitoxantrone; these included complete heart block with fatal outcome in one case, decreased ventricular ejection fraction in one, and sinus tachycardia in two. Nausea, vomiting, fever, diarrhea, and alopecia were mild and occurred in 15%-45% of the patients Therefore, patients with PHC following hepatitis B infection may be less tolerant to mitoxantrone, resulting in the apparent increase in toxicities.
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PMID:Phase II study of mitoxantrone in unresectable primary hepatocellular carcinoma following hepatitis B infection. 253 94

Cisplatin suspension in Lipiodol (LPS) was prepared for the treatment of hepatocellular carcinoma by intra-hepatic arterial injection. In a rabbit liver cancer model, concentrations of cisplatin in tumor were more than 20 times higher than those in a nontumorous part of the liver at 5 min after LPS injection into the hepatic artery. Cisplatin at high concentrations was detected at 7 days after injection. The concentrations in other organs were lower except in the gall-bladder. In clinical trials for 71 patients with hepatocellular carcinoma, partial response was observed in 33 cases (46.5%) and minor response in 20 cases (28.2%). The survival rate was 77% at 6 month and 55% at one year. Although fever, nausea, vomiting and epigastralgia were observed as side effects, these were temporary. Acute gastroduodenal mucosal lesions, cholecystitis, pancreatitis, delayed jaundice and hepatic encephalopathy were observed as complications and super selective cannulation was necessary for their prevention.
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PMID:[Intra-arterial injection of cisplatin suspension in Lipiodol (LPS) in the treatment of hepatocellular carcinoma]. 255 Dec 47

It is very common for intraarterial infusion therapy of some anticancer agent to be effective against hepatocellular carcinoma. In this case, the patient was a 74-year-old man who suffered from very advanced hepatocellular carcinoma with tumor thrombus of the intrahepatic portal vein and IVC. He was treated with intraarterial infusion of CDDP, Etoposide, 5-FU, through a catheter placed in the proper hepatic artery. CDDP (30 mg/day) and Etoposide (60 mg/day) were given once every 5 days, and then 5-FU(250 mg/day) was infused daily for 26 days. The patient underwent this protocol study twice in 3 months. After the intraarterial infusion, transarterial embolization using CDDP (100 mg) powder added to lipiodol and aluminum stearate as suspension was done a month later. The tumor regression rate was 84% after intraarterial infusion of CDDP, Etoposide and 5-FU. The tumor thrombus in the intrahepatic portal vein and IVC had completely disappeared. We could not find lipiodol accumulated in the tumor after TAE. Thus, we assumed that the remaining tumor was a necrotic scar and that a complete response was obtained in the patient. There were some side effects, such as nausea, vomiting, pancytopenia and gastritis but no severe complication occurred.
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PMID:[A case of hepatocellular carcinoma effectively treated by intraarterial infusion of CDDP and other agents]. 255 Dec 53

Four cases of brain tumors associated with hemorrhage from tumors as their first manifestation were reported. These were malignant astrocytoma in two cases, brain metastasis of hepatocellular carcinoma in one case and skull metastasis of hepatocellular carcinoma in one case. Clinical symptoms and sings were generalized convulsion, sudden onset of headache, vomiting and hemiparesis. It was difficult to confirm the diagnosis of brain tumors in such cases. Therefore it is important to perform follow-up plain and enhanced CT repeatedly and it is also important to make adequate biopsy of hematoma wall and surrounding tissue during operation.
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PMID:[Brain tumors associated with hemorrhage from tumors as their first manifestation]. 255 50

The drug 5-fluoro-2-deoxyuridine-C8 (FUdR-C8), one of the lipophilic prodrugs of FUdR, was dissolved in an oily lymphographic agent (Lipiodol Ultra Fluid, Andre Gelbe Laboratory, Paris, France; Ethiodol, Savage Laboratories, Melville, NY) and used for the intraarterial treatment of malignant liver tumors. From August 1985 to June 1988, 33 patients with hepatocellular carcinoma and 13 patients with metastatic liver tumors were treated with this agent at the Kumamoto University Hospital and its affiliated hospitals. The response rate (complete remission [CR] and partial remission [PR]) was 27.6% for hepatocellular carcinomas and 46.1% for metastatic liver tumors. The cumulative 1-year survival rate was 55.1% for hepatocellular carcinomas and 70.0% for metastatic liver tumors. More than a 50% decrease in the tumor marker level was observed in ten of 21 patients with hepatocellular carcinoma and in two of eight patients with metastatic liver tumors. The side effects, which were transient and controlled with conservative treatment, included fever, abdominal pain, nausea, vomiting, and acute gastritis.
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PMID:Intraarterial infusion of 5-fluoro-2-deoxyuridine-C8 dissolved in a lymphographic agent in malignant liver tumors. A preliminary report. 255 39


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