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)

Many chemotherapeutic agents have been evaluated during the last 40 years and some have now an established place in the management of malignant disease. However these agents have a level of toxicity well above any other group of drugs. Chemotherapeutic agents do not discriminate between normal and neoplastic tissue. Chemotherapeutic regimens that are toxic to rapidly dividing malignant cells, are liable to be particularly harmful to lymphoid tissues, bone marrow and the epithelium of the gastrointestinal tract. The side effects due to chemotherapy are classified as immediate, early, delayed and late. Immediate side effects are those that may occur within the first 24 hours of treatment. The most common immediate side effect is nausea and vomiting, due to direct central effect on the vomiting center of the brain. Cisplatin and nitrogen mustard are particularly prone to this complication. The antiemetics usually used are metoclopramide, domperidone and steroid. The efficacies of these drugs are not so good for nausea and vomiting due to cisplatin administration, however several blockades against serotonin M-receptor recently developed are quite effective to nausea and vomiting of chemotherapeutic regimens including cisplatin. Early side effects commence within about one month of therapy. The most common is bone marrow toxicity and can occur after therapy with the vast majority of anticancer drugs. The relative importance of leukopenia and thrombocytopenia vary between the drugs and their route of administration. Recently, hematopoietic cytokines, such as granulocyte-colony stimulating factor (G-CSF) and granulocyte-macrophage-colony stimulating factor (GM-CSP) have been introduced to granulocytopenia developed by cancer chemotherapy. In the phase II study of G-CSF, a rapid recovery of granulocytes after chemotherapy and marked efficacy on infection in granulocytopenic patients were observed. In addition to this, autologous bone marrow transplantation after chemotherapy has been described in patients with solid tumors.
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PMID:[Palliative therapy in cancer. 5. Side effects by anticancer drugs and their treatments]. 169 55

Sixty-six patients with locally advanced (Stages III and IV) carcinoma of the head and neck were treated with three cycles of induction chemotherapy, consisting of cisplatin, fluorouracil (FU) infusion, bleomycin, mitomycin, and hydroxyurea, followed by radiotherapy and/or surgery. There were 48 men and 18 women with a median age of 55 years (range, 18 to 75 years) and Karnofsky performance status of 80 (range, 40 to 90). Primary site was nasopharynx (28 patients), followed by larynx (12) and others (26). Forty-one (62%) patients were presented with Stage IV disease. The response rate to induction chemotherapy was 27% complete response, 50% partial response, 20% stable disease, and 3% progressive disease. There was no significant difference in response rate between patients with cancer of nasopharynx or other sites (P greater than 0.1). Survival was 61% at 24 months. Patients with cancer of nasopharynx had a better survival than those with other primaries (P = 0.033). Toxicities from chemotherapy included alopecia (73%), nausea/vomiting (66%), leukopenia (54%), stomatitis (36%), anemia (32%), thrombocytopenia (16%), and diarrhea (9%). Grade IV toxicity was not observed. Induction chemotherapy with this new regimen resulted in a high response rate but may not be superior to cisplatin and FU alone. It can be safely combined with radiotherapy as a potentially curative therapy in squamous cell carcinoma of the head and neck. Chemotherapy followed by radiation therapy may yield survival similar to radical surgery in laryngeal and other head and neck cancers.
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PMID:Induction chemotherapy with a new regimen alternating cisplatin, fluorouracil with mitomycin, hydroxyurea and bleomycin in carcinomas of nasopharynx or other sites of the head and neck region. 169 26

A retrospective study of 76 children with hemolytic uremic syndrome (HUS) who were admitted to the Alberta Children's Hospital in Calgary. Alberta between January 1982 and December 1988 was undertaken to explore the gastrointestinal manifestations of the syndrome. The children (mean age of 4.0 +/- 3.1 years) presented primarily during the summer months with a microangiopathic hemolytic anemia (Hgb 94 +/- 26 g/L), thrombocytopenia (platelets 87 +/- 83 X 10(9)/L), and acute renal failure (oligoanuria with a BUN of 26 +/- 15 mmol/L, and a creatinine of 294 +/- 90 mumol/L). Forty-three children required dialysis for 10 +/- 17 days. The duration of hospitalization was 17 +/- 17 days. Four children died of complications attributable to HUS. The following symptoms and gastrointestinal manifestations of HUS were noted: fever (33%), vomiting (80%), abdominal discomfort/tenderness (59%), diarrhea (100%), hemorrhagic colitis (79%), rectal prolapse (13%), colonic stricture (3%), colonic perforation (1%), intussusception (1%), indirect hyperbilirubinemia (49%), and elevated hepatocellular enzymes (58%). Of the last 29 children studied, 19 (66%) had elevated levels of amylase and lipase in the presence of acute renal failure, and six (21%) had a marked elevation of lipase (more than four times normal) with additional supportive evidence of pancreatitis. The additional supportive evidence included persistent elevation of lipase after the resolution of acute renal failure in four children, a marked increment in lipase in association with abdominal pain and an abnormal ultrasound of the pancreas after the initiation of oral feeding in a fifth child, and pancreatic exocrine and endocrine necrosis at autopsy in a sixth child.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gastrointestinal manifestations of hemolytic uremic syndrome: recognition of pancreatitis. 170 51

Twenty-five adult patients with resistant or early relapsing Hodgkin's disease have been treated with CAV combination chemotherapy (CCNU, melphalan and etoposide). All patients had previously received both MOPP and ABVD regimens (23 patients as primary therapy and two as first salvage). High-energy radiotherapy had been administered in one case. The CAV chemotherapy was used as first salvage therapy in 15 cases (60%); the remaining patients had been heavily pretreated with different regimens including alkylating agents, vinblastine, and/or nitrosourea derivatives before CAV for multiple relapses or progressive disease. At the initiation of CAV chemotherapy, 64% of patients had extranodal disease (20% with more than one site), and bone marrow was involved in 16% of total cases. Thirty-two percent of CAV patients had progressed during primary therapy, while only 20% of cases had relapsed after complete remission (CR). The CR rate after CAV therapy was 17% (4 of 24); partial responses were observed in 33% of patients, giving an overall response rate of 50%. The response was influenced by the presence of nodal disease and by a prior response to chemotherapy. Considering the 15 patients who received CAV therapy as first salvage, the CR rate was 37%. The median survival from the initiation of CAV therapy was 23 months for the whole group of patients, and was not reached at 2 years for those who received CAV as first salvage therapy. Toxicity consisted of nausea (100% of cases), vomiting (63%), reversible alopecia (83%), mild to moderate leukopenia and thrombocytopenia (54% and 21%, respectively). No therapy-related deaths were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:CAV chemotherapy (CCNU, melphalan, etoposide) as salvage treatment for relapsing or resistant Hodgkin's disease. 170 10

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

Twenty-four cases of dengue haemorrhagic fever/dengue shock syndrome were studied in Delhi in the months of September and October, 1988. The majority of these cases were boys aged 6-10 years. Classical symptoms of dengue (fever, headache, aesthesia, myalgia) occurred in all the patients. Digestive symptoms (nausea, vomiting, anorexia, abdominal pain and hepatomegaly) were also common. Haemorrhagic manifestations were present in 41.7% of the cases. Of these, 90% had gastrointestinal haemorrhages. Shock occurred in 17 cases (70.8%). Thrombocytopenia and prolongation of coagulation profile were found in 62.5% of cases. Three patients (12.5%) who presented with encephalopathy died. The other 21 patients recovered after an average period of 2-8 days.
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PMID:An epidemic of dengue haemorrhagic fever and dengue shock syndrome in Delhi: a clinical study. 170 58

A combination of mitomycin C, vindesine and melphalan was administered to 33 patients with heavily pretreated refractory breast cancer. The overall response rate was 27% with a mean duration of more than 10.2 months. A stabilization with a mean duration of 5.1 months was seen in 56% of cases, while 20% of patients progressed. Gastrointestinal toxicity, mostly grade 1 or 2 nausea/vomiting was seen in 85% of cases, grade 1 or 2 leukopenia in 60% of patients, and grade 1 or 2 thrombocytopenia in 42%. Considering the good compliance of this regimen and the poor prognosis of patients with refractory advanced breast cancer, this combination can be useful as a palliative treatment of breast carcinoma.
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PMID:Combination chemotherapy with mitomycin C, vindesine and melphalan for refractory metastatic breast cancer. 170 43

Forty-five patients with metastatic neuroendocrine tumors were treated with a regimen of etoposide 130 mg/m2/d for 3 days plus cisplatin 45 mg/m2/d on days 2 and 3. Both drugs were given by continuous intravenous infusion. Among 27 patients with well-differentiated carcinoid tumors or islet cell carcinomas, only two partial objective tumor regressions were observed (7%). Among 18 patients prospectively classified as having anaplastic neuroendocrine carcinomas, however, there were nine partial regressions and three complete regressions, an overall regression rate of 67%. For anaplastic disease, the median duration of regression was 8 months (range to 21 months). Tumor response was unrelated to primary site, endocrine hyperfunction, or prior therapy experience. The median survival of all patients with anaplastic tumors was 19 months; this seemed favorable when considering the small experiences with these rare tumors reported in the literature. Toxicity, which was severe for most patients, consisted primarily of vomiting, leukopenia, thrombocytopenia, anemia, alopecia, and neuropathy. The anaplastic neuroendocrine tumor is strongly responsive to therapy with combined etoposide and cisplatin. Patients with undifferentiated carcinomas, originating in typical neuroendocrine tumor sites (small and large bowel, pancreas, and stomach) or of unknown origin, who have consistent histologic findings by light microscopy should be evaluated for this possibility with appropriate immune staining or electron microscopy.
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PMID:Treatment of neuroendocrine carcinomas with combined etoposide and cisplatin. Evidence of major therapeutic activity in the anaplastic variants of these neoplasms. 171 61

Ifosfamide is an oxazaphosphorine alkylating agent with a broad spectrum of antineoplastic activity. It is a prodrug metabolised in the liver by cytochrome P450 mixed-function oxidase enzymes to isofosforamide mustard, the active alkylating compound. Mesna, a uroprotective thiol agent, is routinely administered concomitantly with ifosfamide, and has almost eliminated ifosfamide-induced haemorrhagic cystitis and has reduced nephron toxicity. Therapeutic studies, mostly noncomparative in nature, have demonstrated the efficacy of ifosfamide/mesna alone, or more commonly as a component of combination regimens, in a variety of cancers. In patients with relapsed or refractory disseminated nonseminomatous testicular cancer, a salvage regimen of ifosfamide/mesna, cisplatin and either etoposide or vinblastine produced complete response in approximately one-quarter of patients. As a component of both induction and salvage chemotherapeutic regimens, ifosfamide/mesna has produced favourable response rates in small cell lung cancer, paediatric solid tumours, non-Hodgkin's and Hodgkin's lymphoma, and ovarian cancer. Induction therapy with ifosfamide/mesna-containing chemotherapeutic regimens has been encouraging in non-small cell lung cancer, adult soft-tissue sarcomas, and as neoadjuvant therapy in advanced cervical cancer. As salvage therapy, ifosfamide/mesna-containing combinations have a palliative role in advanced breast cancer and advanced cervical cancer. Ifosfamide/mesna can elicit responses in patients refractory to numerous other antineoplastic drugs, including cyclophosphamide. With administration of concomitant mesna to protect against ifosfamide-induced urotoxicity, the principal dose-limiting toxicity of ifosfamide is myelosuppression; leucopenia is generally more severe than thrombocytopenia. Reversible CNS adverse effects ranging from mild somnolence and confusion to severe encephalopathy and coma can occur in approximately 10 to 20% of patients after intravenous infusion, and the incidence of neurotoxicity may be increased to 50% after oral administration because of differences in the preferential route of metabolism between the 2 routes of administration. Other adverse effects of ifosfamide include nephrotoxicity, alopecia, and nausea/vomiting. In general, intravenously administered mesna is associated with a low incidence of adverse effects; however, gastrointestinal disturbances are common following oral administration. Thus, ifosfamide/mesna is an important and worthwhile addition to the currently available range of chemotherapeutic agents. It has a broad spectrum of antineoplastic activity and causes less marked myelosuppression than many other cytotoxic agents. At present, the role of ifosfamide/mesna in refractory germ cell testicular cancer is clearly defined; however, its overall place in the treatment of other forms of cancer awaits delineation in future well-controlled comparative studies.
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PMID:Ifosfamide/mesna. A review of its antineoplastic activity, pharmacokinetic properties and therapeutic efficacy in cancer. 172 Mar 82

In conjunction with autologous bone marrow rescue, high-dose mitozolomide was given i.v. to 16 patients with refractory malignancies at doses ranging from 100 to 400 mg/m2 over 1 h. Neutropaenia occurred consistently at 300 mg/m2, and three trivial infective episodes were recorded. Thrombocytopaenia occurred consistently at 150 mg/m2, and three patients experienced episodes of minor bleeding. The death of one subject was attributable to pulmonary thromboembolism during the bone marrow reinfusion. Transient emesis and mild alopecia were the only other toxicities. Three of six evaluable patients receiving greater than or equal to 300 mg/m2 exhibited measurable reductions in tumour dimensions, although these failed to fulfil the criteria for a partial response. Mitozolomide was undetectable in plasma at 12 h after drug administration. The plasma pharmacokinetic data fitted mono- or biexponential models in all patients. Model-independent pharmacokinetic parameters were: peak plasma drug concentration, 3.4-46 mg/l; AUC, 8-82 mg h l-1; clearance, 7.6-45 l/h; steady-state volume of distribution, 11-85 l; and plasma elimination half-life, 1.4-2.8 h. Dose-dependent pharmacokinetics were not observed, and only a small percentage of the delivered dose was eliminated unchanged in the urine. The maximally tolerated dose of mitozolomide given with autologous bone marrow rescue was greater than 400 mg/m2. At this dose myelosuppression was the only major toxicity, and the plasma drug levels and AUC values were comparable to those obtained after therapeutic doses in experimental models.
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PMID:A clinical and pharmacological study of high-dose mitozolomide given in conjunction with autologous bone marrow rescue. 173 52


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