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)

Chemotherapy-induced emesis is dependent not only on individual parameters but also on treatment parameters (type and dose of the cytotoxic drug, combination with other cytotoxic drugs). Cyclophosphamide-based chemotherapy is potentially emetogenic and the emtogenicity is proportionally dependent on the dose. Therefore, the preventive antiemetic treatment must be adapted to this emetogenic risk. A number of studies have assessed the efficacy of ondansetron, a highly selective 5-HT3 receptor antagonist, for the control of 'non cisplatin' chemotherapy. In mild emetogenic regimens, oral ondansetron is more effective than placebo and its efficacy is similar to the classic antiemetic regimen metoclopramide-dexamethasone. Concerning moderately emetogenic chemotherapies, iv ondansetron is highly effective and its effecicay is superior to that of metoclopramide and alizapride. Delayed nausea and vomiting can be controlled by an oral ondansetron treatment. This allows to maintain the good response obtained by the initial antiemetic regimen. With very high doses of cyclophosphamide, as in conditioning chemotherapy and total body irradiation prior to bone marrow transplantation, no optimal antiemetic treatment has still been defined; but the combination of ondansetron with dexamethasone should be used according to the poor control obtained with ondansetron alone. However, studies combining 5-HT3 receptor antagonists with dexamethasone are warranted in order to define the optimal treatment in this particularly emetogenic treatment setting.
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PMID:[Optimal control by ondansetron of acute and prolonged emesis induced by chemotherapy without cisplatin]. 867 59

Emesis is a common side effect of chemotherapeutic drugs. Cisplatin, nitrogen mustard and dacarbazine induce increases in urinary 5-hydroxyindoleacetic acid (5-HIAA) in parallel with the development of the period of emesis which is sensitive to 5-HT3 receptor antagonists ('acute emesis'). It is suggested that these cytotoxics release serotonin from enterochromaffin cells, which then acts on 5-HT3 receptors to trigger the emetic response. Cyclophosphamide, on the other hand, induces a modest emetic response, partly sensitive to 5-HT3 receptor antagonists, but not associated with increases in urinary 5-HIAA. It is suggested that cyclophosphamide-induced emesis is not mediated by the release of serotonin from enterochromaffin cells. Although after high-dose cisplatin most emesis is sensitive to 5-HT3 receptor antagonists, patients often present a milder, although more prolonged form of emesis which is mostly resistant to 5-HT3 receptor antagonists (also known as 'delayed emesis'). This form of emesis is not associated with increases in urinary 5-HIAA (not due to serotonin released from the enterochromaffin cells). Treatment with p-chlorophenylalanine (a serotonin synthesis inhibitor) inhibited cisplatin-induced emesis and cisplatin-induced increases in urinary 5-HIAA excretion. In summary, these results indicate that in human patients, serotonin plays a fundamental role in chemotherapy-induced emesis. Serotonin released from enterochromaffin cells seems to mediate emesis sensitive to 5-HT3 receptor antagonists induced by cisplatin, dacarbazine and nitrogen mustard. Emesis sensitive to 5-HT3 receptor antagonists associated with cyclophosphamide treatment, is not mediated by the release of serotonin from enterochromaffin cells by the cytotoxic. Therefore, cyclophosphamide could induce serotonin release either from enteric serotonin nerves or from the CNS. Cisplatin-induced emesis resistant to 5-HT3 receptor antagonists ('delayed emesis') is not mediated by serotonin released from enterochromaffin cells.
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PMID:Serotonin mechanisms in chemotherapy-induced emesis in cancer patients. 869 46

Cyclophosphamide induces moderate to severe emesis. The severity of emesis is dependent on the dose of cyclophosphamide and on the addition of other cytotoxic drugs. A review of the literature dividing studies according to the dose of cyclophosphamide and the specific cytotoxic combination shows that ondansetron plus dexamethasone provides optimal antiemetic therapy in patients receiving standard or high-dose cyclophosphamide (> or = 450 mg/m2). These studies also show that it is important to give antiemetic therapy to cover the prolonged duration emesis and nausea induced by these regimens, e.g. intravenous CMF/(F)AC/(F)EC. For continuous 'oral' (low-dose) CMF chemotherapy, oral ondansetron or oral metoclopramide plus intravenous (or possibly oral) dexamethasone are effective antiemetic therapies.
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PMID:Optimal control of cyclophosphamide-induced emesis. 869 48

The aim of the work was to evaluate the impact of cyclophosphamide and ondansetron on serotonin metabolism measured by urinary 5-hydroxyindoleacetic acid (5-HIAA) excretion. The pattern of urinary 5-HIAA excretion was analysed within 24 h following cyclophosphamide, epirubicin and 5-fluorouracil (FEC) chemotherapy (n = 14), ondansetron as single agent (n = 31), and in a control group (n = 62). 5-HIAA was measured by a fluorescence/polarisation immunoassay. Both FEC and ondansetron alone induced a significantly higher 5-HIAA increase following the first 12 h after drug administration when compared to the control group. The comparison of quantitative variables of 5-HIAA excretion between FEC and ondansetron failed to reveal any statistical differences. Cyclophosphamide-based chemotherapy is associated with only minor increases of 5-HIAA excretion. Analysis of 5-HIAA excretion does not help in the description of the pathophysiology of cyclophosphamide-induced emesis. In contrast to experimental data, serotonin 3 receptor antagonism with ondansetron induces an increase of 5-HIAA excretion in humans.
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PMID:5-Hydroxyindoleacetic acid excretion following combination chemotherapy with cyclophosphamide, epirubicin and 5-fluorouracil plus ondansetron compared to ondansetron alone. 888 33

In Japan, 5-FU/5-FU derivatives or the combination therapy of CAF (cyclophosphamide, CPA; adriamycin, ADM; 5-fluorouracil; 5-FU) have been commonly used for the adjuvant treatment of breast cancer. Recently, a combination of CEF (CPA; Epirubicin, EPI; 5-FU) has come to the stage of adjuvant setting, because the cardiotoxicity was reduced in EPI. In this study, we investigated the feasibility of 6 cycles of CEF (CPA 700 mg/m2, EPI 70 mg/m2, 5-FU 700 mg/m2; day 1 iv every 3-4 weeks) in the adjuvant treatment of primary breast cancer patients with nodal involvements. All 12 patients completed 6 cycles of CEF within 8 months. The median treatment duration was 6.2 months. More than Grade III side effects of neutropenia, nausea/vomiting and alopecia were observed in 7/12 (58.3%), 5/12 (41.7%) and 12/12 (100%), respectively. No serious side effects, including cardiotoxicity, were shown. CEF seems to be feasible regimen as an adjuvant treatment for breast cancer.
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PMID:[The feasibility of CEF (cyclophosphamide, epirubicin, 5-FU) regimen in the adjuvant setting of primary breast cancer]. 912 4

On 24 February 1995, six U.S. soldiers serving with the Multinational Force in Haiti became ill after eating a locally caught fish identified as the greater amberjack Seriola dumerili. The victims presented with nausea, vomiting, watery diarrhea and abdominal cramps 5-8 hr after consumption. Also present in some victims were numbness in the extremities or perioral region, bradycardia and scalp paresthesia. Patients were treated with i.v. hydration therapy and antiemetics. All recovered without sequelae over the course of 1-3 months. A portion of the cooked fish was obtained for analysis. A semipurified lipid extract was prepared according to standard methods and analyzed for the presence of Na+ channel site 5 binding activity using a brevetoxin receptor binding assay. By this assay, the fish sample contained the equivalent of approximately 20 ng Caribbean ciguatoxin/g flesh. The presence of the major Caribbean ciguatoxin (C-CTX-1) was confirmed by liquid chromatography-mass spectrometry. Using the receptor binding assay to monitor activity in TSK and PRP-1 column fractions, two minor toxins were detected in addition to C-CTX-1. One of these minor toxins was more polar, and the other less polar, than C-CTX-1. These data provide firm evidence that a family of C-CTX-1 is responsible for ciguatera in the Caribbean.
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PMID:Identification of Caribbean ciguatoxins as the cause of an outbreak of fish poisoning among U.S. soldiers in Haiti. 920 98

From June 1984 to October 1995, forty seven consecutive patients (pts) with a confirmed diagnosis of diffuse malignant mesothelioma (MM) of the pleura (41) and peritoneum (6), were treated with cisplatin (CDDP) (24 pts) (Group A), or Doxorubicin (ADM) (14) based chemotherapy (Group B), or a combination of CDDP and ADM (9 pts) (Group C). Chemotherapy for Group A was CDDP 100 mg/m2 Dl with Viblastine 6 mg/m2 Dl, 8 (24 pts) for Group B ADM 40 mg/m2 D I with Vincristine (VCR) 2 mg Dl and DTIC 200 mg/m2 Dl-3 (5 pts) or instead of DTIC Cyclophosphamide 600 mg/m2 Dl instead (pts 4). A Total of 11/47 (23%) of the pts responded to chemotherapy; Group A: I complete and 5 partial responders, Group B: 3 partial responders and Group C: 2 partial responders. Pts with MM of peritoneum showed I complete (Group A) and 4 partial (Group B: 2, Group B: 1, Group C: I) responses, a total of 5/6 (83%). There was no difference in survival time, duration of response and time to progression between the examined groups. A statistically significant difference between responders and non responders in terms of survival was seen: responders 20.8 (3-35), non-responders 5.05 (1-12) months (P = 0.03). Toxicity was acceptable and no treatment-related deaths occurred. Myelo-suppression, mild anemia, nausea-vomiting, anorexia and fatigue were the main toxicities. We conclude that CDDP or ADM-based chemotherapy or a combination of both drugs are equally effective in MM.
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PMID:Combination chemotherapy with cisplatin and/or doxorubicin in malignant mesothelioma. A retrospective study [corrected from prospective]. 942 83

We recently reported that chronic administration of cyclophosphamide significantly increased urinary 5-hydroxyindole acetic acid (5-HIAA) excretion in rats indicative of a release of 5-hydroxytryptamine (5-HT) from intestinal enterochromaffin (EC) cells. Cyclophosphamide is considered to be an inactive prodrug and require conversion to active emetic metabolities (e.g. phosphoramide mustard) by hepatic metabolism. However the presence of cytochrome P450 in the intestine raises the possibility of cyclophosphamide metabolism in the wall of the intestine, a site which would have considerable significance for 5-HT release and the emetic effects of cyclophosphamide. The aim of this study was to investigate whether cyclophosphamide could induce the release of 5-HT from the isolated ileum and to examine its mechanism of action. Cyclophosphamide (10(-6)M and 10(-7)M) induced a concentration dependent increase of 5-HT from rat isolated ileum. This cyclophosphamide-induced 5-HT release was significantly reduced by granisetron (10(-6)M and 10(-7)M) or atropine (10(-7)M and 10(-6)M). Tetrodotoxin (10(-6)M completely inhibited the increased 5-HT release induced by cyclophosphamide. These results suggest that cyclophosphamide has the capacity to induce 5-HT release via activation of enteric cholinergic neurons. In addition the in vitro study demonstrate for the first time that cyclophosphamide may be activated to emetic metabolites at extra-hepatic sites (e.g. intestine) and that conversion at these sites could contribute to the mechanism of cyclophosphamide induced emesis.
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PMID:Cyclophosphamide increases 5-hydroxytryptamine release from the isolated ileum of the rat. 950 64

Small cell mucosa-associated lymphoid tissue (MALT) lymphomas rarely affect the duodenum, and optimal treatment has not been defined. The aim of this case series was to determine the clinical features and outcome of duodenal MALT lymphoma in four patients (three men, one woman; median age 52 yr) treated with cyclophosphamide p.o. Initial manifestations were abdominal pain (n = 4), vomiting (n = 2), and an obstructive syndrome (n = 1). MALT lymphoma was diagnosed on the basis of endoscopic biopsies. It was localized in the duodenum in three cases and involved the entire small bowel in one case. Tumor infiltration was limited to the duodenal wall in one case and was associated with locoregional lymphadenopathy in three cases. The patients were graded EI (n = 1) and EII1 (n = 3), respectively, according to the Ann Arbor classification revised by Musshof. Cyclophosphamide, 100 mg daily, was administered p.o. for 18 months. Gastroscopy with biopsies, radiography of the small intestine and abdominal CT (CT) were performed every 6 months. Complete remission was defined by morphological and histological normalization, and partial remission as morphological normalization only. Follow-up lasted from 9 to 65 months. Three patients were in complete remission at 18 months: two relapsed after 2 yr and one was still in complete remission at 65 months. The patient with 9 months of follow-up was in complete remission at 6 months. The two patients who relapsed did not complain of symptoms, and no morphological abnormalities were seen. Relapse was diagnosed on histological grounds. Cyclophosphamide monotherapy p.o. thus seems well adapted to this slowly progressive disease, but it is unclear whether it should be resumed in the case of histological relapse or only in the case of symptomatic relapse. (Am J Gastroenterol 2000;95:536-539. (O 2000 by Am. Coll. of Gastroenterology)
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PMID:Duodenal mucosa-associated lymphoid tissue lymphoma: treatment with oral cyclophosphamide. 1068 64

We designed a randomized, prospective three-arm mobilization study to determine the kinetics of peripheral blood stem cell (PBSC) mobilization in 60 non-Hodgkin's lymphoma (NHL) patients primed with cyclophosphamide (CTX) in combination with granulocyte colony-stimulating factor (G-CSF) (arm A), granulocyte-macrophage (GM)-CSF (arm B) or GM-CSF/G-CSF (arm C). We also compared mobilization and transplant-related toxicities, pre- and post-transplant support and the probability of survival among the three arms. To date, 35 patients have been enrolled in the study; 13 patients have been enrolled in arm A, 10 patients in arm B, and 13 patients in arm C. Successful collection of the target of > or = 2 X 10(6) CD34+ cells/kg in one to four apheresis collections was 10/13, 6/10, and 7/12 in arms A, B, and C, respectively. The differences between arms were not statistically significant. The median time to achieve the target CD34+ cells in patients who successfully mobilized the target CD34+ cells was 3 days, 2 days, and 1 day, in patients in arms A, B, and C, respectively. The time for neutrophil engraftment was 11, 10, and 10 days in arms A, B, and C, respectively. The time for platelet engraftment was 11 days for patients in all arms of the study. Most importantly, no significant differences were observed among the three arms in the duration of neutropenic fever, the extent of mucositis, diarrhea, and nausea/vomiting, or in the number of units of platelets or red cells transfused after transplantation. Risk factors associated with poor mobilization were > or = 3 regimens of chemotherapy prior to mobilization, older age, and disease histology (follicular versus diffuse). Therefore, we conclude that the type of growth factor used for mobilization did not play a major role in the outcome of mobilization and recommend mobilizing NHL patients before they receive multiple regimens of chemotherapy.
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PMID:Peripheral blood stem cell mobilization with cyclophosphamide in combination with G-CSF, GM-CSF, or sequential GM-CSF/G-CSF in non-Hodgkin's lymphoma patients: a randomized prospective study. 1109 98


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