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)

In 75 children with mainly lymphoid malignancies, adriamycin was used as part of the treatment. Three groups were distinguished: group I (n = 18), with an adriamycin dose of 30 mg/m2 as bolus; group II (n = 30), with a dose of 100 mg/m2 divided over 2 subsequent days; and group III (n = 27), with a dose of adriamycin of 100 mg/m2 given as a 24-h infusion. The tolerance of the low dose was the best. In group III small differences in the tolerance were observed. The recovery of the white blood cell count showed a delay in the infusion group, whereas the bolus injection group showed more vomiting. Severe vascular lesions occurred in the infusion group. The use of 24-h infusions of adriamycin is feasible when central venous accesses or totally subcutaneous intravenous devices are used. According to the literature, when long-term invasions of adriamycin are used, the risk of cardiomyopathy is diminished, without influencing the antitumor activity of adriamycin.
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PMID:Tolerance of 24-hour infusions or low- and high-dose bolus injections of adriamycin in children. 315 26

We conducted a phase I and pharmacokinetic study of i.v. idarubicin, a new anthracycline analogue, in 42 evaluable children 1-19 years old. Twenty-seven had leukemia and 15 had various solid tumors. The drug was administered in escalating doses of 10 to 40 mg/m2/course in 3 equal fractions over 3 consecutive days at 14- to 21-day intervals. Myelosuppression and mucositis were the limiting toxicities for short-term administration. Nausea, vomiting, and elevation of liver enzymes and bilirubin were the other toxicities encountered. Peak toxicity occurred 2 weeks after drug administration with median recovery by day 24. All but 4 patients with solid tumors had prior anthracyclines. Mild cardiac function changes without clinical symptoms were observed in 17 of 35 patients measured by serial cardiac evaluations. In addition, there were 4 patients with congestive heart failure. On postmortem examination, 4 patients had changes consistent with anthracycline cardiomyopathy at a prior median total anthracycline dose of 175 mg/m2. The maximum tolerated dose for patients with solid tumors was 15 mg/m2 course in 3 divided doses. Patients with leukemia tolerated 30 mg/m2/course. Six of 15 evaluable patients with acute lymphoblastic leukemia who received greater than or equal to 30 mg/m2 idarubicin achieved a remission (M1 marrow status). The plasma clearance of idarubicin fits a 3-compartment model with a harmonic mean half-life of 2.4 min, 0.6 h, and 11.3 h for alpha, beta, and gamma phases, respectively. Idarubicinol was the only metabolite detected in the plasma and it accumulated during the 3 days of therapy. Idarubicin is similar to daunorubicin in pharmacology and toxicity. While the cardiotoxic dose still must be delineated, the complete remission achieved in multiple relapsed patients with acute lymphoblastic leukemia indicate promising activity in at least that disease.
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PMID:Phase I and clinical pharmacological study of 4-demethoxydaunorubicin (idarubicin) in children with advanced cancer. 347 21

Tiazofurin is a novel C-nucleoside with significant antitumor activity in murine tumor models. In a phase I clinical trial, patients received tiazofurin by bolus iv infusion daily for 5 days. Six doses ranging from 550 to 4100 mg/m2/day were evaluated. Thirty-one treatment courses were initiated in 21 patients. Tiazofurin induced multiple, transient toxic effects at all but the lowest dose level, and treatment interruption was a common result. Nine of 28 treatment courses initiated at doses greater than or equal to 1100 mg/m2/day were interrupted at less than 5 days; only five of eight courses initiated at 1100 mg/m2/day were completed. Symptoms leading to treatment interruption included headache, nausea and emesis, and lethargy and malaise. Other significant, transient toxic effects included skeletal muscle injury manifest as pain, weakness, or serum biochemical abnormalities; mucocutaneous effects; and mental or mood changes. One case each of transient pericarditis and fatal cardiomyopathy occurred at the highest dose. Myelosuppression was observed but was transient and not dose limiting. In addition to leukopenia and thrombocytopenia, unexpected declines in serum hemoglobin were observed, although these were of uncertain significance. Tiazofurin induced significant increases in uric acid production which could be reversed with coadministration of allopurinol. Pharmacokinetic analysis revealed tiazofurin plasma elimination to be at least biphasic, with a beta-half-time of 4.2 hours; most of an injected dose could be recovered from the urine as unaltered compound within 24 hours. From this study we conclude that an appropriate dose for phase II trials with this schedule is less than or equal to 1000 mg/m2/day. The schedule may be a difficult one for clinical evaluation of antitumor activity, however, because of the possibility of frequent treatment interruption due to multiple systemic toxic effects.
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PMID:Phase I trial of tiazofurin administered by i.v. bolus daily for 5 days, with pharmacokinetic evaluation. 380 11

Five cardiology centers conducted open-label prospective trials of meobentine sulfate, an intravenously and orally available analog of bethanidine, to assess its potential for treatment of recurrent, drug refractory ventricular tachycardia (VT) or fibrillation (VF), and complex ventricular arrhythmias. The study population comprised 26 patients (mean age, 61 years); 18 were men. Coronary artery disease was present in 15, cardiomyopathy in six, and valvular heart disease in three. Patients presented with both VT and VF (seven), sustained VT alone (12), or frequent ventricular ectopy (PVCs) and nonsustained VT (seven). Of the 26 patients, 5 were enrolled in antiarrhythmic studies (chronic PVC suppression) and 21 were enrolled in programmed electrical stimulation (PES) studies. Two of five in the chronic PVC study showed greater than 75% arrhythmia suppression. Among 21 patients in PES studies, there were eight intravenous (16 mg/kg) and 19 oral trials (400 to 1000 mg every 6 hours, 3 days/dose interval). Five of 22 patients showed efficacy at repeat PES study (neither VT nor VF), one showed partial efficacy, and four were not restudied because of clinical arrhythmia (three) and/or adverse effects (two). Overall, three patients (12%) were continued on the drug for an extended period of time. Adverse experience included hypotension in 50% and gastrointestinal effects (nausea, vomiting, or diarrhea) in 56% (oral trials only). Adverse reactions led to drug discontinuation in six and dosage reduction in eight patients. Thus, meobentine may prevent induction of VT or VF or reduce frequency of complex PVCs in selected patients refractory to other antiarrhythmic agents, but the response rate is relatively low. Symptomatic hypotension or gastrointestinal adverse effects are common and may limit utility of meobentine as a chronic oral antiarrhythmic agent.
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PMID:Meobentine sulfate: antiarrhythmic and electrophysiologic effects assessed by programmed electrical stimulation and ambulatory monitoring in patients with complex ventricular tachyarrhythmia. Report of a multicenter evaluation. 390 15

Eighty-three patients with advanced soft tissue sarcoma who had received no prior chemotherapy entered a randomised phase II study comparing carminomycin (CMM) 20 mg/m2 with adriamycin (ADM) 75 mg/m2, both administered i.v. bolus every 3 weeks. Six patients were ineligible and response could not be evaluated in 6 additional patients. Thirty-eight evaluable patients received ADM and 33 received CMM. There was one complete response to ADM and 10 partial responses, an overall response rate of 29%. CMM showed significantly (P = 0.01) lower antitumour activity--one partial response (3%). Stabilisation of disease was similar in both arms (47 and 45%), but fewer patients progressed on ADM (24 compared to 52%). Durations of response dating from the start of chemotherapy were 5 months for complete remission on ADM, a median of 7 months (range 4-17) for partial response on ADM and 14 months for the one partial remission on CMM. Although the median time to progression for all patients receiving CMM (2 months) was significantly (P = 0.001) shorter than for those receiving ADM (5 months), patients on ADM had only a marginally significant longer duration of survival (P = 0.06) than the patients receiving CMM. A leucocyte nadir less than 2.0 X 10(9)/l occurred in 38% of patients receiving ADM and 43% receiving CMM. Anaemia and thrombocytopoenia were uncommon. Other toxicities such as nausea, vomiting, anorexia and alopecia were more severe in the ADM group. There was one infective death secondary to leucopoenia in the ADM arm, and one patient who had received 109 mg/m2 CMM + 255 mg/m2 ADM developed progressively fatal cardiomyopathy.
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PMID:Carminomycin vs adriamycin in advanced soft tissue sarcomas: an EORTC randomised phase II study. 635 80

Twenty-two patients who had metastatic breast cancer previously treated with combination chemotherapy, cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) or CMF with vincristine and prednisone, were treated with Carminomycin (carubicin) 20 mg/m2 body surface area by intravenous bolus injection once every 3 weeks. Of 21 evaluable patients, 1 patient achieved complete remission, 5 patients achieved partial responses, and 11 remained stable. Cases of acute drug toxicity included myelosuppression, phlebitis, and gastrointestinal symptoms; there were four cases of mild alopecia, which consisted of thinning of the scalp hair. There were three cases of biopsy-proven cardiomyopathy, contrary to previous reports from the United Soviet Socialist Republic, which indicated that this drug was relatively free of cardiotoxicity. The median duration of remission for responders was 23 weeks. It is believed that Carminomycin has significant activity against metastatic breast cancer and, because its side effects, especially nausea, vomiting, and alopecia, were considerably milder than those experienced with Adriamycin, further investigation of this drug is warranted.
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PMID:Carminomycin. A new anthracycline analog in the treatment of advanced breast cancer. 654 98

A boy, aged 7 months, of consanguineous parents presented with an acute onset of vomiting, fever, nonketotic hypoglycemia and acidosis and died from cardiac arrest after ventricular fibrillation. He had hepatomegaly and echocardiographically a non-obstructive cardiomyopathy. Autopsy was not allowed. After birth the child had suffered from a severe respiratory distress syndrome, transient metabolic acidosis and had a sweaty feet odour. Later on, development was retarded with a severe muscular hypotonia. Post mortem, numerous unusual organic acids were found in high concentrations in urine, e.g. dicarbonic acids, 2-hydroxyisobutyric, isovaleric, 3-hydroxyisovaleric acid, N-acyl glycines, isovalerylglutamic acid and sarcosine. This pattern indicated deficiencies of several acyl-Co A dehydrogenases in the metabolism of leucine, isoleucine, valine, lysine, short-chain fatty acids and sarcosine. This could be confirmed using cultured skin fibroblasts which were shown to degrade the corresponding labeled substrates insufficiently to 14CO2. It is assumed that the functional multiple acyl-Co A dehydrogenation deficiency is caused by a deficiency of a common link in the electron transfer system of these dehydrogenases which is inherited autosomal recessively in this family. Among the 12 patients reported, 7 died within the first 5 days of age.
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PMID:Multiple acyl-Co A dehydrogenation deficiency (MADD) in a boy with nonketotic hypoglycemia, hepatomegaly, muscle hypotonia and cardiomyopathy. Detection of N-isovalerylglutamic acid and its monoamide. 686 97

The haemodynamic effects and pharmacokinetics of single intravenous doses of tolmesoxide, a new vasodilator agent, were studied in 6 patients with severe cardiac failure secondary to ischaemic cardiomyopathy and refractory to conventional therapy. The mean (+ SEM) baseline cardiac index (CI) and pulmonary artery diastolic pressure (PADP) were 1.7 +0.11/min/m2 and 30.5 +4.1 mm Hg respectively. The mean % rise in CI was 78.8 +23.3 and the mean % fall in PADP was 35.2 +5.2. The mean half life of tolmesoxide in these patients was markedly prolonged at 15.6 +6.6h. Side effects were minimal - vomiting was seen in 1 patient. This agent warrants further study in the long term management of refractory cardiac failure.
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PMID:Clinical pharmacology of tolmesoxide in refractory heart failure. 731 77

Chronic adriamycin (ADR) intoxication with cardiomyopathy developed in young Beagle dogs given weekly IV injections (1 mg/kg of body weight) for 20 weeks (cumulative dose 400 mg/m2). Eighteen dogs were allotted equally to three groups: group A received ADR only, group B was given ADR and simultaneous weekly doses of vitamin E (17 mg/kg of body weight as alpha-tocopherol acetate), and group C received ADR, weekly doses of vitamin E as in group B, and selenium (0.06 mg/kg of body weight as selenite). The dogs reacted with cutaneous hyperemia, head shaking, and vomiting immediately after ADR injection. After 4 to 6 weekly injections, all the dogs developed alopecia that was present initially over the head and subsequently extended to the ventral portions of the neck, thorax, and abdomen and the proximal inner areas of the limbs. Other skin lesions present in alopecic areas were secondary ulcerative dermatitis and melanosis. Testicular atrophy and cachexia developed in the dogs, but damage was not present in bone marrow, alimentary tract, kidney, and bone with the dosage schedule utilized. Hematologic studies showed no significant alterations. Supplementation with vitamin E alone or with selenium failed to alter the incidence and severity of extracardiac ADR-induced lesions. This study shows that the dog is a good model for studies of chronic ADR-induced cardiotoxicity, as cardiac damage was consistently produced and ADR-associated extracardiac lesions were of minimal severity.
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PMID:Clinical observations, cutaneous lesions, and hematologic alterations in chronic adriamycin intoxication in dogs with and without vitamin E and selenium supplementation. 740 87

Toxic Shock Syndrome (TSS) is a potentially fatal illness caused by a particular strain of Staphylococcus aureus. The clinical presentation is similar to that of septic shock. The incidence of TSS peaked in the late 1970s and early 1980s, probably as a result of availability of super absorbent tampons. Although most commonly associated with menstruation, the overall incidence of menstrual and nonmenstrual TSS in men and women ranges from 1 to 3 per 100,000. There are almost equal numbers of menstrual and nonmenstrual cases of TSS identified annually. S aureus, the causative microorganism in cases of TSS, has been isolated from many body tissues. Toxic shock syndrome presents as a flu-like illness with high fever, vomiting, diarrhea, general malaise, and muscle weakness. Nursing and medical management focus on controlling or preventing potentially serious complications, such as adult respiratory distress syndrome, renal failure, electrolyte imbalances, disseminated intravascular coagulation, encephalopathy, and cardiomyopathy. Judicious use of tampons and barrier contraceptive devices may decrease the risk of developing TSS.
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PMID:Toxic shock syndrome: an opportunity for nursing intervention. 865


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