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)

With estramustine phosphate the clinician has the possibility to ensure complete hormonal as well as cytotoxic control of advanced prostate cancer with a single drug. EMP is considered as a first choice for treatment of hormone refractory prostate cancer. It is at least as effective as conventional chemotherapy, yet less aggressive with regard to its toxicity profile. EMP is particularly useful in patients with limited bone marrow reserve, e.g. in case of prior or associated radiotherapy. As to the use of EMP in primary treatment, more information is required before we can define with certainty subgroups of patients who would benefit more from an early course of EMP than from other hormonal therapy. The existing data point in the direction of poorly differentiated tumors, patients with bone pain and poor prognosis. EMP treatment is associated with an increased risk of cardiovascular morbidity. This should be avoided as much as possible by proper selection of patients or by prophylaxis. Gastro-intestinal side effects, such as nausea, diarrhea and anorexia are dose-dependent. These adverse events tend to interfere with compliance at dosages over 560 mg/day. Dosage modifications or an anti-emetic may help. The intravenous administration of EMP offers the possibility for high loading doses at a substantially reduced risk for cardiovascular and gastrointestinal side effects.
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PMID:The present role of estramustine phosphate in advanced prostate cancer. 192 66

One hour after suicidal ingestion of about 20 mL of a 38% solution of bromofosmethyl, CAS: 2104-96-3 (bromophos), a 52 year-old female was admitted to the hospital with extreme miosis, hypersalivation, hyperperistalsis and muscular fibrillation. Gastric lavage was performed and activated charcoal administered. Cholinergic symptoms were antagonized by repeated doses of 0.5 mg atropine. Because of the high dose of bromophos, hemoperfusion was performed with amberlite XAD4. The bromophos clearance during hemoperfusion was 95 mL/min (flow 200 mL/min). The patient received two doses of 500 mg obidoxime for recurrent muscular fibrillation. The further clinical course was uneventful. On day 4, the patient was transferred to a psychiatric ward because of persistent suicidality. In contrast to poisoning by most organophosphates, red blood cell acetyl cholinesterase was only minimally depressed but the plasma butyryl cholinesterase was initially decreased and normalized within a few days. The records of 25 patients reported to our Poison Control Center with ingestion of more than 1 g bromophos were also evaluated. The most frequent symptoms were miosis, hyperperistalsis, hypersalivation, agitation, nausea/vomiting and convulsions. Nine of the patients had no symptoms. Bromophos is relatively less toxic than its phosphate derivative, parathion.
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PMID:Acute poisoning with bromofosmethyl (bromophos). 205 7

Estramustine phosphate, an anti-prostatic cancer agent, was investigated on eleven patients to evaluate the efficacy in a treatment of advanced breast cancers. The daily dose of medication was 840 mg. According to criteria of Japan Society for Cancer Therapy, none was assessed as CR, three as PR, four as NC and PD. The response rate was 27.3%. There was no differences in response rates among estrogen receptor status. A favourable response was observed in postmenopausal patients but no response in premenopausal, as well as a good response in lesions of soft tissue and lung, a poor response in lesions of liver and bone. As to toxicity of estramustine phosphate, gastrointestinal disorders such as nausea, vomiting and diarrhea were noted frequently during the treatment, and a long term administration was not able to perform in premenopausal patients because of vaginal bleeding and discharge, and pain in breast. The estramustine phosphate therapy for advanced breast cancers was regarded as one of modalities for a treatment of postmenopausal patients as a second line therapy. This is the first report in Japan discussing the efficacy of estramustine phosphate for a treatment of breast cancer.
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PMID:[Clinical evaluation of estramustine phosphate in the treatment of patients with advanced breast cancers]. 239 6

F-Ara-AMP (fludarabine phosphate) is an adenosine analogue that is resistant to deamination; it is a more potent cytotoxic compound than ara-A in experimental tumor systems. F-Ara-AMP was given by continuous IV infusion over 5 days once every 4 weeks to 27 evaluable adult patients with advanced cancer. The median Karnofsky performance status was 70% (range 50%-90%), and the median age was 58 years (range 41-74). In addition to adequate blood counts, a creatinine clearance of at least 60 ml/min was required. The initial dose level was 35 mg/m2/day. Dose-limiting myelosuppression was seen in the first patient. Subsequent patients were treated at lower doses. Myelosuppression was the only major toxicity. Leukopenia was generally more prominent than thrombocytopenia, but 2 patients experienced prolonged thrombocytopenia which prevented further therapy. Nausea was minimal, and neither renal nor neurologic toxicity was encountered. In patients with good renal function a dose of 25 mg/m2/day can be safely administered. However, because of apparent cumulative myelosuppressive effects a lower dose is more appropriate for patients who have had extensive prior chemotherapy or radiotherapy.
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PMID:Phase I clinical trial of fludarabine phosphate (F-ara-AMP). 241 21

Fludarabine phosphate (NSC 312878), an adenosine deaminase resistant analogue of 9-beta-D-arabinofuranosyladenine, has entered clinical trials. Eleven patients with acute leukemia in relapse received 14 courses of fludarabine phosphate as a 5-day continuous infusion administered at doses of 40 to 100 mg/m2/day. Toxicity was characterized by uniform myelosuppression, as well as occasional nausea, vomiting, and hepatotoxicity. Three episodes of metabolic acidosis and lactic acidemia were noted. In addition, three patients suffered neurotoxicity. Two of these three patients had a severe neurotoxicity syndrome characterized by blindness, encephalopathy, and coma. Neither patient recovered neurological function. Neuropathological findings at autopsy were characterized by a diffuse, necrotizing leukoencephalopathy which was most severe in the occipital lobes. The medullary pyramids and posterior columns were also severely affected. This sporadic fatal neurotoxicity was observed only at doses greater than 40 mg/m2/day. The maximum tolerated dose for a 5-day infusion of fludarabine phosphate is thus 40 mg/m2/day.
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PMID:Fludarabine phosphate (NSC 312878) infusions for the treatment of acute leukemia: phase I and neuropathological study. 242 88

Eighteen episodes of peritonitis in 16 CAPD patients were treated with oral ofloxacin 400 mg initially, followed by 300 mg daily for a total of 10 days. The culture-positive rate was 72.2% with Staphylococcal species as the most frequent isolates. The overall cure rate as defined by negative cultures 1 and 2 months after discontinuation of antibiotics was 83.3%. The time taken for the peritoneal effluent to clear completely was 5 days. With such a dosing regime, there was a significant increase in the mean serum trough level of ofloxacin from 2.28 mg/l on day 1 to 5.83 mg/l on day 10 (P less than 0.001). There was no significant difference in the serum levels attained whether or not phosphate binders were concurrently given. Side-effects were nausea and non-specific dizziness. No patients had to discontinue treatment because of side-effects. Ofloxacin appeared to diffuse from the blood into the peritoneal fluid, and a highly significant correlation existed between simultaneous blood and peritoneal effluent ofloxacin levels (r = 0.88, P less than 0.0001).
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PMID:Oral treatment of peritonitis in CAPD patients with ofloxacin. 314 86

Amino-hydroxy-propylidene bisphosphonic acid (APD) is a potent inhibitor of bone resorption. Its oral use in Paget's disease of bone has proved effective and safe when the drug is administered on a long-term basis. Since APD was found not to impair bone mineralization, it was assumed that a long remission would be obtained by administering a high dose of the compound over a very short period of time. Therefore, 12 patients with symptomatic Paget's disease received 1200 mg/d APD orally over 5 consecutive days. Follow-up is 2 months for all patients, 6 months for 6 patients and one year for one patient. Clinical improvement and biochemical remission were observed in all patients. Side effects were negligible (transient nausea in 2 patients and +1 degree C temperature increment noted for 2 days in 3 patients). Urinary hydroxyproline started decreasing within 2 days and became normal as a mean (+/- SEM) after 5 days (1.9 +/- 0.3 mumol/lGF, nl less than 2.3) and in all cases after 15 days. Thereafter it remained within the normal range (1.9 +/- 0.2 mumol/lGF) for 6 months. Plasma alkaline phosphatase activity fell progressively and significantly, and became normal after 1-3 months in all patients but one, a man with very active disease in whom the parameter remained slightly above normal and stable. At the end of the sixth month, mean plasma alkaline phosphatase activity was 100 +/- 13 U/l (nl less than 120 U/l). Plasma calcium and phosphate fell transiently between days 4 and 15.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Paget's disease of bone treated per os with APD in 5 days]. 379 71

Impromidine (SK&F 92676), a potent selective histamine H2-receptor agonist in animals has been studied in healthy male volunteers. Impromidine 10 micrograms kg-1h-1 i.v. produced near maximal acid secretion and cimetidine 2 mg kg-1h-1 inhibited this output by a mean of 65% in 5 subjects. The log dose-response curve to impromidine in 5 subjects was linear over the dose range 2.5--20 micrograms kg-1h-1. Cimetidine 0.5 mg kg-1h-1 caused a highly significant parallel shift of the dose-response curve, consistent with direct competitive antagonism. The gastric secretory responses to impromidine 10 micrograms kg-1h-1 i.v., histamine acid phosphate 40 micrograms kg-1h-1 i.v., and pentagastrin 6 micrograms kg-1h-1 i.v. were similar. Cardiovascular effects of impromidine were less marked than those due to histamine. Gastric secretory and cardiovascular effects of impromidine are dose dependent. No significant difference was seen in peak acid output between impromidine 10 micrograms kg-1 and pentagastrin 6 micrograms kg-1 whether injected intramuscularly or subcutaneously. Headache which accompanied infusion with histamine occurred less frequently with impromidine, and nausea and abdominal discomfort which occurred with pentagastrin did not occur with impromidine. Impromidine will be valuable in the study of gastric secretion and the role of histamine H2 receptors in other systems.
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PMID:Gastric secretory studies in humans with impromidine (SK&F 92676)--a specific histamine H2 receptor agonist. 615 65

To assess the value of high-dose dexamethasone therapy in preventing the gastrointestinal (GI) side effects of chemotherapy, a randomized double-blind study was conducted in women receiving outpatient therapy for breast cancer. Single-dose dexamethasone sodium phosphate (10 mg) or placebo was administered intravenously in 57 trials in 22 women immediately before chemotherapy. Questionnaires (administered before therapy and 24 hours later) were compared for evidence of nausea, vomiting, and anorexia produced by chemotherapy. No GI intolerance to chemotherapy was noted in 24 (83%) of the 29 dexamethasone trials v 16 (57%) of the 28 placebo trials. Dexamethasone trials produced the following results: no side effects in 50% (14/29), insomnia the night after chemotherapy in 21% (6/29), an increase in energy levels in 24% (7/29), and an improvement in mood in 14% (4/29). High-dose dexamethasone therapy has useful application in alleviating the emetic effects of cancer chemotherapy.
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PMID:Antiemetic efficacy of dexamethasone therapy in patients receiving cancer chemotherapy. 634 9

The basis of conservative treatment in chronic uremia is the restriction of protein, which lowers blood urea and diminishes nausea, vomiting and other uremic symptoms. Protein restriction to less than 25-30 g per day in adult patients may lead to negative nitrogen balance and protein depletion, which can be prevented by supplementing the diet with essential amino acids or a mixture of essential keto acid analogues and amino acids. The traditional view has been that low protein diet affords symptomatic relief in chronic uremia but does not effect the progression of renal failure. However, recent clinical results, mostly retrospective, suggest that protein restriction may retard or halt progression. This has led to a renewed interest in therapy with low protein diet and essential amino acids or keto analogues, since this form of treatment may postpone the time when the patient has to be started on dialysis, or even make dialysis unnecessary. It is not settled by which mechanism protein restriction effects progression of renal failure. According to one hypothesis, hyperphosphatemia (high Ca X P product) is harmful for the diseased kidneys; protein restriction is beneficial, since a low protein diet is generally also low in phosphate. An alternative hypothesis suggests that glomerular hyperfiltration in the remaining nephrons of the diseased kidneys is harmful and leads to glomerulosclerosis; low protein intake protects the kidney by abolishing glomerular hyperfiltration.
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PMID:Discovery and rediscovery of low protein diet. 636 67


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