Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A phase I clinical study of intravenous Tegafur was conducted in nineteen previously treated patients with primary lung cancer. The dose of Tegafur was elevated from 1.0 to 3.0 g/m2/day for five consecutive days to determine the maximum tolerated dose. The dose-limiting factors were gastrointestinal and neurological toxicity and fatigability observed with the dose level of 2.5 g/m2/day for 5 days. Hematologic, hepatic and renal toxicities were not observed. Gastrointestinal toxicity including nausea, vomiting, anorexia and diarrhea of over grade 2 were seen to result from the dose of 2.5 g/m2/day. Neurological toxicity consisted of headache, dizziness, anxiety and depression. At the dose level of 2.0 g/m2/day, one patient, who had epileptic seizures in the past, experienced a psychomotor seizure. Depression (Grade 2 CNS toxicity) was observed at the dose level of 3.0 g/m2/day. Dose limiting factors were neurological toxicities. The pharmacokinetics of tegafur and 5-FU (the active form of Tegafur) has been studied in all patients. Serum level of tegafur was measured by HPLC method, and serum level of 5-FU was analyzed by GC-MS method. At the dose level greater than 2.0 g/m2/day for 5 days, the mean serum 5-FU values appear over the therapeutic range (0.1 micrograms/ml). In conclusion, 2.5 g/m2/day for 5 days was considered to be MTD, and 2.0 g/m2/day for 5 days intravenous administration was recommended for the phase II trial of single agent chemotherapy.
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PMID:[High-dose Tegafur (FT) for primary lung cancer: a phase I trial]. 201 1

Seven weeks after a generalized cerebral seizure a 27-year-old woman from Ghana developed nausea, vomiting and weight loss, gradually increasing over two weeks. Cranial computed tomography revealed several hyperdense formations with extensive associated oedema and a midline shift. Among extensive biochemical tests only a raised erythrocyte sedimentation rate of 24/50 mm and leukopenia of 2,600/microliters (with normal differential count) were notable. Diagnostic laparotomy was performed because of sonographic and computed tomographic evidence of enlarged abdominal lymph nodes. Histological examination of representative lymph nodes and of tiny nodules deposited on the peritoneum revealed caseous granulomatous inflammation. Mycobacterium tuberculosis was cultured from these specimens. Antituberculosis treatment was started with 0.3 g/d isoniazid, 0.6 g/d rifampicin, 2 g/d pyrazinamide and 1 g/d streptomycin, plus dexamethasone, 4 mg four times daily. After eight weeks treatment an intracerebral focus, removed to exclude neoplasm, proved histologically to be a tuberculoma. Only after four months was it possible to reduce the glucocorticoid dosage to prednisone, 20 mg/d. The antituberculosis treatment was continued for 18 months, with only isoniazid and rifampicin taken during the last 14 months. Final clinical and biochemical examinations were unremarkable. Computed tomography demonstrated regression of the abdominal lymph nodes and the cerebral foci. The patient was without any symptoms.
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PMID:[The manifestations of extrapulmonary tuberculosis]. 201 78

A patient presented without symptoms 30 minutes after ingesting acetonitrile, also known as methylacyanide. He had prompt gastric lavage and activated charcoal administration. Hours later, the onset of clinical toxicity was heralded by mental status abnormalities and vomiting prior to a generalized seizure. Following administration of sodium thiosulfate, the patient made an uneventful recovery. A blood cyanide level drawn shortly after presentation, but reported after the patient had been discharged, documented significant exposure. During hospitalization, cyanide toxicity was inferred from the history of ingestion of acetonitrile, plus a significant absence of venous blood hemoglobin desaturation. Because even small amounts can be harmful and toxicity is delayed, all acetonitrile ingestions should be presumed dangerous. Patients should be observed and repeatedly evaluated for at least 24 hours. In the absence of cyanide level determinations, lethargy, vomiting, seizures, and the lack of normal venous blood hemoglobin desaturation are clues to cyanide toxicity.
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PMID:Cyanide toxicity from acetonitrile-containing false nail remover. 201 1

Cocaine abuse is associated with a constellation of serious medical complications. An unrecognized and recently described complication of cocaine use is rhabdomyolysis with acute renal failure. We describe the first patient identified in our institution with this entity, admitted to the medical services with oliguric acute renal failure. Three days prior to admission the patient had a cocaine snorting binge. He presented with bilateral flank pain, gross hematuria, vomiting and chills. No history of crush injury, prolonged immobilization and or seizures was reported. On admission the vital signs were normal, physical exam revealed periorbital edema and marked soft tissue neck swelling. Lab values: Bun 120 mgs%, Creat. 10.7 mgs%, Na 132 meq/lt, Co2 13mq/lt, Cl, 103meq/lt, Co2 13meq/lt, Ca 5.3 mgs%, CPK 30,800 U/L with a MM fraction of 98%, LDH 600 U/L, SGOT 300 U/L. The urine was dark red with a ph of 6.5 and 100 rbc/hpf. The anti-GBM antibody and blood cultures were negative. An abdominal sonogram was normal. He received peritoneal dialysis and was discharged on his 14th hospital day with a CPK of 2,800 U/L and decreasing azotemia. Cocaine associated rhabdomyolysis has only been recently described in the literature (AJM April, 88). Acute myoglobinuric renal failure needs to be added to the growing list of medical complications of cocaine use.
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PMID:Cocaine and rhabdomyolysis: report of a case and review of the literature. 207 48

A 12 year old girl with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes (MELAS) is reported. After a normal childhood, at 9 years of age she developed generalized and hemilateralized seizures. Posteriorly, these episodes became more frequent and were accompanied by headache, homonimous hemianopsia, ataxia, vomiting, photophobia, left hemiparesis, slurred speech and even convulsive status. Laboratory tests evidenced lactic acidosis, brain lucencies at CT Scan and ragged skeletal muscle fibers at muscle biopsy.
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PMID:[Mitochondrial encephalomyopathy, lactic acidosis and features of cerebrovascular disorders]. 207 86

42 dogs with non-Hodgkin's lymphoma (NHL) were randomized for treatment with either PEG-L-asparaginase 10 IU/kg intramuscularly (n = 22) or L-asparaginase 400 IU/kg intraperitoneally (n = 20). Another 20 dogs were treated with either PEG-L-asparaginase 30 IU/kg (n = 10) or L-asparaginase 400 IU/kg (n = 10). Each treatment protocol consisted of two asparaginase treatments followed by a 10-week period of induction chemotherapy and then maintenance on asparaginase until progression occurred. No significant differences were found between treatments in the response rates after 2 weeks of asparaginase therapy or in the time to relapse, the time to treatment failure or the remission period. The reaction to asparaginase after the initial 2 weeks was a prognostic factor for the total duration of remission under asparaginase maintenance therapy. No side-effects were noted in the dogs treated with PEG-L-asparaginase, whereas 14 (48%) of the L-asparaginase treated dogs had side-effects related to this drug, including anaphylactic shock (9), anorexia or vomiting (4), hypersensitivity-related oedema (3), seizures (1) and acute pancreatitis (1). No abnormalities in clotting times, fibrinogen levels or antithrombin-III levels were found in any of the 62 dogs. PEG-L-asparaginase has the same anti-tumour activity as native L-asparaginase in dogs with NHL, but lacks side-effects.
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PMID:Polyethylene glycol-L-asparaginase versus native L-asparaginase in canine non-Hodgkin's lymphoma. 214 33

The subacute toxicity of compound 1 was investigated in rats and dogs. Compound 1 was administered orally to rats of both sexes at daily doses of 0.5, 1.0 or 2.5 g/kg for 3 months. No change attributable to the administration of compound 1 was found either in blood count or in histopathological examination. Decreases in SGPT, alkaline phosphatase and lactic acid dehydrogenase and an increase in serum cholesterol were detected. Compound 1 was mixed with food and given to dogs of both sexes daily at doses of 0.2 or 0.5 g/kg for 3 months. Severe toxic symptoms including anorexia, emesis, ataxia and convulsive seizures were observed. A decrease in SGPT and increase in alkaline phosphatase were also detected. Hyperemia of the duodenal mucosa and severe kidney lesions were found in histopathological examination. Neither abnormality of appearance nor histopathological change was found in a pig receiving compound 1 at the daily dose of 0.1 g/kg for 3 months. The results suggest that there are differences of compound 1 metabolism among the species used in this study.
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PMID:[Species differences in subacute toxicity of pyrrole aldehyde N4-(4-methoxyphenyl) semicarbazone]. 215 Dec 66

Four mature infants developed intracranial haemorrhage at ages from ten hours to five weeks. No predisposing or provoking factors could be demonstrated. The symptoms were apnoea, vomiting, pyrexia, irritability, tremor, hypertonicity, seizures and tense fontanelle. The diagnosis was established by ultrasound scanning and confirmed by computed tomographic scanning. The infants developed hydrocephalus requiring treatment. During the period of observation, these infants showed normal psychomotor development and the neurological findings were normal.
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PMID:[Intracranial hemorrhage in mature infants without predisposing factors]. 218 Jan 63

With the advent of boric acid insecticides, accidental ingestion of the compound can be encountered in animals. Toxic levels of boric acid most commonly cause vomiting, depression, and, occasionally, diarrhea. Boric acid is, however, cytotoxic to all cells. If a sufficiently high level is ingested, seizures, renal tubular nephrosis, and, rarely, hepatotoxicity may be noted. Gastrointestinal evaluation and supportive care are usually of primary therapeutic importance, although in severe cases, exchange transfusion and/or peritoneal dialysis may be required to decrease blood boron concentrations.
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PMID:Toxicology of selected pesticides, drugs, and chemicals. Boric acid. 218 Jan 82

Poisonings resulting from DEET are rarely encountered in companion animals. In human patients, DEET toxicosis has been associated with the development of a toxic encephalopathy characterized by tremors, seizures, behavioral changes, and abnormal movements. Generally, DEET toxicosis in companion animals is of short duration and is characterized by vomiting, tremors, ataxia, and excitation. Treatment for DEET toxicosis includes symptomatic therapy and decontamination.
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PMID:Diethyltoluamide (DEET) insect repellent toxicosis. 218 Jan 85


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