Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiparkinsonian activity of lergotrile mesylate, a presumed dopaminergic receptor stimulating agent, was investigating in monkeys with surgically induced tremor and in parkinsonian patients. The administration of lergotrile resulted in a dose-dependent reduction in the intensity of tremor in the monkeys. In 13 patients with Parkinson's disease treated with lergotrile (up to 12 mg a day), overall improvement was observed in five. Tremor was the main clinical feature to benefit, and the improvement reached statistical significance. In a subgroup of four patients treated with a higher dose of lergotrile (up to 20 mg a day), further improvement in rigidity and bradykinesia was noted, but again, only improvement in tremor was statistically significant. Adverse effects included orthostatic hypotension, behavioral alterations, and nausea and vomiting. These were severe enough to result in drug withdrawal in three patients.
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PMID:Studies on the antiparkinsonism efficacy of lergotrile. 16 32

Ftorafur is a 5-fluorouracil analogue which is slowly metabolized to 5-FU, resulting in prolonged therapeutic levels of this latter drug. Ninety-one evaluable patients with metastatic breast cancer were treated with Ftorafur, Adriamycin, cyclophosphamide, and BCG (ACFTOR-BCG), in an attempt to increase the effectiveness of the program or decrease its myelosuppressive toxicity. The results of this trial were compared to those previously reported with the combination of 5-FU, Adriamycin, cyclophosphamide, and BCG (FAC-BCG). Overall objective response rates were 65% and 76% for ACFTOR-BCG and FAC-BCG, respectively. Durations of response were 12 months and 14 months for ACFTOR-BCG and FAC-BCG (p = 0.53). The median survival of responders was 22 and 23.9 months, respectively. Substantial toxicity was observed with Ftorafur: nausea and vomiting severe enough to cause weight loss was observed in a substantially higher fraction of the patients treated with this drug than with 5-FU. Other side-effects, which were not observed with the 5-FU combination, were somnolence, dizziness, personality changes, tremor, ataxia, and confusion. No differences in myelosuppressive toxicity were observed between the two combinations, and the incidence of infectious complications was identical. The combination of Ftorafur, Adriamycin, cyclophosphamide and BCG did not offer any advantages with respect to increased effectiveness or reduced toxicity over the FAC-BCG regimen in breast carcinoma.
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PMID:Ftorafur, adriamycin, cyclophosphamide and BCG in the treatment of metastatic breast cancer. 38 55

Twelve parkinsonian patients with an unsatisfactory therapeutic result on L-Dopa alone due to nausea, vomiting and involuntary movements were treated WITH L-Dopa and decarboxylase inhibitor. The daily dose reached 800mg L-Dopa and 200 mg decarboxylase inhibitor. Single doses of each of the components were also given. Electrophysiological examination of hypokinesia, tremor and rigidity, and clinical observation revealed clear evidence of rapid improvement on small doses of L-Dopa combined with decarboxylase inhibitor. Most of the improvement occurred during the 1st week before the maximal dose was reached. A single oral dose of decarboxylase inhibitor resulted in an improvement, suggesting the presence in the organism of a small AMOUNT OF L-Dopa. This work also shows the absence of liver toxicity of the drug used. Elimination of the extracerebral side effects nausea and vomiting in our opinion is a principle advantage of the compound compared to L-Dopa alone, wheras abnormal involuntary movements, which were found in all patients, remain the limiting adverse side effect.
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PMID:Treatment of parkinsonism with l-dopa and a decarboxylase inhibitor. An electrophysiological and clinical study. 114 54

Eighteen patients with parkinsonism were treated with a combination of L-dopa and peripheral decarboxylase inhibitor, L-alphahydrazinomethyldopa (MK-486). Modification of L-dopa effect by MK-486 was also studied in parkinsonian patients as well as in cats. (1) Concentrations of dopa and dopamine in plasma and brain were measured in cats following intraperitoneal injection of L-dopa alone (100 mg/kg) or combined with MK-486 (10 mg/kg). Dopa levels in plasma and brain in the combination with MK-486 were three times as high as in L-dopa alone. Dopamine levels in caudate nucleus and putamen were increased nearly fourfold with the combination. (2) Plasma dopa and dopamine levels were measured in parkinsonian patients. Clinical pharmacological studies disclosed that a 1 : 10 ratio of MK-486 to L-dopa in dosage was preferable. (3) Maximum plasma dopa levels with the combination were four times those following L-dopa alone. Plasma dopa sustained a high level over a period of five hours. MK-486 markedly reduced plasma levels of dopamine. (4) There was no significant difference in dopa and dopamine levels in cerebrospinal fluid between L-dopa alone and a combination of MK-486, but dopamine levels in the CSF were still high at four hours after the combination of MK-486. (5) In clinical studies of eighteen patients with parkinsonism, the effectiveness of the combination therapy (mean dosage of L-dopa: 750 mg/day) was observed in all cases. Marked improvement was noted in 10 cases out of 15 (67%) with akinesia, in 12 cases out of 17 (71%) with rigidity and in six cases out of 14 (43%) with tremor. Maximum plasma dopa levels were higher in those cases with marked improvement, and were highest in patients with diskinesias as a side effect. (6) An addition of vitamin B6 did not show adverse effects. (7) Transient nausea and vomiting as a side effect, less severe than those experienced with L-dopa alone, were noted in five cases (28%). Dyskinesias in extremities, face, mouth and tongue were observed in six cases (33%). These dyskinesias were seen in a high percentage of cases with marked improvement and were never observed in the extremities contralateral to the side of thalamotomy.
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PMID:L-dopa therapy combined with peripheral decarboxylase inhibitor (MK-486) in Parkinsonism. 115 13

Mitoxantrone is a new effective antineoplastic agent with activity against a wide range of tumors. Compared with the anthracycline drugs doxo- and daunorubicin, it exhibits a clearly lower toxicity and, most importantly, a reduced cardiotoxicity. The analysis of the side-effects recorded after accidental overdosage of the drug gives additional insight into its tolerability. Here we describe our observations in three patients who inadvertently received 100 mg m-2 (two pts) and 183 mg m-2 (one pt) as single slow bolus injections. The main side-effects were moderate nausea and vomiting, shaking chills, and profound but reversible neutro- and thrombocytopenia. There was no immediate cardiac toxicity. One patient with extensive previous daunomycin exposure developed congestive heart failure after 4 months. Two patients were not evaluable for late cardiac complications because of early death due to tumor progression.
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PMID:Accidental overdose of mitoxantrone in three patients. 255 63

Ethanol, a highly lipid-soluble compound, appears to exert its effects through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the gamma-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolised at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute ethanol poisoning and the ethanol withdrawal syndrome. 304 Dec 44

Ifosfamide was given to 61 patients with malignant solid tumors diagnosed before the age of 21 years. In this phase II study, all patients received 1.6 g/m2/day X 5 iv over 15 minutes followed by mesna at a dose of 400 mg/m2 iv at 15 minutes and 4 and 6 hours after ifosfamide. Responses were observed in five of 15 patients with osteosarcoma, two of ten with neuroblastoma, two of six with Wilms' tumor, two of five with rhabdomyosarcoma, four of eight with other soft tissue sarcomas, one of one with retinoblastoma, one of two with germ cell tumors, one of one with B-cell lymphoma, and one of one with a primitive neuroectodermal tumor. Fifty-nine of 61 patients had received prior alkylating agent therapy which included cyclophosphamide, cisplatin, mechlorethamine, melphalan, or dacarbazine. Fourteen of 19 responses developed in patients whose tumors were resistant to treatment with cyclophosphamide. A patient with malignant Schwannoma who had received no prior chemotherapy developed a complete response which lasted 12 months. A patient with brain metastases of osteosarcoma has had complete response for greater than 2 years. Complete response was also observed in a patient with B-cell lymphoma. Toxicity consisted of mild to moderate nausea and vomiting, transient reversible myelosuppression, occasional elevation of serum BUN or creatinine, and transient neurotoxicity characterized by somnolence, confusion, weakness, tremor, hallucinations, or seizures. We conclude that ifosfamide is an important alkylating agent without apparent complete cross-resistance with cyclophosphamide, and as such should be further investigated for determination of its activity in patients with pediatric neoplasms and considered for incorporation into phase II-III trials for certain tumors.
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PMID:Phase II trial of ifosfamide in children with malignant solid tumors. 310 34

A rare complication of nonsteroidal antiinflammatory drug (NSAID) use, particularly in patients with collagen vascular or autoimmune diseases, is aseptic meningitis. A healthy 21-year-old man receiving naproxen for muscle spasm was admitted with a chief complaint of severe headache. Approximately one week after beginning naproxen, the patient developed headache, fever (T 38.8 degrees C), shaking chills, and nuchal rigidity with occasional nausea and vomiting resulting in a 15-lb weight loss. Findings from a cerebrospinal fluid examination revealed polymorphonuclear pleocytosis and elevated protein, but no evidence of infection with bacteria, fungi, mycobacteria, or viral agents was noted. Within 36 hours of discontinuing naproxen, the meningitis-like symptoms markedly improved. Rechallenge with naproxen was not performed. In patients exhibiting meningitis-like symptoms, a thorough drug history, including that of recent or intermittent NSAID use, should be obtained.
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PMID:Aseptic meningitis associated with naproxen. 339 Nov 11

A 58-year-old woman was receiving chemotherapy for carcinoma of the breast. She was given 1,700 mg metoclopramide IV for 2 months to prevent nausea and vomiting. Within hours after metoclopramide was given, she had hand tremor, akathisia, and truncal and orofacial dyskinesia. These symptoms resolved, but she was left with persistent shoulder stump chorea, the perception of the phantom left arm involuntarily adducted at the shoulder and flexed at the elbow, and dystonic pronation and extension of the hand away from her body. The motor aspects of the phantom dyskinesia will be emphasized.
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PMID:Metoclopramide-induced phantom dyskinesia. 397 6

The symptoms include, by ascending order of severity: nightmares and insomnia, nausea and vomiting, muscular weakness or tremor, postural hypotension, hyperthermia, muscle twitching, convulsions, confusional state or psychosis. Prominent features are the late onset of these symptoms, several days after treatment has been discontinued, and the sometimes difficult diagnosis, since patients are usually unaware of their dependence on these drugs. Reinstituting benzodiazepine treatment, then withdrawing it progressively are the best curative measures. Prevention is easy if treatment is gradually rather than abruptly withdrawn in all patients who receive the compound in high dosage for more than one month.
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PMID:[Benzodiazepine physical dependence. 6 cases (author's transl)]. 610 22


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