Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy, serum concentration and side effects of CBZ for partial seizures in children were evaluated. The study was undertaken on 27 patients with partial seizures ranging from 5 to 17 years of age. Further 15 patients with various types of epilepsy taking CBZ with other anticonvulsants were selected as controls to compare the serum levels of CBZ. In nineteen of the 27 patients seizures were controlled completely, in whom serum CBZ levels varied fro trace to 15.6 mcg/ml, average being 8.18 +/- 3.40 mcg/ml, while those of uncontrolled ones ranged from 3.5 to 11.3 mcg/ml, average being 7.50 +/- 2.97 mcg/ml. There was no significant difference between both groups of the above. EEG was improved in the seven of 19 seizure-free cases, serum levels of which ranged from 5.9 to 13.2 mcg/ml. With regard to the side effects, transient leucopenia was observed in four patients and serum GOT and GPT slightly elevated in two. Correlation between dose and serum level in the monotherapy group was not significant as well as in the combined therapy group. Serum DBZ levels in the monotherapy group were significantly higher than those in combined therapy group.
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PMID:Carbamazepine as a sole anticonvulsant for partial seizures. 12 70

Liver function tests were carried out in 206 adults and children taking anticonvulsants to ascertain the prevalence of biochemical abnormalities in asymptomatic patients. It was observed that serum gamma-glutamyl transpeptidase was elevated in 74.6% of patients, alkaline phosphatase in 29.7% and alanine aminotransferase in 25.2% of cases. These figures are similar to those previously reported in the literature and probably reflect hepatic enzyme induction by the anticonvulsants. It is suggested that there is no value in the routine performance of liver function tests in patients with epilepsy. However, such patients should be informed of the symptoms of hepatic dysfunction and asked to report for liver function tests should they have such symptoms.
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PMID:Liver function tests in persons receiving anticonvulsant medications. 134 66

The effect of the experimental antiepileptic drug gabapentin (1-(aminomethyl) cyclohexane acetic acid; GPT) on the feline trigeminal complex was compared with the effect of established antiepileptic drugs and with the effect of GABAA and GABAB agonists and antagonists. Intravenous injection of 10-60 mg/kg GPT depressed the descending periventricular facilitation of trigeminal nucleus neurons, as well as segmental excitatory mechanisms. On the other hand, GPT usually facilitated, but sometimes depressed, both segmental and periventricular inhibitory mechanisms. GPT thus resembled carbamazepine and phenytoin in its action on excitatory mechanisms and on segmental inhibition, but differed in its effect on inhibitory pathways descending from the reticular formation. In agreement with our observations, GPT has been found to be effective against partial and generalized tonic-clonic seizures, similar to the spectrum of activity of carbamazepine and phenytoin. The action of GPT in our model also resembled that of the GABAB agonist baclofen in its facilitation of reticular and segmental inhibitory mechanisms and its depression of segmental excitatory mechanisms, but differed in its effect on excitatory mechanisms descending from the reticular formation. GPT has also been reported to mimic GABAB receptor activation in other experiments but appeared to act by a GABA-receptor independent mechanism.
Epilepsy Res 1991 Apr
PMID:Comparison of gabapentin with other antiepileptic and GABAergic drugs. 186 22

A cross-sectional study was performed to define patients at risk of developing liver disease due to long-term treatment with anticonvulsive drugs. The activities of gamma-glutamyltransferase, aspartate aminotransferase, and alanine aminotransferase and the concentrations of primidone, phenobarbital, phenytoin, and valproic acid in serum were estimated. Epileptic children before therapy were used as controls. The results indicated enzyme induction due to phenobarbital and both enzyme induction and liver cell damage or plasma membrane leakage due to phenytoin. Gamma-glutamyltransferase may be an early indicator of liver disease due to valproic acid.
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PMID:Effects of anticonvulsive drugs on the activity of gammaglutamyltransferase and aminotransferases in serum. 287 3

The anticonvulsant drug, primidone, was believed to be responsible for the development of hepatic cirrhosis in a 9-year-old German Shepherd Dog with idiopathic epilepsy. Marked increases in serum alanine aminotransferase, serum alkaline phosphatase, total bilirubin, and sulfobromophthalein retention, as well as decreases in albumin and BUN supported the diagnosis of hepatic failure. Biochemical abnormalities improved after primidone was discontinued. Previous reports indicated a poor prognosis for anticonvulsant-induced hepatic failure; however, this dog has remained stable for over a year after diagnosis and proper therapy.
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PMID:Hepatic cirrhosis associated with long-term primidone therapy in a dog. 399 53

A case of deletion of the short arm of chromosome 3 (46,XY,del(3)(p253) is described. The patient is a youth of 18 years in an institution for the mentally retarded. Phenotypically, he presents congenital heart disease, hypertelorism, ptosis, epicanthus, blepharophimosis, strabismus, nystagmus, synophrys, low-set ears, frequent infections, epilepsy (abnormal EEG and grand mal seizures), "rocker bottom" feet, flat occiput and muscular hypotonia. The parents are healthy and with normal karyotypes. A silent allele in the GPT system was found in the mother, the propositus and 4 of the 5 siblings.
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PMID:Partial deletion of the short arm of chromosome 3. 722 94

Serum amino acid (AA) profiles are altered in epilepsy. It is not clear whether this is due to the disease process itself or to other variables such as seizure type, seizure frequency, duration of illness, medication, or altered liver function. We investigated serum AA profiles and liver enzymes in 73 epileptic patients and 90 healthy subjects and evaluated the data by analysis of variance to discriminate between age, sex, seizure type, duration of illness, seizure frequency, antiepileptic drug (AED) and increased serum liver enzyme levels, and their putative interaction with the serum AA profile. There was no correlation between the changes in the AA profile and age, duration of illness, seizure frequency, and seizure type. Seventy-two percent of the AED-treated patients and 33% of the unmedicated patients showed an increase in one or several serum liver enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), and/or gamma-glutamyl transferase (gamma-GT)]; particularly gamma-GT. We observed a significant increase in serum concentrations of glutamine and glycine and decreased levels of taurine, threonine, serine, valine, methionine, isoleucine, leucine, phenylalanine, histidine, tryptophan, and arginine in AED-treated patients but not in unmedicated patients. These results show that the changes in the serum AA profiles of epileptic patients treated with AEDs occur in patients with alteration of serum liver enzymes; whether this implies a causal relation is still uncertain.
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PMID:Serum amino acids, liver status, and antiepileptic drug therapy in epilepsy. 809 92

Chemotherapy with a combination of synthetic ACTH (ACTH-Zn) and valproic acid (VPA) induced remarkable hypofibrinogenemia in three children (5 months, 8 months, and 5 years and 10 months old) with intractable epilepsy. The lowest blood fibrinogen (Fbg) levels by this combination therapy were 22, 51 and 64 mg/dl (mean 45.7 mg/dl), respectively. These levels occurred, when ACTH-Zn was administered at an average dose of 0.33 mg/day (0.03 mg/kg/day) and the mean blood concentration of VPA was 59.7 micrograms/ml. With the administration of VPA without ACTH-Zn, the lowest blood Fbg levels were 232, 108 and 170 mg/dl (mean 170 mg/dl), respectively. The mean blood concentration of VPA was 109.0 micrograms/ml. The inadvertent-effects associated with this combination therapy consisted of thrombocytopenia (59,000/microliters) in one case and a mild GPT increase (65-109 IU/l) in three cases. However, all these changes were transient. No bleeding tendency was detected clinically, when this hypo-Fbg-emia appeared. The concentration of VPA and the blood level of Fbg were found inversely correlated with a correlation coefficient of -0.22 (p < 0.01) in 150 serum samples from 91 patients with childhood epilepsy treated with VPA without ACTH-Zn. In the three cases presented, the combination with ACTH-Zn resulted in considerably lower blood Fbg levels than those predicted from the blood VPA concentrations. This indicates that the combination of ACTH-Zn and VPA induces a further decrease of Fbg in blood. The reason why hypo-Fbg-emia results from this combination therapy is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Three cases of hypofibrinogenemia induced by chemotherapy with a combination of synthetic ACTH and valproic acid]. 828 Apr 48

Gabapentin is a novel anticonvulsant drug. The anticonvulsant mechanism of gabapentin is not known. Based on the amino acid structure of gabapentin we explored its possible effects on glutamate and gamma-aminobutyric acid (GABA) metabolism in brain as they may relate to its anticonvulsant mechanisms of action. Gabapentin was tested for its effects on seven enzymes in the metabolic pathways of these two neurotransmitters: alanine aminotransferase (AL-T), aspartate aminotransferase (AS-T), GABA aminotransferase (GABA-T), branched-chain amino acid aminotransferase (BCAA-T), glutamine synthetase (Gln-S), glutaminase (GLNase), and glutamate dehydrogenase (GDH). In the presence of 10 mM gabapentin, only GABA-T, BCAA-T, and GDH activities were affected by this drug. Inhibition of GABA-T by gabapentin was weak (33%). The Ki values for inhibition of cytosolic and mitochondrial forms of GABA-T (17-20 mM) were much higher than the Km values for GABA (1.5-1.9 mM). It is, therefore, unlikely that inhibition of GABA-T by gabapentin is clinically relevant. As with leucine, gabapentin stimulated GDH activity. The GDH activity in rat brain synaptosomes was activated 6-fold and 3.4-fold, respectively, at saturating concentrations (10 mM) of leucine and gabapentin. The half-maximal stimulation by gabapentin was observed at approximately 1.5 mM. Gabapentin is not a substrate of BCAA-T, but it exhibited a potent competitive inhibition of both cytosolic and mitochondrial forms of brain BCAA-T. Inhibition of BCAA-T by this drug was reversible. The Ki values (0.8-1.4 mM) for inhibition of transamination by gabapentin were close to the apparent Km values for the branched-chain amino acids (BCAA) L-leucine, L-isoleucine, and L-valine (0.6-1.2 mM), suggesting that gabapentin may significantly reduce synthesis of glutamate from BCAA in brain by acting on BCAA-T.
Epilepsy Res 1995 Sep
PMID:Effects of anticonvulsant drug gabapentin on the enzymes in metabolic pathways of glutamate and GABA. 856 62

In a prospective study 50 children with new onset epilepsy were investigated. Routine screening for complete blood count, serum protein, albumin, gamma-glutamyltransferase (gamma-GT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and coagulation studies before, 3, 6 and 9 weeks after commencement of antiepileptic therapy with valproate were carried out. Serum B12 and folate levels were also determined in 29 patients. The aim of the study was to evaluate the effect of VPA on these laboratory findings. We found a significant reduction of red blood count and platelet count, whereas MCV showed a significant upward trend. Vitamin B12 levels were elevated after starting VPA therapy. We found no elevations of liver enzymes, but a significant transient reduction of ALT after 3 and 6 weeks and significantly reduced serum protein and albumin after 3, 6 and 9 weeks. Coagulation studies revealed a significant downward trend in serum fibrinogen and upward trend in thrombin time. The other parameters showed no significant changes after onset of VPA treatment. We think that reduced red blood cell and platelet counts, and elevated MCV indicate a direct toxic effect on a hematopoietic precursor or stem cell in patients treated with VPA. Furthermore, reduced protein, albumin and fibrinogen indicate an impaired liver synthetic function in asymptomatic children treated with VPA monotherapy.
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PMID:Hematologic manifestations and impaired liver synthetic function during valproate monotherapy. 873 99


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