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PubMed2006

Anticonvulsant hypersensitivity syndrome: cross-reactivity with tricyclic antidepressant agents.

BACKGROUND: Aromatic anticonvulsant agents such as carbamazepine and phenytoin can induce anticonvulsant hypersensitivity syndrome (AHS) at a frequency of 1 in 10,000 to 1 in 1,000 treated patients. The hypersensitivity syndrome is a potentially life-threatening adverse drug reaction with multiorgan involvement, and incidental reexposure must be strictly avoided. Patients and treating physicians must be informed and educated about the causal drug and its potential immunologic or toxicologic cross-reactivity with other compounds. It has been well established that for future antiepileptic drug therapy, carboxamides (carbamazepine and oxcarbazepine), phenytoin, and barbiturates (phenobarbital and primidone) have to be avoided owing to their high degree of cross-reactivity. Other anticonvulsant agents, such as valproic acid, benzodiazepines, and gabapentin, may be prescribed. OBJECTIVES: To present the clinical data for and to describe the potential cross-reactivity between aromatic anticonvulsant and tricyclic antidepressant agents in patients with carbamazepine- and phenytoin-induced AHS. METHODS: The knowledge of cross-reactivity among aromatic anticonvulsant agents mainly emerged from clinical experience and observations because diagnostic challenge tests are not advisable. Thirty-six patients with the diagnosis of AHS were instructed to contact our unit if the symptoms relapsed. RESULTS: Despite better knowledge of AHS, one third of the patients had avoidable recurrences after exposure to cross-reactive drugs. Besides the known cross-reactivity among aromatic anticonvulsant agents, we observed a recurrence of the hypersensitivity syndrome in 5 patients after the administration of tricyclic antidepressant agents. CONCLUSION: The important potential cross-reactivity between aromatic anticonvulsant and tricyclic antidepressant drugs should be brought to the attention of treating physicians.

Adolescent↗
PubMedDate not supplied

[Efficacy of gabapentin in a sample of bipolar patients].

INTRODUCTION: Field studies support the idea of gabapentin being helpful in the maintenance, and in the treatment of some symptoms in bipolar patients. Our study evaluates relapse rates previous and after gabapentin administration in severe bipolar patients. METHODOLOGY: Gapabentine was administered to all consecutive bipolar patients from a relapse prevention program who could not be given lithium, valproic acid or carbamacepin because of his current medical condition or his past history of secondary effects or lack of response to those treatments. Number and severity of relapses were evaluated before and after gabapentin administration. RESULTS: Seven patients were included in the study. Medium maintenance period with gabapentine was 9 months. In the gabapentin period, relapses per month increased from 0.18 in the previous three years to 0.29. This may be due because six patients interrupted abruptly previous treatment in less than 1 week. Relapses severity, evaluated by measuring length and number of hospitalisations, and number of interviews by month, was similar to the three previous years, and better than the period from the beginning of the condition. Clinical Global Impression evaluated gabapentin as similar to previous mood stabilizers in five patients and better in two. Irritability and dysphoria improved in all the patients. CONCLUSION: Although gabapentin may be helpful in some patients, a clinical essay that shows its efficacy as add-on treatment is need.

Acetates↗
PubMed1995

Effects of idrapril calcium on tissue angiotensin-converting enzyme in rats.

Tissue angiotensin-converting enzyme (ACE) inhibition was measured in rats after single intravenous (i.v.) and oral (p.o.) doses of idrapril calcium, and the correlation between peak inhibition and tissue concentration of the drug was investigated. Five minutes after idrapril calcium (3 mg/kg i.v. as free acid), ACE in the examined tissues (serum, lungs, kidneys, heart, aorta, adrenals, testes, and brain) showed > 50% inhibition, always associated with measurable amounts of idrapril. After 90 min, ACE activity was still inhibited only in serum, lungs, kidneys, and aorta, recovering to basal values by 8 h in all samples but serum. Oral idrapril calcium (30 mg/kg) produced > 50% peak ACE inhibition in serum, lungs, and kidneys, in which measurable levels of the drug were detected, and in the aorta, where idrapril was not detected. Other tissues showed neither marked inhibition nor measurable drug levels. Kinetics of ACE inhibition in affected tissue mirrored those observed after intravenous administration. Idrapril, despite its hydrophilic nature, is able to reach extravascular tissues and to inhibit local ACE. However, in no tissue did the effect on ACE last longer than in serum and the hypothesis of a peculiar role of tissue RAS in determining the hypotensive activity of idrapril calcium is not supported in rats.

Administration, Oral↗
PubMed1988

The effects of gabaculine in vivo on the distribution of GABA-like immunoreactivity in the rat retina.

gamma-Aminobutyric acid (GABA) is an inhibitory transmitter found in the retinae of mammals largely within certain amacrine cells. In previous studies from this laboratory, subcutaneous administration to rats of gabaculine, an enzyme-activated irreversible inhibitor of gamma-aminobutyric acid (GABA)-transaminase, produced large, rapid and long-lasting increases in levels of retinal GABA. We employed immunocytochemistry to determine whether such changes in the levels of retinal GABA are accompanied by changes in the cellular distribution of GABA. Using a recently developed antiserum to a GABA-protein conjugate, and the peroxidase-antiperoxidase method, we examined retinae from control rats and from rats 2 or 8 h after administration of 10 mg/kg gabaculine. From previous work, retinal levels of GABA were respectively elevated 3- or 6-fold at those postgabaculine times. In the present study, marked changes in the distribution of GABA-like immunoreactivity (GABA-LIR) were apparent by 2 h after injection of gabaculine, and were more striking at 8 h postgabaculine. The pattern of staining for GABA-LIR strongly suggested that much of the GABA in gabaculine-treated retinae was within Müller glial cells. That observation provides evidence for the importance of those cells in the uptake and degradation of GABA after its release from retinal neurons.

Animals↗
PubMed1972

Mapping of the tryptophan genes of Acinetobacter calcoaceticus by transformation.

Auxotrophs of Acinetobacter calcoaceticus blocked in each reaction of the synthetic pathway from chorismic acid to tryptophan were obtained after N-methyl-N'-nitro-N-nitrosoguanidine mutagenesis. One novel class was found to be blocked in both anthranilate and p-aminobenzoate synthesis; these mutants (trpG) require p-aminobenzoate or folate as well as tryptophan (or anthranilate) for growth. The loci of six other auxotrophic classes requiring only tryptophan were defined by growth, accumulation, and enzymatic analysis where appropriate. The trp mutations map in three chromosomal locations. One group contains trpC and trpD (indoleglycerol phosphate synthetase and phosphoribosyl transferase) in addition to trpG mutations; this group is closely linked to a locus conferring a glutamate requirement. Another cluster contains trpA and trpB, coding for the two tryptophan synthetase (EC 4.2.1.20) subunits, along with trpF (phosphoribosylanthranilate isomerase); this group is weakly linked to a his marker. The trpE gene, coding for the large subunit of anthranilate synthetase, is unlinked to any of the above. This chromosomal distribution of the trp genes has not been observed in other organisms.

Alcaligenes↗
PubMed1994

Clinical pharmacokinetics of gabapentin.

Pharmacokinetic properties are important to consider in evaluating the usefulness of new antiepileptic drugs (AEDs). Gabapentin is a new, water-soluble, antiepileptic agent with properties of an amino acid. This drug is rapidly absorbed and exhibits dose-dependent bioavailability as a result of a saturable transport mechanism. Plasma concentrations are essentially proportional to dosages up to 1,800 mg daily, which is the highest dosage used in double-blind, placebo-controlled clinical trials. Gabapentin is not protein-bound. A high volume of distribution indicates greater concentration in tissue than in plasma. It is not metabolized and does not induce hepatic enzymes or inhibit metabolism of other antiepileptic drugs. As a result, metabolism-related factors do not necessitate dosage alterations of gabapentin and concomitant AEDs after prolonged therapy. The drug is excreted unchanged in urine; plasma clearance is linearly related to creatinine clearance; and dosage is readily adjusted based on renal function. The elimination half-life is approximately 5 to 9 hours. Consequently, three divided doses are usually required per day, but steady state is rapidly achieved. No significant interactions between gabapentin and standard antiepileptic drugs or oral contraceptives have been observed. These and other pharmacokinetic properties make gabapentin unique among available AEDs.

Acetates↗
PubMed2001

Function of leucine in excitatory neurotransmitter metabolism in the central nervous system.

A novel hypothesis for the role of branched-chain amino acids (BCAA) in regulating levels of the major excitatory neurotransmitter glutamate in the central nervous system is described. It is postulated that the branched-chain aminotransferase (BCAT) isoenzymes (mitochondrial BCATm and cytosolic BCATc) are localized in different cell types and operate in series to provide nitrogen for optimal rates of de novo glutamate synthesis. BCAA enter the astrocyte where transamination is catalyzed by BCATm, producing glutamate and branched-chain alpha-keto acids (BCKA). BCKA, which are poorly oxidized in astrocytes, exit and are taken up by neurons. Neuronal BCATc catalyzes transamination of the BCKA with glutamate. The products, BCAA, exit the neuron and return to the astrocyte. The alpha-ketoglutarate product in the neurons may undergo reductive amination to glutamate via neuronal glutamate dehydrogenase. Operation of the shuttle in the proposed direction provides a mechanism for efficient nitrogen transfer between astrocytes and neurons and synthesis of glutamate from astrocyte alpha-ketoglutarate. Evidence in favor of the hypothesis is: 1) The two BCAT isoenzymes appear to be localized separately in the neurons (BCATc) or in the astroglia (BCATm). 2) Inhibition of the shuttle in the direction of glutamate synthesis can be achieved by inhibiting BCATc using the neuroactive drug gabapentin. Although gabapentin does not inhibit BCATm, it does block de novo glutamate synthesis from alpha-ketoglutarate. 3) Conversely, gabapentin stimulates oxidation of glutamate. Inhibition of BCATc may allow BCKA to accumulate in the astroglia, thus facilitating conversion of glutamate to alpha-ketoglutarate.

Acetates↗
PubMed1995

Mechanisms of action of antiepileptic drugs.

Depending on their mechanism of action, anticonvulsant drugs in clinical use may be divided into three groups: those drugs which facilitate gamma-aminobutryic acid (GABA)ergic neurotransmission; those which block neuronal ion channels; and those whose mechanism of action is unresolved. The compounds acting on GABAergic systems may be further subdivided into those which modulate transmission through chloride channels, e.g. the barbiturates and the benzodiazepines; those compounds, in particular vigabatrin, which reduce the degradation of GABA by blocking GABA transaminase; and those which inhibit the re-uptake of GABA into the presynaptic terminal. The other group of compounds whose mechanism of action is known are those which block neuronal ion channels. Blockage of voltage-operated sodium channels by lamotrigine, phenytoin or carbamazepine leads to decreased electrical activity and, probably, a subsequent reduction in glutamate release. Conversely, ethosuximide, blocks voltage-operated calcium channels, especially those which mediate calcium currents in thalamic neurones. Of those drugs in which the mechanism of action is unknown, sodium valproate is the prime example. An antagonistic action at the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor might also be a possibility, which could be the case with some of the newer compounds currently undergoing evaluation.

Acetates↗
PubMed1981

Gabaculine and m-carboxyphenyl-pyridoxamine 5-phosphate as probes of the catalytic binding sites of 4-aminobutyrate aminotransferase.

A homogeneous 4-aminobutyrate aminotransferase isolated from pig brain exhibits a k(cat) of 9.6 s-1 and contains one mole of pyridoxal 5-phosphate/mole of dimer. THe reaction of the enzyme with gabaculine (5-amino-1,3-cyclohexadiene carboxylic acid) was studied by observing changes in the absorption spectrum of the bound cofactor and by monitoring loss of catalytic activity. The enzyme is completely inactivated by gabaculine, but the dialyzed inactive sample containing 0.5 mol of gabaculine/mol dimer is fully reconstituted by addition of pyridoxal 5-phosphate. Stopped-flow kinetic studied reveal that gabaculine reacts with the cofactor bound to the aminotransferase with a second-order rate constant of 2.5 X 10(3) M-1 s-1. Fluorometric titrations of the apoprotein with m-carboxyphenyl-pyridoxamine 5-phosphate show the binding of two moles of inhibitor/mole of enzyme. The binding process is reversible and the affinity of the apoprotein for the inhibitor is at least 10-fold higher than the affinity for the cofactor. It is postulated that the dimeric enzyme contains two potential active sites per dinner, but the binding site characterized by a weaker affinity constant for pyridoxal 5-phosphate becomes functional only after specific chemical modification of the molecule of cofactor tightly bound to the protein.

4-Aminobutyrate Transaminase↗
PubMed1969

Organization of enzymes in the polyaromatic synthetic pathway: separability in bacteria.

ULTRACENTRIFUGATION IN SUCROSE DENSITY GRADIENTS WAS EMPLOYED TO ESTIMATE THE MOLECULAR WEIGHTS AND TO DETERMINE POSSIBLE PHYSICAL AGGREGATION OF THE FIVE ENZYMES CATALYZING STEPS TWO TO SIX IN THE PRECHORISMIC ACID PORTION OF THE POLYAROMATIC SYNTHETIC PATHWAY IN SIX SPECIES OF BACTERIA: Escherichia coli, Salmonella typhimurium, Aerobacter aerogenes, Bacillus subtilis, Pseudomonas aeruginosa, and Streptomyces coelicolor. The five enzymes were not aggregated in extracts of any of the species examined, nor are the genes encoding these enzymes clustered in those bacterial species for which genetic evidence exists. (An initial examination of the blue-green alga Anabaena variabilis indicates nonaggregation in this species also.) This situation in bacteria is in marked contrast to that found in Neurospora crassa and other fungi in which the same five enzymes are associated as an aggregate encoded (at least in the case of N. crassa) by a cluster of five genes. In addition, also in contrast to N. crassa, no evidence was obtained for more than one kind of dehydroquinase activity in any of the bacteria examined. These comparative results are discussed in relation to the origin, evolution, and functional significance of the gene-enzyme relationships existing in the early steps of aromatic biosynthesis in bacteria and fungi.

Alcohol Oxidoreductases↗
PubMed1999

Gabapentin in the management of convulsive disorders.

Gabapentin, in clinical use since 1993, is indicated as an adjunctive antiepileptic drug (AED) for treatment of complex partial seizures, with or without secondary generalization, in patients over 12 years of age. Although several cellular actions have been described in the literature, the molecular mechanism(s) of action responsible for the anticonvulsant effect of gabapentin has not been conclusively determined. It is likely that gabapentin has multiple concentration-dependent actions that combine in a unique manner to produce antiepileptic efficacy. The pharmacokinetic properties of this water-soluble, amino-acid AED are generally favorable. Absorption appears to be dependent on transport by the L-system amino acid transporter. Elimination of unmetabolized drug occurs by the renal route. Although its therapeutic range is not well characterized, gabapentin has a broad therapeutic index. This implies that a wide range of doses can be used, based on individual patient needs, without significant limitation due to dose-dependent side effects. Gabapentin has few drug-drug interactions, none of which is clinically limiting. Several studies have demonstrated the long-term efficacy of gabapentin with no systematic evidence of tachyphylaxis. In addition, there is increasing evidence to support the use of gabapentin as monotherapy. Gabapentin is safe and is generally well tolerated. To date, nearly 3 million patients have been treated in studies and in open use without causal relationship to a specific life-threatening organ toxicity. Seizure control superior to that observed in well-controlled trials has been reported at higher doses used in clinical practice and in studies. Therefore, gabapentin dosing must be optimized on an individual basis to achieve an adequate trial of the drug and obtain the best seizure control.

Acetates↗
PubMed1992

Pharmacology of idrapril: a new class of angiotensin converting enzyme inhibitors.

Idrapril is the prototype of a new chemical class of angiotensin converting enzyme (ACE) inhibitors, the hydroxamic non-amino acid derivatives. Idrapril strongly inhibited rat and human plasma ACE and rabbit lung ACE (IC50: 7-12 nM) as well as the pressor response induced by angiotensin I in anesthetized rats (ED50: 63 nmol/kg i.v.). Idrapril (0.04-23 mumol/kg i.v.) lowered the blood pressure dose dependently, up to 20-35%, in different models of hypertension (sodium-depleted spontaneously hypertensive rat, two-kidney-one-clip renal hypertensive rat, and aortic-coarctated rat), its profile being similar to that of captopril in terms of potency and efficacy. Idrapril and captopril reduced the blood pressure and potentiated substance P-induced bronchoconstriction in the guinea pig to the same extent, suggesting a similar degree of ACE inhibition in the circulation. However, idrapril potentiated capsaicin-induced bronchoconstriction (a model that has been related to the liability of ACE inhibitors to produce cough in patients) less effectively than captopril. We conclude that effective ACE inhibition in vitro and in vivo can be obtained with this novel class of compounds.

Angiotensin I↗
PubMed2005

Rapid quantification of gabapentin in human plasma by liquid chromatography/tandem mass spectrometry.

A simple, sensitive and rapid liquid chromatography/tandem mass spectrometry (LC-MS/MS) method was developed and validated for the quantification of gabapentin, a new antiepileptic drug, in human plasma using its structural analogue, 1,1-cyclohexane diacetic acid monoamide (CAM) as internal standard. The method involved a simple protein precipitation by means of acetonitrile followed by a rapid isocratic elution with 10mM ammonium formate buffer/acetonitrile (20/80, v/v, pH 3.0) on Waters Symmetry C(18 reversed phase chromatographic column and analyzed by mass spectrometry in the multiple reaction monitoring mode. The precursor to product ion transitions of m/z 172-->154 and m/z 200-->182 were used to measure the analyte and the IS, respectively. The assay exhibited a linear dynamic range of 40-10000 ng/mL for gabapentin in human plasma. The limit of detection and lower limit of quantification in human plasma were 10 and 40 ng/mL, respectively. Acceptable precision and accuracy were obtained for concentrations over the standard curve ranges. A run time of 2 min for each sample made it possible to analyze a throughput of more than 400 human plasma samples per day. The validated method has been successfully used to analyze human plasma samples for application in pharmacokinetic, bioavailability or bioequivalence studies.

Amines↗
PubMed1996

The novel anticonvulsant drug, gabapentin (Neurontin), binds to the alpha2delta subunit of a calcium channel.

Gabapentin (1-(aminomethyl)cyclohexane acetic acid; Neurontin) is a novel anticonvulsant drug, with a mechanism of action apparently dissimilar to that of other antiepileptic agents. We report here the isolation and characterization of a [3H]gabapentin-binding protein from pig cerebral cortex membranes. The detergent-solubilized binding protein was purified 1022-fold, in a six-step column-chromatographic procedure, with a yield of 3.9%. The purified protein had an apparent subunit Mr of 130,000, and was heavily glycosylated. The partial N-terminal amino acid sequence of the Mr 130,000 polypeptide, EPFPSAVTIK, was identical to that reported for the alpha2delta subunit of the L-type Ca2+ channel from rabbit skeletal muscle (Hamilton, S. L., Hawkes, M. J., Brush, K., Cook, R., Chang, R. J., and Smilowitz, H. M. (1989) Biochemistry 28, 7820-7828). High levels of [3H]gabapentin binding sites were found in membranes prepared from rat brain, heart and skeletal muscle. Binding of [3H]gabapentin to COS-7 cells transfected with alpha2delta cDNA was elevated >10-fold over controls, consistent with the expression of alpha2 delta protein, as measured by Western blotting. Finally, purified L-type Ca2+ channel complexes were fractionated, under dissociating conditions, on an ion-exchange column; [3H]gabapentin binding activity closely followed the elution of the alpha2 delta subunit. [3H]Gabapentin is the first pharmacological agent described that interacts with an alpha2delta subunit of a voltage-dependent Ca2+ channel.

Acetates↗
PubMed2003

Gabapentin: in postherpetic neuralgia.

Gabapentin is a structural analogue of the neurotransmitter gamma-aminobutyric acid (GABA) approved for use in adults with postherpetic neuralgia. Gabapentin does not bind to GABA(A) or GABA(B) receptors. Its mechanism of action in humans is unclear, but may involve binding to alpha2delta calcium channel subunits in animal models. Reductions in the mean daily pain score from baseline to week 7 or 8 of treatment (primary endpoint) were significantly greater with gabapentin 1800-3600 mg/day than placebo therapy in two well designed trials in patients with postherpetic neuralgia. The proportion of responders (patients showing a > or =50% reduction in mean daily pain score at endpoint versus baseline) was significantly greater with gabapentin than placebo. Daily sleep rating scores, the Short Form McGill Pain Questionnaire (total pain scores), Patient and Clinician Global Impression of Change and measures on the Short Form-36 Health Survey (including physical functioning, role-physical, bodily pain, vitality or mental health) improved to a significantly greater extent with gabapentin than placebo. Adverse events associated with gabapentin in patients with postherpetic neuralgia were usually mild to moderate in intensity, with dizziness, somnolence and peripheral oedema being commonly reported.

Acetates↗
PubMed1982

Feline generalized epilepsy induced by tranexamic acid (AMCA).

Epileptic activities induced by topical application of tranexamic acid (AMCA) and penicillin to the cortex of 12 cats in acute experiments were compared. Both substances when diffusely applied on a wide cortical area of both hemispheres at very low concentration produced an EEG pattern consisting of spike-wave bursts similar to the electrographic manifestations seen in feline generalized epilepsy induced by large parenteral doses of sodium penicillin. These epileptic bursts could be triggered by repetitive stimulation of nucleus centralis medialis. Increased concentrations of both AMCA and penicillin led to the appearance of bilaterally synchronous spikes and poly-spikes which were not further excited by NCM stimulation. Two factors seem to play an important role in eliciting spike-wave bursts in both models: (1) the area of the cortex exposed to the epileptogenic agent and (2) the concentration of the epileptogenic agent used. The similar effects observed in 5 chronic animals either by intravenous injection of high doses of AMCA or by intramuscular injection of sodium penicillin confirm the results obtained in acute experiments and suggest a new way of inducing feline generalized epilepsy.

Administration, Topical↗
PubMed2002

Newer antiepileptic drugs in bipolar disorder: rationale for use and role in therapy.

Antiepileptic drugs (AEDS) are used regularly in the treatment of patients with bipolar disorders. Carbamazepine and valproic acid (sodium valproate) are effective as antimanic treatments, and the success of these medications has prompted investigation of other AEDs as possible treatments in patients with mood disorders. Lamotrigine appears to be the most promising of the newer AEDs with respect to effects in mood disorders. Current evidence suggests efficacy of this drug both as monotherapy and as an adjunctive agent in bipolar depression, and studies are underway to clarify its efficacy in mood stabilisation and rapid cycling, as currently available data are equivocal. Use of gabapentin is not as well supported in the literature, although data from open trials using it as an adjunctive agent suggest that it may be helpful in patients with bipolar depression. There have been some open trials and case reports supporting the use of topiramate as an adjunctive agent for the treatment of mania; however, data from controlled trials are not yet available. Further controlled trials of lamotrigine, gabapentin or topiramate as monotherapy and adjunctive treatment are needed to clarify their potential roles in the treatment of patients with mood disorders.

Acetates↗
PubMed1981

The role of antifibrinolytic therapy in the preoperative management of recently ruptured intracranial aneurysms.

In a retrospective study of the use of antifibrinolytic therapy in a series of patients with recently ruptured intracranial aneurysms, 131 patients were selected based on the following criteria: commencement of therapy within 3 days of the last subarachnoid hemorrhage (SAH); continuation of therapy for at least 6 days; and apparently uncomplicated surgery. Two main modalities of antifibrinolytic therapy were used: Group A, tranexamic acid (AMCA) 3 gm daily plus aprotinin k.i.u. (kallikrein inactivating units) daily (82 cases); Group B, AMCA 6 gm daily (41 cases). The remaining 8 patients were treated with epsilon-aminocaproic acid alone or in combination with aprotinin and were not considered to constitute a large enough group for statistical comparison. The rest of the preoperative treatment consisted of bed rest; mild sedation; antihypertensives, if the blood pressure exceeded 160 mm Hg; and osmotic diuretics as needed. The mean interval between last SAH and operation was about 13 days in both groups. The rates of rebleeding and thromboembolism were similar in the two groups but the rates of ischemic complications and post-SAH hydrocephalus were higher in Group B. The difference in the rate of severe cerebral ischemic complications was statistically significant (11 of 82 in Group A versus 12 of 41 in Group B, p less than 0.02), and in the main they were present preoperatively. The rates of rebleeding (approximately 10%) and of death from rebleeding (approximately 5%) are lower than in other published series on the natural history of this condition. In cases in which antifibrinolytics are indicated, present evidence indicates that low-dose AMCA plus aprotinin seems to be a rational combination for lowering the rebleeding, ischemic complication, and post-SAH hydrocephalus rates.

Adult↗