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)

Both isoniazid (INH) and cefazolin (CEZ) can have serious adverse effects on the central nervous system (CNS), causing seizures. In this study, we investigated the effect of INH on the pharmacodynamics of CEZ-induced seizures in rats. Male Wistar rats pretreated with INH (150 mg/kg i.p.) or saline received an intravenous infusion of CEZ at 3.2 g/h/rat until the onset of seizures, then samples of cerebrospinal fluid (CSF), blood (for serum), and brain were obtained immediately. The administration of INH was associated with a reduction in the total dose of CEZ required to produce seizures. The concentrations of CEZ in serum, brain, and CSF in INH-treated rats at the onset of seizures were significantly lower than those in control rats. In rats coadministered with pyridoxine (150 mg/kg s.c.), the concentration of CEZ in CSF at the onset of seizures was significantly higher than that in rats administered INH only. These results suggest that INH potentiates the sensitivity of the CNS to CEZ-induced seizures, and that the increased sensitivity is associated with the inhibition of vitamin B(6) metabolism by INH.
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PMID:Effect of isoniazid on the pharmacodynamics of cefazolin-induced seizures in rats. 1585 23

Isoniazid is an anti-tuberculosis drug, used commonly for treatment and prophylaxis of tuberculosis. Acute isoniazid intoxication is characterized by a clinical triad consisting of metabolic acidosis resistant to treatment with sodium bicarbonate, seizures which may be fatal and refractory to standard anticonvulsant therapy, and coma. Treatment requires admission to the intensive care unit for ventilatory support, management of seizures and metabolic acidosis. Pyridoxine, in a dose equivalent to the amount of isoniazid ingested, is the only effective antidote. We report the successful treatment of two isoniazid intoxication cases: the case of a child developing an accidental acute isoniazid intoxication and an adult case of isoniazid intoxication with the intent of suicide.
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PMID:Seizures, metabolic acidosis and coma resulting from acute isoniazid intoxication. 1611 96

Isoniazid (INH) has neurotoxic effects such as seizure, poor concentration, subtle reduction in memory, anxiety, depression and psychosis. INH-induced toxic effects are thought to be through increased oxidative stress, and these effects have been shown to be prevented by antioxidant therapies in various organs. Increased oxidative stress may be playing a role in these neurotoxic effects. N-methyl D-aspartat receptors (NMDA) are a member of the ionotropic group of glutamate receptors. These receptors are involved in a wide variety of processes in the central nervous system including synaptogenesis, synaptic plasticity, memory and learning. Erdosteine is a potent antioxidant and mucolytic agent. We aimed to investigate adverse effects of INH on rat hippocampal NMDAR receptors, and to elucidate whether erdosteine prevents possible adverse effects of INH. In the present study, compared to control group, NMDAR2A (NR2A) receptors were significantly decreased and malondialdehyde (MDA), end product of lipid peroxidation, production was significantly increased in INH-treated group. On the other hand, administration of erdosteine to INH-treated group significantly increased NR2A receptors and decreased MDA production. In conclusion, decreasing NR2A receptors in hippocampus and increasing lipid peroxidation correlates with the degree of oxidative effects of INH and erdosteine protects above effect of INH on NR2A receptors and membrane damage due to lipid peroxidation by its antioxidant properties.
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PMID:The effects of isoniazid on hippocampal NMDA receptors: protective role of erdosteine. 1613 24

A 25-year-old, 54-kg Hispanic man who had recently started multidrug therapy for pulmonary tuberculosis presented in status epilepticus after ingesting 9 g of isoniazid in a suicide attempt. Successful management of this patient required collaboration between several institutions to provide the large amount of necessary intravenous pyridoxine. Ultimately, this single overdose depleted the supply of intravenous pyridoxine for a significant region of the state of Nebraska. Isoniazid is commonly used to treat tuberculosis, but it is encountered relatively infrequently as the cause of an acute overdose. Severe isoniazid overdoses may present as seizure activity that is refractory to conventional antiepileptic therapy. Although intravenous pyridoxine is an effective antidote for isoniazid overdoses in patients presenting with status epilepticus, this agent has few indications and is typically stocked in limited quantities. In regions with large populations of patients who receive antituberculosis therapy, collaborative networks must be created to ensure that adequate supplies of intravenous pyridoxine (> or = 20 g) are available for effective treatment of isoniazid poisonings.
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PMID:Acute isoniazid toxicity and the need for adequate pyridoxine supplies. 1699 64

Tuberculosis has re-emerged as a significant public health threat over the last decade both globally and within Australia. This is thought to be largely due to the HIV epidemic, a growing itinerant population, and immigration. The antibiotic isoniazid remains an integral part of drug therapy. With the numbers of patients receiving isoniazid remaining high, the number of cases of acute poisoning is expected to be significant. This paper presents a series of two cases of isoniazid poisoning presenting to a tertiary referral centre in North Queensland. Isoniazid toxicity produces a triad of coma, metabolic acidosis and seizures. The seizures are often refractory to traditional antiepileptics. A specific antidote is available (pyridoxine [vitamin B6]) and both patients were administered this as part of their treatment. We also surveyed all hospitals in Australia with an accredited adult Emergency Department to assess the availability of pyridoxine.
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PMID:Isoniazid overdose : a case series, literature review and survey of antidote availability. 1753 59

Isoniazid is an effective and widely used drug in tuberculosis treatment. The administration of toxic amounts of INH causes recurrent seizures, profound metabolic acidosis, coma and even death but therapeutic dose of isoniazid is a very rare cause of seizures. We present a case of 44-year-old HIV positive African-American female who was recently started on a preventive dose of INH after being found purified protein derivative (PPD) positive. She developed status-epilepticus that did not respond to most of the antiepileptics. As soon as she received intravenous pyridoxine, the seizures terminated abruptly.
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PMID:INH induced status epilepticus: response to pyridoxine. 1861 Jun 79

Isoniazid is widely used to treat tuberculosis. In populations with a high prevalence rate of tuberculosis, acute ingestion of isoniazid has been reported as a potential cause of coma. In this study, we present the diagnosis and treatment of isoniazid poisoning in a case with acute coma as the major clinical presentation.A 32-year-old male who ingested 12 g isoniazid (2 hours prior to medical attention) was brought to the emergency department while in a coma and experiencing frequent seizures. Initial treatment with large doses of pyridoxine (for 6 hours) failed to awaken this patient. The patient was then given hemodialysis and pyridoxine; after 3 days he awoke from coma, with no further reported seizures.Isoniazid poisoning should be suspected in patients whose major symptoms are coma and seizure, especially those who have access to isoniazid. Monitoring the blood level of isoniazid will establish the diagnosis and help clinical management. A combination of hemodialysis and pyridoxine is effective in treating isoniazid poisoning.
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PMID:Coma caused by isoniazid poisoning in a patient treated with pyridoxine and hemodialysis. 1880 28

We report here an 11-year-old previously healthy girl with isoniazid intoxication who sustained a seizure-induced thoracic compression fracture. The following might be the first such case reported in the medical literature. Isoniazid toxicity should be suspected in any patient who comes to the emergency department with refractory seizures and metabolic acidosis. Forceful muscle contractions during a convulsive seizure can result in vertebral compression fracture, especially in the midthoracic region. A complaint of back pain after isoniazid-induced seizures in patients raises a strong suspicion of vertebral fracture and should be evaluated radiologically.
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PMID:Thoracic spine compression fracture during isoniazid-induced seizures: case report. 1909 63

Isoniazid (INH) is an integral component of treatment of tuberculosis. An acute overdose is potentially fatal and is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. The diagnosis of INH overdose should be considered in any patient who presents to emergency medical services (EMS) with the triad. We report a patient presenting with multiple generalised tonic clonic (GTC) convulsions with severe metabolic acidosis as a manifestation of INH toxicity.
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PMID:Isoniazid toxicity presenting as status epilepticus and severe metabolic acidosis. 1975 63

A series of 9H, 10H, 3-[N- 4 methyl -2-benzamido thiophen 3-yl carbonyl amino [2-(2'-phenyl 1'- ethylenyl)] 10-(aryl) thiazolidino [4, 5-b] 1, 5 benzodiazepine [7a-7h] were designed and synthesized to meet the structural requirements essential for anticonvulsant activity. Anticonvulsant activity was determined after intra-peritoneal administration to mice by supramaximal electroshock seizures model and Isoniazide Hydrazone induced seizures model. Motor impairement was determined using actophotometer and rotarod apparatus. Among the synthesized compounds two [JG 7a and JG 7e] compounds exhibited significant anticonvulsant activity after intra-peritoneal administration. Active compounds carry hydroxy substitutent at 2-position and methoxy at 4-position in the phenyl ring at C(5) of benzodiazepine. In present we study conclude that small polar and electron rich groups contribute significantly for anticonvulsant activity while electronegative substitutents showed lesser contribution for anticonvulsant activity.
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PMID:Design, synthesis and pharmacological screening of potential anticonvulsant agents using hybrid approach. 2003 7


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