Indication
Seizure due to isoniazid toxicity
Seizure due to isoniazid toxicity is a severe, life-threatening neurological complication resulting from acute supratherapeutic exposure or overdose of the antitubercular agent isoniazid. Read more about Seizure due to isoniazid toxicity
4 drugs 4 manufacturers
Drugs that treat it
Common Seizure due to isoniazid toxicity therapies.
PYRIDOXINE HCL (pyridoxine HCl (vitamin B6))
PYRIDOXINE HCL (pyridoxine HCl (vitamin B6))
PYRIDOXINE HCL (pyridoxine HCl (vitamin B6))
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Coming soonSeizure due to isoniazid toxicity is a severe, life-threatening neurological complication resulting from acute supratherapeutic exposure or overdose of the antitubercular agent isoniazid.
It predominantly affects the central nervous system, occurring across all patient populations exposed to toxic levels.
Pathophysiologically, isoniazid inhibits pyridoxine phosphokinase and binds pyridoxal 5'-phosphate, depleting active vitamin B6 and arresting glutamic acid decarboxylase activity.
This depletion profoundly diminishes gamma-aminobutyric acid synthesis, leading to widespread loss of central inhibitory neurotransmission.
Clinically, this manifests as intractable, recurrent generalized tonic-clonic convulsions or status epilepticus that typically resist standard anticonvulsant therapy and are frequently accompanied by profound high-anion-gap lactic acidosis and coma.
- nih.gov
Seizure due to isoniazid toxicity is a severe, life-threatening neurological complication resulting from acute supratherapeutic exposure or overdose of the antitubercular agent isoniazid
- mhmedical.com
Seizure due to isoniazid toxicity is a severe, life-threatening neurological complication resulting from acute supratherapeutic exposure or overdose of the antitubercular agent isoniazid Pathophysiologically, isoniazid inhibits pyridoxine phosphokinase and binds pyridoxal 5'-phosphate, depleting active vitamin B6 and arresting glutamic acid decarboxylase activity This depletion profoundly diminishes gamma-aminobutyric acid synthesis, leading to widespread loss of central inhibitory neurotransmis...
- nih.gov
It predominantly affects the central nervous system, occurring across all patient populations exposed to toxic levels
- nih.gov
It predominantly affects the central nervous system, occurring across all patient populations exposed to toxic levels
- nih.gov
Clinically, this manifests as intractable, recurrent generalized tonic-clonic convulsions or status epilepticus that typically resist standard anticonvulsant therapy and are frequently accompanied by profound high-anion-gap lactic acidosis and coma
- nih.gov
Clinically, this manifests as intractable, recurrent generalized tonic-clonic convulsions or status epilepticus that typically resist standard anticonvulsant therapy and are frequently accompanied by profound high-anion-gap lactic acidosis and coma
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