Encephalopathy secondary to isoniazid in patients on hemodialysis (original) (raw)
Related papers
Isoniazid-induced Encephalopathy in a Chronic Kidney Disease Patient: A Case Report
2020
Drug-induced encephalopathy is a well-known side effect of many drugs. Isoniazid (INH), a first-line drug used in the treatment of tuberculosis, can cause encephalopathy in chronic kidney disease (CKD) patients though other isoniazid-related neurotoxicities are more commonly encountered in general population. We report isoniazid-induced encephalopathy in a female patient with CKD. She has been given rifampicin, INH, pyrazinamide, and ethambutol with pyridoxine and prednisolone for the treatment of Pott’s disease of cervical spine. The patient developed recurrent episodes of altered consciousness following the treatment. After exclusion of other causes, isoniazid-induced encephalopathy was suspected, which was further proved by symptomatic improvement after stopping isoniazid.
Journal of Rangpur Medical College
We report an isoniazid-induced encephalopathy in a man with chronic renal failure. Drug-induced encephalopathy is a common side effect of many drugs. Isoniazid (INH), a first-line drug for tuberculosis, can cause encephalopathy in patients with chronic kidney disease (CKD). For Pott's disease of the thoracic spine, he received rifampicin, INH, pyrazinamide, and ethambutol with pyridoxine and prednisolone. But the patient is free of pyridoxine for two and a half months. Subsequently, after treatment, the patient experienced recurrent episodes of altered consciousness, irrelevant conversations, and disorientation. After ruling out other causes, isoniazid-induced encephalopathy was suspected and confirmed by improvement of symptoms after discontinuation of high-dose isoniazid and pyridoxine. J Rang Med Col. March 2023; Vol. 8, No. 1:72-75
BMC Nephrology, 2017
Background: Isoniazid is the most widely used anti-tuberculosis agent, yet it may lead to life-threatening complications. Case presentation: Here we report the case of a chronic hemodialysis patient who developed severe encephalopathy after the start of isoniazid. Blood levels of isoniazid were elevated, and acetyl-isoniazid over isoniazid ratio was decreased 3 h after intake of the medication, suggesting that a slow acetylator phenotype may have contributed to drug toxicity, in addition to pyridoxal phosphate removal by dialysis. This hypothesis was confirmed by sequencing of NAT2, the gene responsible for isoniazid elimination, and identification of NAT2 polymorphisms compatible with a slow acetylator phenotype. Isoniazid withdrawal along with supplementation using high doses of pyridoxine successfully reversed the drug toxicity. Isoniazid toxicity occurs in populations at risk, including patients with chronic kidney failure or NAT2 polymorphisms, who have a disturbed metabolism of pyridoxine or isoniazid, respectively, and those on renal replacement therapies, in whom pyridoxal phosphatethe active metabolite of pyridoxineis inadvertently removed by dialysis. Conclusions: Physicians should be aware of the increased risk of isoniazid toxicity in patients on dialysis and in those with a slow acetylator phenotype conferred by NAT2 polymorphisms. Adaptation of prescriptioneither with higher doses of pyridoxine or decreased doses of isoniazid, respectivelyhas been suggested to reduce the risk of potentially life-threatening toxicity of isoniazid.
Seizures, Metabolic Acidosis and Coma Resulting from Acute Isoniazid Intoxication
Anaesthesia and Intensive Care, 2005
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.
Isoniazid induced Acute Metabolic Acidosis and Neurotoxicity–A Case Report and Review of Literature
Pharmacology, Toxicology and Biomedical Reports, 2015
Isoniazid (INH) is a crucial drug in the prevention and treatment of tuberculosis. INH is commonly known to cause derangements in liver function tests and peripheral neuropathy due to pyridoxine deficiency in slow acetylators. However, in toxic doses it is known to cause severe neurologic manifestations and acute metabolic acidosis. INH toxicity is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. Hence, the diagnosis of INH overdose should be considered in any patient who presents to Emergency medical services (EMS) with the triad. Though accidental overdose of anti-tuberculosis drugs have been reported in children and adults, acute toxicity is rare. When recognized, intravenous pyridoxine and correction of acidosis with sodium bicarbonate and supportive treatment is effective. The condition is easily treated with intravenous pyridoxine but if not treated in time could prove fatal. Unlike other poisonings, serum INH levels do not co-relate with either symptomatology or liver injury.
Pinar Tosun Tasar, Sevnaz Sahin, Niyazi Bozkurt, Abdullah Sayıner, Soner Duman, Fehmi Akcicek
Isoniazid is the most important antituberculosis medicine. Adverse effects are generally fever and rash. There are few case reports in the literature which identified high fever without rash associated with INH use. In this case report, we present a case with tuberculosis lymphadenitis and isoniazid-induced fever.
Seizures with single therapeutic dose of isoniazid
The Indian journal of tuberculosis, 2012
Isoniazid (INH) is an integral component of treatment of tuberculosis. An acute overdose is potentially fatal and is characterised by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. A case of isoniazid induced seizures after therapeutic dose of 600 mg. as a part of CAT I thrice weekly intermittent anti-tuberculosis regimen for pulmonary tuberculosis is reported. The frequency of the usage of Isoniazid as antituberculosis therapy requires that physicians be aware of such toxicity.
Case Report: Acute isoniazid intoxication after intentional ingestion
Wellcome Open Research
Isoniazid is an anti-tuberculosis medication that is extensively used for treatment and prevention of tuberculosis. Acute isoniazid poisoning is characterized by a clinical triad of recurrent seizures, raised anion gap metabolic acidosis and coma. The seizures are unresponsive to standard anticonvulsant drugs, instead requiring pyridoxine administered in a dose equal to the amount of isoniazid consumed. Due to the high incidence of tuberculosis in low-income countries like Nepal, isoniazid intoxication should be considered in any patient who present with such unresponsive seizures and coma. We report a case of a 31 years old woman from Nepal, who intentionally ingested 12 grams of isoniazid and presented with generalized tonic-clonic seizures. She was successfully managed with 10 grams of pyridoxine along with other supportive management, including sodium bicarbonate for metabolic acidosis and mechanical ventilation. Doctors working in low-income countries, like Nepal, where tubercu...