Chronic dialysis, NAT2 polymorphisms, and the risk of isoniazid-induced encephalopathy - case report and literature review.

ABSTRACT:

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 dose

SUBMITTER: Constantinescu SM 

PROVIDER: S-EPMC5584033 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature