NAT2 slow acetylator — isoniazid metabolism
One copy of the NAT2*6 slow-acetylator variant detected.
You have one slow-acting copy of the NAT2 gene.
Likely intermediate or slow acetylator status. Slightly slower clearance of isoniazid (TB therapy) and several other drugs. Effect varies; full NAT2 phenotyping requires multiple SNPs.
Your body likely clears the TB drug isoniazid and a few other medicines slightly more slowly than average. The effect is small, and a full picture would need additional DNA testing.
What this means
NAT2 is a liver enzyme that conjugates aromatic amines, including isoniazid (used for TB), hydralazine, procainamide, and sulfasalazine. About half of European-descent and African-descent populations and a much smaller fraction of East Asian populations are slow acetylators. Slow acetylators have a modestly higher risk of isoniazid-induced hepatotoxicity and of drug-induced lupus from hydralazine.
NAT2 is an enzyme in your liver that breaks down a handful of specific medicines, including the TB drug isoniazid, the blood-pressure drug hydralazine, the heart-rhythm drug procainamide, and the inflammatory bowel medicine sulfasalazine. People naturally split into "fast" and "slow" acetylators depending on which versions of this gene they have: about half of European- and African-descent populations are slow, while it's much less common in East Asian populations. Slow acetylators have a modestly higher chance of liver side effects from isoniazid, and of a drug-induced form of lupus from hydralazine. For most medicines you encounter, this gene doesn't matter.
Caveats
- True NAT2 phenotype requires multiple SNPs to determine fully; this is one of several.
- The clinical effect is small unless one of the relevant drugs is prescribed.
- There's been longstanding debate about whether routine NAT2 testing improves TB treatment outcomes.