What is the relationship between isoniazid and fast-acetylators?

Fast-acetylators metabolize isoniazid (INH) quickly due to the presence of specific genetic variants that enhance their ability to process the drug. This rapid metabolism can affect the drug's efficacy, as the quick breakdown may lead to lower levels of the drug in the system for an extended period.

Patients identified as fast-acetylators tend to excrete INH more efficiently, which can necessitate careful management of their treatment regimen to ensure adequate therapeutic levels are maintained. The concept of fast and slow acetylation is fundamentally linked to how individual differences in genetics impact drug metabolism, influencing not only dosing strategies but also the overall effectiveness of the therapy.

The other options did not accurately capture this relationship, as fast-acetylators do not require lower doses of the drug, do not metabolize it slowly, and still respond to INH, albeit potentially in a different dosage or regimen than slow-acetylators. Understanding these pharmacogenomic principles is crucial for optimizing treatment for tuberculosis with isoniazid and similar medications.