Drug penetrates well into sites of infection, including CSF and center of areas of caseous necrosis. Elimination is primarily biotransformation and to lesser extent, renal elimination. There are both fast and slow acetylators, genetically determined. This results in blood levels that vary by a factor of 4 to 6 fold. Slow acetylation predominant phenotype in most Scandinavians, Jews, and North African Caucasians.
Drug interaction is more likely with slow acetylators given 'normal' doses.
Isoniazid inhibits hepatic mixed function oxidases. Adverse Effects ca. Isoniazid increases the elimination of pyridoxine. Phenytoin, e.g., is metabolized by these oxidases and could accumulate in the presence of excess isoniazid. Mostly occurs 4 to 8 weeks after start of therapy.