Individuals who are slow acetylators (i.e. have a relatively low activity of hepatic N-acetyltransferase):
Correct Answer: D
Rationale: Slow acetylators have reduced hepatic N-acetyltransferase (NAT2) activity, affecting metabolism of drugs like hydralazine, isoniazid, and procainamide. In European Caucasians, prevalence is actually 50-60%, not 15-20%, making that statement inaccurate. Gold treatment side effects like thrombocytopenia or nephrotic syndrome aren't strongly linked to acetylation status, but rather to immune responses, so that's less relevant. Halothane hepatotoxicity relates to immune-mediated reactions or metabolites, not acetylation speed. Hydralazine, metabolized by NAT2, accumulates in slow acetylators, increasing risk of drug-induced lupus with antinuclear antibodies (ANA), a well-documented association. Agranulocytosis with clozapine isn't tied to acetylation but to idiosyncratic reactions. The ANA risk with hydralazine is the most accurate, reflecting its pharmacogenetic implications, critical for personalized dosing and monitoring.