Pharmacogenetic factors, especially genetic aspects that modulate the plasma concentration of cocaine, could play a role in cocaine susceptibility and have yet to be studied. Once absorbed, cocaine is rapidly transformed in two main metabolites, benzoylecgonine and ecgonine methyl ester, both of which are pharmacologically inactive [18]. The hydrolysis that leads to the formation of ecgonine methyl ester is catalyzed by butyrylcholinesterase (BChE), which is an enzyme involved in the metabolism of certain drugs (including cocaine and heroin), various local anesthetics, and short-acting muscle relaxants [19]. BChE is synthesized primarily in the liver and is distributed throughout the intestinal mucosa, in plasma, and in the white matter of the central nervous system [20]. The enzyme is encoded by the BChE gene (BCHE), which is located on chromosome 3q26 [21]. The BCHE genomic region spans approximately 70 kb, with four exons and three large introns [22]. Although more than 65 BCHE mutations have been identified, not all of them have been fully studied [23]. In general, these mutations produce enzymes with lower levels of catalytic activity than that of those produced
