Do the distinctive BChE phenotypes (i.e., atypical or fluoride resistance) indicate which genetic mutation is responsible?
Not necessarily. All the atypical (dibucaine-resistant) cholinesterase mutations around the world so far have been exactly the same point mutation. Perhaps these will all be traced back to some common ancestor that was the founder of this mutation. However, there are at least two different point mutations that produce fluoride resistance (Fluoride-1 and Fluoride-2). Special tests can be used to distinguish between the two fluoride-resistant phenotypes, but these two variants are very similar and would be confused in most diagnostic laboratories. Why bother to keep track of the people with succinylcholine sensitivity? The importance of BChE in the metabolism of other drugs is not as well-established, except for mivacurium, which was designed to be inactivated by this enzyme. Some other drugs hydrolyzed by BChE are aspirin, several local anesthetics, heroin, cocaine and bambuterol.2 However, the importance of BChE in the metabolic inactivation of these and other new drug substrates depen