CONCLUSION
In summary,
this
study was the first PPK model for busulfan that successfully
incorporated GSTA1 genotypes in a Chinese pediatric population
and partly explained the source of large variability of busulfan
exposure, suggesting that TDM would be necessary for optimization of
pediatric Bu treatment. Moreover, a BSA-based dosing regimen is
recommended for individual busulfan therapy in order to weaken
variability in busulfan exposure and to enhance the safety and efficacy
of Bu treatment. Finally, an optimal LSS (C2h and
C4h) would be convenient for TDM in the future.