Advances in genetic testing have confirmed the presence of susceptibility loci on chromosomes 12 and 16 for UC and CD. These loci show a strong association with particular disease phenotypes that may explain the clinical heterogeneity of IBD. Whether multiple genotypes will be found to explain these phenotypes remains to be determined. Pharmacogenetic differences in 6-mercaptopurine metabolism can be used clinically to predict patient susceptibility to drug-induced toxicity. Novel treatment strategies are being developed at The Johns Hopkins Medical Center Hospital based on these inherent genetic differences. The aim is to improve treatment efficacy and clinical response times and prevent untoward drug-induced toxicity.
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