| The approval of anti-tumor necrosis factor (TNF) agents has led to a dramatic improvement in the care of patients with Crohn's disease. Since these medications do not work in everyone, and are associated with rare, but serious side effects, the ideal scenario would be to selectively treat patients who have the highest chance of responding, ie. the right medication, for the right patient, at the right time, and at the right dose. The approvals of newer therapies for Crohn’s disease including anti-trafficking (ie. natalizumab, vedolizumab) and anti IL12/23 (ustekinumab) agents has compounded the need to a priori identify factors that might render an individual patient more likely to respond to a specific mechanism of action, or to medical therapy in general. Many variables have been studied to determine their association with response to anti-TNF agents. Clinical parameters include patient characteristics, disease duration, body mass index, smoking status and disease phenotype, concomitant immunomodulators and biologic markers including C-reactive protein, serum TNF levels, immune responses to microbial antigens, and drug/anti-drug antibody concentrations. More recently, research has focused on genetics to identify polymorphisms associated with treatment response. Results from individual studies of these factors have not yet allowed for reliable clinical applicability. These agents work, but not in everyone. To limit toxicity, save cost and more precisely deliver effective treatment, further work in this area along with multivariate clinical prediction modeling may soon allow us to deliver ‘personalized medicine’ by predicting individualized treatment responses in patients with Crohn’s disease. |
