Conclusions

The advent of biological therapy provides the opportunity to advance the care of patients with IBD because we have opportunities to interrupt the disease pathophysiology in a more specific way. The infliximab experience teaches that interfering with cytokine-mediated inflammation improves the clinical outcome of severe CD.

New biological drugs are coming in the near future. Can we treat severe CD by blocking more than one inflammatory mediator? The mechanism of inflammation in cytokine-mediated CD is quite complex. Cytokines are numerous, act at very low titre (potent biological activity), have many target cells and the cytokine response is mediated by specific cellular receptors. Furthermore, different cytokines produce the same effects, and large interactions among cytokines are documented. We can postulate that interfering with two or more cytokines may improve the clinical course of CD. However, we do not know yet if this approach may alter immune defence towards pathogens and immune surveillance on carcinogenesis, and we must consider that biolog-ics are expensive drugs.

Biological drugs present a major challenge: the more effective they are, the more side effects they can produce. Therefore, biological therapy should carefully managed, with close observance for possible adverse events and provision for any complication resulting from treatment. Inappropriate management of these potent drugs will compromise their use in clinical practice.

Future clinical studies should address efficacy, safety and cost effectiveness of biologic therapies for CD and should provide the necessary information to take maximum advantage of these new therapies.

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