Overview: New Directions in Inflammatory Bowel Disease Therapy

Summary

Although the etiology of IBD is unclear, progress has been made in identifying the cells and the mediators that cause inflammatory response. The inflammatory cells and the biochemical mediators that are evidenced in excess, the enzymes that are activated and the receptors that bind these mediators during ‘acute’ exacerbation of IBD appear to be pathologically similar to inflammation observed in various other organ systems. Progress has been made in modifying the empirical therapy with 5-ASA and its congeners suitable for topical therapy as enemas. Oral therapy with 5-ASA has also met with changes by complexing it with less toxic pharmaceutical adjuvants for delivery to target areas. Progress in steroid therapy has focused on not only increasing the glucocorticoid activity, but also chemically modifying corticosteroids such that they are absorbed less readily and rapidly metabolised to reduce their adverse side-effects. The use of cyclosporin and azathioprine has met with some success. However, recent progress in understanding inflammatory diseases in pharmacological terms has provided an impetus for pharmaceutical companies to discover novel therapies to combat the disease by preventing the production or binding of inflammatory mediators to their respective receptors. It is too early to predict how efficacious these drugs will be in suppressing the inflammatory response. Clearly more controlled studies are needed to substantiate the efficacies of these drugs. Be that as it may, recent enthusiasm emerging from the discovery of novel therapeutic agents to combat inflammation in general has changed the trends in IBD therapy. The next few years will tell whether these drugs are therapeutically useful and whether a single drug is efficacious to combat both Crohn's disease and ulcerative colitis.