Biological therapies for inflammatory bowel disease: controversies and future options.

Over the last few years, advances in understanding the pathogenesis of inflammatory bowel disease, together with progress in biotechnology, have led to the availability of several biological drugs that have dramatically changed the therapeutic approach to these disorders. Indeed, several molecules targeting crucial inflammatory cytokines, blocking T-cell activation/proliferation or the recruitment of inflammatory cells into the inflamed bowel, have been discovered and commercialized. However, the increasing use of biological agents has raised some concerns regarding their short- and long-term safety.

Use of infliximab in particular clinical settings: management based on current evidence.

With the increasingly widespread use of the anti-tumor necrosis factor-alpha agent infliximab for the treatment of Crohn's disease and ulcerative colitis, there have been some concerns raised about the potential consequences of such therapy in particular clinical settings. In this review, we report the current strategies for optimizing treatment outcomes and minimizing the risks of some of the most serious events attributable to infliximab therapy. In particular, an up-to-date overview is provided on how to treat patients with inflammatory bowel disease using infliximab therapy, with regard to the diagnosis and management of latent tuberculosis infection and the risk of reactivation of hepatitis B and C infections.

Vascular involvement in inflammatory bowel disease: pathogenesis and clinical aspects.

Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel disease (IBD), are chronic inflammatory conditions, characterized by a microvascular and also macrovascular involvement. Chronically inflamed intestinal microvessels of IBD patients have demonstrated significant alterations in their physiology and function compared with vessels from healthy and uninvolved IBD intestine. Recently, some studies have revealed that the poor mucosal healing, refractory inflammatory ulcerations and damage in the IBD intestine could depend on microvascular dysfunction, resulting in diminished vasodilatory capacity and tissue hypoperfusion in the IBD gut.