Korean J Med.  2013 Dec;85(6):578-585.

Natural Course of Crohn's Disease and Novel Treatment Drugs

• Lee JH
• Cheon JH

Abstract

Crohn's disease is a chronic recurrent inflammatory disease, mainly affecting the gastrointestinal tract. The pathogenesis of inflammatory bowel disease is believed to be caused by the complex interplay of many factors including host genetic susceptibility, the external environment such as infectious agents or the commensal enteric flora, and the immune system dysfunction. Advances in the understanding of the pathophysiology of inflammatory bowel disease have resulted in the development of multiple biological agents that all represent an alternative to the use of current therapies in patients with refractory Crohn's disease. Moreover, these biologic agents are expected to change the natural course of inflammatory bowel disease. Among them, anti-tumor necrosis factor (TNF)-alpha agent is the first developed drug, and it dramatically improved the IBD management. However, more than one-third of the patients do not respond to the drugs due to antibody formation and loss of response. To increase treatment efficacy, enormous efforts have been made to develop novel anti-cytokines which can be an alternative to anti-TNF-alpha agents. They are anti-CD4+ T cell cytokines including interleukin (IL)-12/23, IL-17A, and IFN-gamma blockers, selective anti-adhesion molecules, anti-inflammatory cytokine IL-10, and immune stimulators. This paper reviews the natural history of Crohn's disease, natural course modifiers, and the efficacy and safety of biologic agents other than anti-TNF alpha agents.

Keyword

Crohn's disease; Inflammatory bowel disease; Natural history; Biologic agent; Anti-TNF agent

MeSH Terms

Antibody Formation
Biological Agents
Crohn Disease*
Cytokines
Gastrointestinal Tract
Genetic Predisposition to Disease
Humans
Immune System
Inflammatory Bowel Diseases
Interleukin-10
Interleukin-17
Interleukins
Natural History
Necrosis
Treatment Outcome
Biological Agents
Cytokines
Interleukin-10
Interleukin-17
Interleukins