Crohn’s disease and ulcerative colitis are two chronic inflammatory bowel diseases (IBD).  Crohn’s disease most commonly affects the end of the small intestine (the ileum) and the beginning of the large intestine (the colon), yet it may involve any part of the gastrointestinal tract.  By contrast, ulcerative colitis affects only the colon.

Patients with IBD have frequent diarrhea, abdominal pain, fever, and rectal bleeding.  Symptoms of both conditions can be very similar.  The most common complications of Crohn’s disease include obstruction or blockage of the intestinal passage, ulcers within the intestinal tract, and fistulas.  Fistulas connect different parts of the intestine and may even tunnel into surrounding tissues such as skin, bladder and vagina.  Some patients with IBD also develop arthritis in their joints and spine.

IBD is an autoimmune disease that involves a complex interaction between the genes, the immune system, and the environment.  IBD occurs when our immune system goes astray, mistaking our own bowel tissue for a foreign invader, such as bacteria or virus, and subsequently launching an attack, and causing inflammation.  When the inflammatory process advances, white cells are attracted to the lining of the bowels and release chemical mediators, which eventually cause tissue damage.  tumor necrosis factor (TNF) is one of the key chemical mediators and plays a significant role in the inflammatory process.

In the past few years, due to an increased understanding of IBD pathogenesis, the strategic plan in treating IBD has changed.  Treatment has evolved from the conventional use of anti-inflammatory drugs such as sulfasalazine, 5-aminosalcylates (Asacol or Pentasa) and corticosteroids to control symptoms, to so-called immunomodulators such as 6-mercaptopurine (6-MP), methotrexate, azathioprine, and cyclosporine, which further alter the immune system and inflammatory process.   However, these treatments still have unsatisfactory results for some patients with moderate to severe IBD.

Thanks to scientific breakthroughs in molecular biology and genetic engineering, we are able to produce anti-TNF biologic agents.  Like anti-missiles, anti-TNF biologic agents can lock in on a target (TNF) and block the enemy’s offensive maneuver.  Anti-TNF agents have proved very effective in reducing inflammation of the spine and bowels and closing draining fistulas in Crohn’s disease.  Currently, there are four anti-TNF agents effective in the treatment of IBD: adalimumab (Humira), infliximab (Remicade), golimub (Simponi) and certolizumab (Cimzia).  Stelara (ustekinumab), another kind of biologics, targets IL-12/IL-23 cytokines, is also an approved treatment of moderate to severe Crohn’s colitis.

In May 2014, Vendolizumab was approved for moderate to severe ulcreative colitis, and crohn’s disease.  Vedolizumab (Entyvio), another different biologic agent, works by binding to cell surface receptors and inhibits the migration of leukocytes (white blood cells) from the bloodstream to sites of inflammation in the bowel tissue.   Recently Xelianz, an oral JAK (Janus Kinase) inhibitor, has been approved for the treatment of IBD.  Unlike other biologics that target extracellular molecules, such as pro-inflammatory cytokines, Xelianz target the intracellular signaling pathways that operate as hubs in the inflammatory cytokines network.  Even through severe IBD is a debilitating disease, these new biologic agents give us good reason to be optimistic.