© Springer International Publishing AG 2018 129
A.S. Cheifetz, J.D. Feuerstein (eds.), Treatment of Inflammatory
Bowel Disease with Biologics, https://doi.org/10.1007/978-3-319-60276-9_9
Chapter 9
Use of Biologics in Crohn’s Disease
and Ulcerative Colitis Prior to Surgery
and Perioperative Risks
Afrin Kamal and Bret Lashner
Medical therapy plays a critical role for induction and maintenance of luminal
inflammatory bowel disease (IBD) and fistulizing Crohn’s disease. The mechanism
of disease is thought to be caused by an exaggerated T-cell immune response to
enteric bacteria in a genetically vulnerable host. Considering that an exaggerated
immune response is responsible for the pathogenesis of IBD, the market developed
agents focusing on diminishing this immune activity. Of these therapies, a large
bulk falls into the category of “biologic therapy.” These agents are monoclonal anti-
bodies targeting tumor necrosis factor, including infliximab (Remicade©), adalim-
umab (Humira©), certolizumab (Cimzia©), and golimumab (Simponi©), and
targeting integrin α 4 β7 such as vedolizumab (Entyvio©) [ 1 ].
Biologic agents attempt to alter the natural history of IBD by aiding in steroid
withdrawal while preserving disease remission [ 2 ]. These agents have been proven
effective. For example, since the commercial availability of infliximab in 1998, the
overall rate of IBD surgery has decreased. Unfortunately medical therapy has not
been able to erase the need for bowel resection; on average 75% Crohn’s disease
and 30% ulcerative colitis patients will undergo surgery due to refractory disease or
complications. Often, medical therapy proceeds the need for surgery, bringing up
concerns regarding perioperative risks with anti-TNF agents [ 3 , 4 ].
Tumor necrosis factor alpha encompasses several effects on a cellular level.
First, as a product of activated macrophages, it regulates cell signal protein of sys-
temic inflammation and thus immune cells [ 5 ]. Second, biologic therapies bind to
both the soluble and membrane-bound forms of TNF, leading to apoptosis of TNF-
expressing inflammatory cells [ 4 ]. Inhibition of this key cytokine in the inflamma-
tory process is the primary therapeutic effect for inflammatory bowel disease. Third,
TNF-α plays an important role in mediating neutrophil chemotaxis and adhesion
during the beginning phases of inflammation, whereas in the proliferative phase of
A. Kamal • B. Lashner (*)
Cleveland Clinic, 9500 Euclid Avenue/A30, Cleveland, OH 44195, USA
e-mail: [email protected]; [email protected]