The aim of the thesis was to investigate the mechanisms of action of biological drugs in
chronic inflammatory bowel disease (IBD), which includes Crohn’s disease and
ulcerative colitis. In this work, I also compared the effectiveness of treatments in
influencing disease progression, and included a comparison of efficacy based on
previous treatments with biological drugs. Biological drugs used for the treatment of
IBD include TNF-α inhibitors (infliximab, adalimumab, certolizumab pegol), α4β7
integrin inhibitors (vedolizumab), and interleukin IL-12 and IL-23 inhibitors
(ustekinumab, risankizumab). These drugs specifically target molecules responsible for
the patient’s pathological condition, such as chronic inflammation of the intestinal wall,
ulcerations, and strictures of the intestinal lumen. The mechanisms of action of
biological drugs include neutralizing pro-inflammatory cytokines, reverse signaling
through transmembrane forms of target molecules, inducing apoptosis of T cells,
preventing the migration of immune cells into the intestinal mucosa, and modulating the
balance between pro- and anti-inflammatory immune pathways. I used a review and
analysis of scientific literature, as well as a network meta-analysis of randomized
clinical trials. Results in biologically naïve patients showed that the most effective
combination was infliximab with azathioprine, with an 88 % probability of inducing
clinical remission. In previously treated patients, the most effective were ustekinumab,
adalimumab, and IL-23 inhibitors. Maintenance of clinical remission was successful
with all currently available biological drugs, without significant differences in safety
profiles. Understanding the mechanisms of action and immunological targets allows for
better therapy selection and supports a personalized approach in the treatment of IBD.
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