Real-World Outcomes of Vedolizumab Therapy in Ulcerative Colitis and Crohn’s Disease at a Tertiary Referral Center

Abstract

Background: Vedolizumab was approved for the therapy of ulcerative colitis and Crohn’s disease in mid-2014. Real-world treatment data are necessary for a balanced assessment of its position among other therapeutic options. Summary: Patients with ulcerative colitis or Crohn’s disease, initiating vedolizumab therapy at the outpatient clinic for inflammatory bowel diseases at the University Hospital ­Heidelberg between June 1, 2014 and August 31, 2016, were recruited based on electronic medical records. The primary study endpoint was response at week 30, while the secondary endpoints were the need for surgery and discontinuation of therapy due to inadequate response, or adverse events. Twenty-five patients with ulcerative colitis (40% anti-tumor necrosis factor α [TNFα] naive) and 28 patients with Crohn’s disease (10.7% anti-TNFα naive, 53.6% having undergone at least one intestinal surgery) were enrolled. Among the ulcerative colitis patients, 20% achieved remission, 32% partial response, and 48% were non-responders to vedolizumab. In Crohn’s disease, 14.3% of the patients achieved remission, 46.4% partial response, and 39.4% were non-responders. Two patients discontinued vedolizumab therapy due to suspected side effects. Key Message: In a relatively treatment-refractory cohort of inflammatory bowel disease patients, vedolizumab was efficacious in achieving response. However, the majority of the patients were not satisfactorily treated, as they did not reach remission.

Do Androgens Modulate the Pathophysiological Pathways of Inflammation? Appraising the Contemporary Evidence

“…Recent clinical trials with interleukin-6 receptor monoclonal antibody tocilizumab (TCZ) and tumor necrosis factor inhibitors (TNFi) for the treatment of rheumatoid arthritis demonstrated improvements with anti-TNF-α therapy and anti-IL-6 receptor therapy [4]. Also, vedolizumab therapy was shown to improve ulcerative colitis and Crohn’s disease [5]. Since testosterone deficiency increases the levels of inflammatory cytokines (Table 1), and testosterone therapy in hypogonadal men with chronic inflammatory conditions also reduce TNF-α and IL6 (Table 2), it is possible that testosterone therapy reduces the levels and activities of these inflammatory cytokines, and therefore reducing the burden of disease, and the amelioration of symptoms in such clinical conditions (Table 3).…”

“…In this review, we wish to focus our discussion on the effects of testosterone deficiency (i.e., hypogonadism) and testosterone therapy in men with inflammatory diseases, and the changes in the expression and function of inflammatory biomarkers, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and C-reactive protein (CRP). Our focus on these specific biological markers is, in part, due to recent advances in clinical applications of anti-inflammatory cytokines therapy for various clinical conditions [3,4,5]. For instance, adalimumab (Humira ® ), a TNF-α inhibitor, is the highest-selling drug today, and it is being used in various auto-immune diseases [6].…”

Long‐term efficacy and safety of vedolizumab in patients with inflammatory bowel diseases: A real‐life experience from a tertiary referral center

“…Considering the highly selective character of trial enrollment, it is always fundamental to observe whether real‐life settings support the initially reported results of a new drug . Real‐world publications on this field are accumulating, with some conflicting results, but only a few of them include long‐term evaluation at 1 year with endoscopic assessment . Therefore, we presented an Italian single‐center study on VDZ long‐standing effectiveness and tolerability in patients with UC and CD at a tertiary referral setting.…”

Population Pharmacokinetics of Tofacitinib in Patients With Moderate to Severe Ulcerative Colitis

“…Clinical characteristics of UC include rectal bleeding, fecal urgency, and diarrhea 1 . Therapies used to treat UC include mesalamine (5‐aminosalicylic acid [5‐ASA]), corticosteroids, thiopurines (eg, azathioprine, 6‐mercaptopurine), tumor necrosis factor inhibitors (TNFi; eg, adalimumab, infliximab, golimumab), and integrin inhibitors (eg, vedolizumab) 1–5 . However, many patients either do not respond to these therapies or do not have a sustained response; therefore, novel treatments with different mechanisms of action are required.…”