Literature Reviews

Adalimumab is an effective and safe treatment for Crohn’s Disease (CD). However, both patients and healthcare professionals may wish to mitigate medication exposure due to potential safety and economic concerns in the long term. Since a high relapse rate follows drug discontinuation, treatment de-escalation without actually stopping the medication may allow for decreasing drug exposure while maintaining efficacy. In two observational studies, de-escalation from a 2-week to a 3-week adalimumab dosing interval was successful in most of the patients, though reversal to a 2-week dosing interval...

The SONIC trial yielded seminal findings showing that the combination of infliximab and azathioprine is more effective than either treatment alone for the maintenance of remission in patients with Crohn’s Disease (CD) [1]. In recent years, despite the availability of an increasing number of biologics and small molecules to treat CD, a ceiling of therapeutic efficacy has been reached [2]. Therefore, there has been a resurgence of interest in whether this therapeutic ceiling “effect” can be overcome with new treatment combinations.

Despite an expanding therapeutic arsenal, a considerable proportion of patients with Crohn's Disease (CD) and Ulcerative Colitis (UC) fail to achieve or sustain therapeutic responses [1, 2]. Mechanisms contributing to this failure, particularly with respect to biologic therapy, are only partially understood [3]. Uncovering the mechanisms behind loss of response may help to enhance the efficacy of existing treatment options or to develop alternative options for the future.

Patients will often ask, “What causes Inflammatory Bowel Disease?” Frustratingly, we remain unable to answer this seemingly simple question, beyond the often-quoted paradigm that unknown environmental factors trigger inflammation in genetically susceptible individuals. Although our understanding of the immune response in IBD has reached phenomenally detailed levels of resolution, the nature and identity of the initial environmental triggers of IBD have continued to remain a mystery.