Abstract
For a significant proportion of patients with inflammatory bowel disease (IBD), primary non-response and secondary loss of response to treatment remain significant issues. Anti-tumor necrosis factor therapies have been licensed for use in IBD. Other disease-related pathways have been targeted as well, including the interleukin 12/23 axis and lymphocyte tracking. However, the need for parenteral administration and the associated costs of dispensing and monitoring all biologics remain a burden on healthcare systems and patients. Janus kinase inhibitors are small-molecule drugs that can be administered orally and are relatively inexpensive, thus offering an additional option for treating IBD. They have been shown to be effective in patients with ulcerative colitis (UC), but they are less effective in those with Crohn’s disease (CD). Nonetheless, given the immune-system-based mechanism of these drugs, their safety profile remains a cause for concern. This article provides an overview of Janus kinase (JAK) inhibitors and new trends in the treatment of IBD.
Highlights
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is caused by chronic inflammation of the gastrointestinal tract [1]
The study showed that tofacitinib induced a clinical response in 69% of patients with moderate to severe anti-tumor necrosis factor (TNF)-resistant IBD, including 27% who were in steroid-free clinical remission by 1 year of treatment
A large amount of data is available concerning the risk of deep vein thrombosis and pulmonary embolism in patients with IBD receiving tofacitinib, including a pooled analysis of 1157 patients with UC treated with tofacitinib who were enrolled in three induction studies, one maintenance trial, and one ongoing long-term extension study
Summary
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is caused by chronic inflammation of the gastrointestinal tract [1]. The JAK family comprises four intracellular tyrosine kinases, JAK1, JAK2, JAK3, and tyrosine kinase 2 (TYK2), and seven transcriptional activators, which include signal transducers and intracellular transcription factors (STATs) The binding of these factors activates the JAK-STAT pathway via different cytokine receptors and leads to changes in the levels of immune mediators, such as interferons and interleukins [3]. Among the latter, IL-6 and IL-12 and IL- 23 are important drivers of disease activity in IBD [4,5]. The relevant or comprehensive studies were included in our descriptive review article
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