Advancing drug monitoring for better IBD outcomes

Gastrointestinal disorders are increasingly recognised as a global health challenge, with rising incidence rates and substantial implications for the general population. In fact, research conducted in 2022 revealed that over half a million people in the UK alone are living with Crohn's disease and ulcerative colitis — nearly double that of previous estimates.¹ This equates to a prevalence of approximately 1 in every 123 individuals, and the incidence of gastrointestinal disorders is projected to continue to rise in the coming decades.²

Fortunately, this growing disease burden is being counteracted by significant strides in pharmacological IBD management, particularly through the development of biologic treatments like the TNF-α inhibitors infliximab (IFX) and adalimumab (ADM). Biologics and biosimilars — more affordable biotherapeutic medicines with highly similar structures, functions and efficacy to the original drugs — offer a distinct advantage over systemic small molecule anti-inflammatories, due to their direct mode of action.^3,4 These therapies have transformed IBD care by targeting and inhibiting pro-inflammatory cytokines, markedly reducing the need for surgical interventions⁵ since their integration into routine clinical practice. However, the chronic and often unpredictable nature of IBD continues to pose significant challenges for both patients and healthcare providers. Responses to biotherapies vary widely, from rapid remission in some patients to no therapeutic effect in others. It is not therefore uncommon for patients to experience limited benefit from these treatments; up to 30 per cent of IBD patients show no initial response, and as many as 46 per cent encounter a gradual loss of response (LOR) to biotherapeutics over time.⁶

Understanding how the body metabolises and eliminates anti-TNF drugs is crucial to effective IBD management. Medications like IFX and ADM are cleared through several complex pathways, including proteolysis, loss through mucosal barriers during severe flare-ups, and binding to TNF-α molecules.⁷ In patients experiencing high inflammation levels, substantial amounts of TNF-α inhibitors may be eliminated through these processes, requiring dose adjustments to maintain therapeutic levels. Moreover, treatment efficacy is closely linked to numerous patient-specific characteristics that can increase risk of immunogenicity.⁸