Efficacy and Safety of Dual Biologic Therapy in Patients With Inflammatory Bowel Disease: A Review of the Literature

Abstract

Using 2 or more treatment modalities to achieve a synergistic effect in patients with refractory inflammatory bowel disease (IBD) has been an area of focus for many years. This methodology, known as combination therapy, has been proposed for various therapeutic agents, most commonly biologics and immunomodulators. Although the mainstay of biologic therapy for IBD has traditionally focused on agents targeting tumor necrosis factor, the development of newer biologics with different targets, such as vedolizumab and ustekinumab, has introduced the possibility of concomitant dual biologic therapy. Dual biologic therapy has been proposed in the treatment algorithm for 2 types of patients with IBD: those with well-controlled luminal IBD and uncontrolled extraintestinal symptoms (secondary indications such as arthritis or psoriasis) and those with refractory, uncontrolled IBD. Thus far, the data on the efficacy and safety of dual biologic therapy as a treatment for Crohn's disease or ulcerative colitis remain quite limited. In fact, the overwhelming majority of the literature consists of case reports and case series. Given this paucity of high-level data, physicians have looked to larger studies on dual biologic therapy in other fields of medicine, such as rheumatology and dermatology. The goal of this article is to summarize the current literature on the use of dual biologics in IBD, address the potential adverse effects or risks associated with combination therapy, and highlight future directions in the use of this therapeutic modality.

Keywords: Crohn’s disease; Inflammatory bowel disease; biologic therapy; combination therapy; dual biologics; extraintestinal manifestations; ulcerative colitis.

Figure.

Overview of biologics used for the management of inflammatory bowel disease and their mechanisms of action. Figure created with BioRender.com. IL, interleukin; MAdCAM-1, mucosal addressin cell adhesion molecule 1; Th, T-helper; TNF, tumor necrosis factor.