Large vessel vasculitis combined with inflammatory bowel disease: epidemiology, shared pathogenesis, and therapeutic advances

Abstract

Concomitant existence of large vessel vasculitis (LVV) and inflammatory bowel disease (IBD) is rare but has gained increasing clinical and research attention. LVV, comprising Takayasu arteritis (TAK) and giant cell arteritis (GCA), is characterized by granulomatous inflammation of the aorta and its branches. Accumulating evidence demonstrates a substantial overlap between LVV and IBD in epidemiological patterns, genetic susceptibility loci, immune cell subsets, and proinflammatory cytokine networks, supporting shared immunopathogenic mechanisms. IBD, including Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic immune-mediated inflammatory disorder influenced by genetic predisposition and gut microbiota dyshomeostasis. Patients with concomitant LVV–IBD exhibit heterogeneous and often insidious clinical presentations, with a predominance in young women, frequent multisystem involvement, and significant diagnostic challenges. Multimodal assessment incorporating imaging, endoscopy, and laboratory biomarkers is essential for early detection, although unified diagnostic criteria and disease-specific biomarkers remain lacking. Management requires careful balancing of intestinal and vascular disease control. Current therapeutic approaches include glucocorticoids, conventional immunosuppressants, and biologic agents, with anti-tumor necrosis factor therapies and other targeted agents showing benefit in selected refractory cases. Future multicenter, large-scale prospective studies are needed to refine diagnostic strategies, optimize treatment algorithms, and further elucidate shared immune-inflammatory pathways to improve long-term outcomes and enable precision therapy.