Treatment with tumor necrosis factor antagonists increased steadily for patients with CD (43.4% of all patients in Brazil were treated in 2014) but less so for patients with UC (4.5% of all patients were treated in 2014).Surgery for IBD decreased with time.
Effects of Tumor Necrosis Factor Alpha Inhibitors on Lymph Node and Ileocecal Mucosa-Associated Lymphoid Tissue Architecture in Patients With Inflammatory Bowel Disease.
Adequate serum drug levels of tumor necrosis factor-alpha inhibitors (anti-TNF) have been shown to improve outcomes in patients with inflammatory bowel disease (IBD).
Combination therapies for IBD that include TNF antagonists, especially with corticosteroids, are associated with a higher risk of serious infection, whereas monotherapy with an immunosuppressive agent is associated with a lower risk, compared with monotherapy with a TNF antagonist.
The efficacy of antitumour necrosis factor (TNF)-α biologics has validated the role of inflammatory cytokines notably TNF-α in the exacerbation and perpetuation of IBD.
Is There a Risk of Lymphoma Associated With Anti-tumor Necrosis Factor Drugs in Patients With Inflammatory Bowel Disease? A Systematic Review of Observational Studies.
In recent years, more molecules, both biologically and chemically synthetized, have been developed as potential therapeutic options for IBD that target different molecular pathways aside from TNF blockade, and which have been proposed as targets for novel drugs.
We therefore performed a comprehensive analysis of vedolizumab-induced alterations in mucosal and systemic immunity in patients with inflammatory bowel disease (IBD), using anti-inflammatory therapy with the TNFα antibody infliximab as control.
Corticosteroids and Thiopurines, But Not Tumor Necrosis Factor Antagonists, are Associated With Cytomegalovirus Reactivation in Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis.
Since production of TNFα is a feature of IBD relevant to therapies, we sought to determine whether B cells in GALT or the CD27<sup>-</sup>IgD<sup>-</sup> subset in particular could contribute to pathology by secretion of TNFα or IL-10.
Polymorphisms in the NFkB, TNF-alpha, IL-1beta, and IL-18 pathways are associated with response to anti-TNF therapy in Danish patients with inflammatory bowel disease.
We performed a systematic review of changes in fecal and colon microbiomes of patients with inflammatory bowel diseases (IBD) receiving treatment with monoclonal antibodies against tumor necrosis factor (TNF), integrins, or cytokines.
The clinical success of biologics that inhibit TNF (Tumor Necrosis Factor) in inflammatory bowel diseases (IBD), psoriasis and rheumatoid arthritis (RA) has clearly established a pathogenic role for this cytokine in these inflammatory disorders.
Although KEGG showed inflammatory bowel disease in the E. coli group, the KEGG pathway analysis showed that these DEGs were mainly involved in the tumor necrosis factor signaling pathway, fructose metabolism, and mannose metabolism in both <i>S. aureus</i>- and <i>E. coli</i>-induced sepsis.