Many patients with Crohn's disease (CD) are treated with medications, including steroids, immunomodulators, and anti-tumor necrosis factor alpha (anti-TNF-α) agents, at the time of surgery.
In the multivariate analysis, having anti-TNF drug levels above the cutoff values [odds ratio (OR) 3.1]) and having UC instead ofCD (OR 4) were associated with a higher probability of having mucosal healing.
Polymorphisms of the TNF Gene and Three Susceptibility Loci Are Associated with Crohn's Disease and Perianal Fistula Crohn's Disease: A Study among the Han Population from South China.
We further demonstrated that GSK2256294, a clinical EPHX2i, reduced the production of IL2, IL12p70, IL10 and TNFα in both ulcerative colitis and Crohn's disease patient-derived explant cultures.
An ability to modulate the release of the proinflammatory mediators, such as TNF-α, is an important goal in the development of therapies for the treatment of diseases, such as Crohn's disease and ulcerative colitis, associated with excessive release of inflammatory mediators.
The pro-inflammatory cytokine, TNF-α, which plays a major role in the development and persistence of diseases such as Crohn's disease, psoriasis, psoriatic arthritis, and rheumatoid arthritis, is the basis for the use of anti-TNF-α therapies.
In multivariate analysis, we confirmed female gender, longer disease duration, IBD-related surgery, presence of other EIM and treatment with anti-TNF to be independent risk factors for the onset of arthritis/arthralgia in CD and UC/IBDU patients.
The approval of ustekinumab, a monoclonal antibody blocking the common p40 subunit of IL12 and IL23, marked an important evolution in medical management for CD: this novel class of biologic therapy demonstrated efficacy in both patients naïve to biologics as well as in patients experiencing inadequate response or loss of response to TNF antagonists.
Twenty-five patients with ulcerative colitis (40% anti-tumor necrosis factor α [TNFα] naive) and 28 patients with Crohn's disease (10.7% anti-TNFα naive, 53.6% having undergone at least one intestinal surgery) were enrolled.
Interestingly, hepcidin was found to be decreased in patients with Crohn's disease after successful therapy with anti-TNF-<i>α</i> mAb (i.e., infliximab), indicating the underlying association between TNF-<i>α</i> and hepcidin expression.
The methylation status of DEFA5 and TNF genes provides a signature biomarker that characterizes patients with CD and supports the possible implication of the environment and the immune system in CD pathogenesis.
Patients with Crohn's disease (CD), but not ulcerative colitis (UC), of shorter duration have higher rates of response to tumor necrosis factor (TNF) antagonists than patients with longer disease duration.
In this analysis, we aimed to compare the cost-effectiveness of ustekinumab, infliximab, or adalimumab for the treatment of moderate-severe Crohn's disease in patients who failed conventional therapy (i.e., corticosteroids and immunomodulators) but were naïve to tumor necrosis factor antagonists (i.e., biologic drugs).
We aimed to investigate the impact of the single nucleotide polymorphisms of rs34436714 of the NOD-like receptor protein 12 gene on the production of tumor necrosis factor-alpha (TNFα) in patients with inflammatory bowel disease (IBD)In a matched case-control study 90 patients with IBD, 56 with Crohn disease (CD) and 34 with ulcerative colitis, were genotyped and compared to 98 healthy comparators matched for age and gender.
The methylation status of DEFA5 and TNF genes provides a signature biomarker that characterizes patients with CD and supports the possible implication of the environment and the immune system in CD pathogenesis.
Tumor necrosis factor alpha (TNFα) has an important role in the body composition of patients with rheumatoid arthritis (RA), Crohn's disease (CD), and spondyloarthritis (SpA).