The impact of severe inflammation on semen quality, including sperm DNA integrity, in men with inflammatory bowel disease [IBD] is unknown, as are the potential effects of anti-tumour necrosis factor-alpha [TNF-alpha] therapy.
The introduction of biological therapies including anti-TNF, anti-IL-12/23, and anti-integrins, has revolutionized the treatment of IBD, but these drugs are not universally effective.
While tumor necrosis factor (TNF) antagonists remain the biologic of choice for majority of patients with moderate-to-severe IBD, IL-12/23, and IL-23 antagonists should be considered for first- or second-line therapy because of their efficacy in biologic-naïve and experienced patients.
Paradoxical reactions were observed in 3 (33.3%) of 9 patients on TNF inhibitors, including 2 (22.2%) with inflammatory bowel disease-like changes and 1 (11.1%) with sarcoid-like granulomas.
Here we explored the regenerative effects of iPSC-MSCs and the mechanisms by which iPSC-MSCs promote mucosal healing via tumor necrosis factor-α-stimulated gene 6 (TSG-6) in mouse models of inflammatory bowel disease (IBD).
Tumour necrosis factor (TNF) is a key cytokine during inflammatory responses and its dysregulation is detrimental in many inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease.
Outcome of elective switching to vedolizumab in inflammatory bowel disease patients under tumor necrosis factor antagonist-maintained clinical remission.
Increased prevalence of anti-TNF therapy in paediatric inflammatory bowel disease is associated with a decline in surgical resections during childhood.
Studies of serum vitamin D (Vit-D) levels in patients with inflammatory bowel disease (IBD) treated with anti-tumor necrosis factor-alpha (anti-TNF-α) agents are scarce.
Hispidulin-7-<i>O</i>-neohesperidoside (HN) is flavone diglycoside isolated from the methanolic extract of aerial parts of <i>Cirsium japonicum var</i>. ussuriense.HN concentration-dependently inhibited NO production and considerably downregulated the levels of the proinflammatory cytokines, IL-1β and TNF-α, and the iNOS protein level in LPS-induced RAW 264.7 cells.HN inhibited the production of the chemotactic cytokine, IL-8, in LPS-induced HT-29 cells.HN has potential as an anti-inflammatory agent to prevent and/or treat IBD.
We aimed to estimate the incidence rate (IR) of psoriasis in children with inflammatory bowel disease (IBD), juvenile idiopathic arthritis (JIA), and chronic noninfectious osteomyelitis (CNO) with tumor necrosis factor-alpha inhibitor (TNFi) exposure as compared to those without TNFi exposure and to the general pediatric population.
Initial evidence for the use of TNF-α inhibitors in HS stemmed from recognition that inflammatory bowel disease patients treated with these medications saw a concurrent improvement in their HS symptoms.