A novel role of the splenic volume in Crohn’s disease: evaluating the efficacy of infliximab

Abstract

Background: A number of patients with Crohn’s disease (CD) suffer from loss of response to infliximab (IFX) therapy. Splenic volume is reported to be enlarged in patients with CD compared to normal individuals. The association between splenic volume and IFX efficacy in CD remains unclear.Methods: We performed a retrospective study of patients with CD who received regular IFX treatment at Zhongshan Hospital, Fudan University, between August 2015 and December 2021. We collected baseline characteristics and clinical features from medical records in the CD database of Zhongshan Hospital. We accurately measured the splenic volume using semi-auto spleen segmentation software, followed by the analysis of splenic volume and IFX efficacy.Results: We included 49 patients with CD receiving IFX treatment, of whom 41 responded to IFX and 8 failed to respond to IFX. Splenic volume, as well as volume adjusted for body mass index (SV/BMI) and body weight (SV/W), was significantly decreased after IFX treatment in responders but increased in non-responders compared to the volume before the treatment. Accordingly, the levels of leukocyte count, platelet count, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were decreased after IFX treatment in responders. Contrarily, the levels of hemoglobin, albumin, and tumor necrosis factor (TNF)-α were elevated in responders. Moreover, both CRP and TNF-α levels were significantly positively correlated with SV/BMI in all patients.Conclusion: Splenic volume, especially SV/BMI and SV/W, was reduced after IFX treatment in CD patients responsive to IFX. SV/BMI was positively correlated with disease activity. Splenic volume is a promising indicator to evaluate IFX efficacy in CD.

ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer

“…Activation of NF-κB upregulates the expression of interleukins IL-1 and IL-6, inducing inflammation and promoting cell survival, thus amplifying the inflammatory cascade reaction. This leads to the disruption of tight junctions and apoptosis of epithelial cells in the intestinal epithelium, impairing the intestinal mucosal barrier, and ultimately causing intestinal mucosal damage ( 160 , 161 ). As mentioned earlier, patients with XP have a significantly higher risk of developing lung and gastrointestinal cancers, but the likelihood of developing IBD-associated CAC is still unknown.…”