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10.3390/ijms19030907 35 ChanetonB.HillmannP.ZhengL.MartinA
Key pathophysiologic mechanisms include: Mucosal barrier dysfunction: Impaired epithelial tight junctions allow bacterial translocation, triggering innate immune activation T-helper cell dysregulation: Predominantly Th1 and Th17 pathways drive chronic inflammation via TNF-, IL-12, IL-23 the basis for biologic therapy targets Transmural inflammation: Unlike UC (mucosal only), CD involves all layers: mucosa submucosa muscularis propria serosa Granuloma formation: Non-caseating granulomas are pathognomonic but present in only ~3050% of biopsies Fibrosis and stricture: Chronic inflammation activates myofibroblasts collagen deposition luminal narrowing obstructive symptoms Fistula formation: Transmural ulcers penetrate serosa form sinus tracts connect to adjacent bowel, bladder, vagina, or skin 7
As described in further detail below, we proposed for CY 2026 an OPD fee schedule increase factor of 2.4 percent for the CY 2026 OPPS/ASC proposed rule (which is the proposed estimate of the hospital inpatient market basket percentage increase of 3.2 percent, less the proposed 0.8 percentage point productivity adjustment)
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