7 Novel and Emerging Therapies One approach to avoiding gastrointestinal toxicity of NSAIDs is to pair them with fixed doses of gastroprotective agents in single-tablet formulations
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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
Variable modifications included mono-methylation of arginine residues (14.01565 Da), dimethylation (28.0313 Da), and oxidation of methionine residues (15.9949 Da)
Patch testing on the inner forearm before facial application is advisable when reintroducing
