Photo Credit: wildpixel

The following is a summary of “Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a lipidomic study,” published in the May 2025 issue of BMC Gastroenterology by Moe et al. 

Researchers conducted a retrospective study to characterize the lipid profile in treatment-refractory, non-immunogenic patients with adequate trough levels in inflammatory bowel disease (IBD).  

They included patients with IBD refractory to anti-tumor necrosis factor (TNF) or vedolizumab from a Norwegian translation study. Mucosal lipid profiles were compared to reference groups comprising treatment-naïve patients with moderate to severe disease at debut who later responded or achieved remission on anti– TNF therapy, patients treated to remission with biological agents, and healthy controls. Lipidomics analyses were conducted on mucosal biopsies. Statistical evaluation of lipid levels used generalized least squares. Lipidomics data were log2-transformed and auto-scaled before analysis, with P-values adjusted via the Benjamini-Hochberg procedure to control the false discovery rate (FDR).  

The results showed that proinflammatory lipids, including ceramides (Cer) and sphingomyelins (SM), and protective lipids, such as glycerophosphocholines (PC) and glycerophosphoethanolamines (PE) were significantly reduced in treatment-refractory patients with ulcerative colitis (UC) compared to treatment-naïve patients with moderate to severe disease. Significant alterations in Cer, hexosyl Cer (HexCer), SM, PC, PE, and glycerophosphoserines (PS) were found in treatment-refractory patients with UC vs controls. Patients with Refractory Crohn disease (CD) exhibited minor lipid changes relative to other CD groups. No significant mucosal lipid differences were observed between patients with inflammatory bowel disease in remission and healthy controls.  

Investigators concluded that treatment-refractory UC exhibited significant mucosal lipid alterations compared to treatment-naïve cases, reflecting dynamic chronic inflammation, while lipid profiles in remission resembled normal states. 

Source: bmcgastroenterol.biomedcentral.com/articles/10.1186/s12876-025-03944-6