Urinary prostaglandin E-major metabolite concentrations were higher in active Crohn’s disease and ulcerative colitis; however, its predictive performance was inferior to fecal calprotectin, according to a recent study.
Researchers investigated the efficacy of prostaglandin E-major urinary metabolite (PGE-MUM) as a noninvasive biomarker for monitoring disease activity in inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC). Conducted at two European centers, the study compared PGE-MUM to fecal calprotectin (FC) and blood C-reactive protein (CRP), widely used biomarkers in IBD management.
Published in Scientific Reports, the study included 214 adults undergoing routine care, 121 of whom had CD and 86 of whom had UC. Clinical disease activity was classified using the Harvey-Bradshaw Index for CD and the Simple Clinical Colitis Activity Index for UC. PGE-MUM concentrations were measured using chemiluminescent assays, normalized to urinary creatinine, and compared with FC and CRP levels.
The researchers found that PGE-MUM concentrations were significantly higher in active disease compared with remission in both CD (59.8 µg/g vs 37.3 µg/g, P = .003) and UC (40.8 µg/g vs 31.3 µg/g, P = .002). However, PGE-MUM was less effective than FC in predicting disease activity. In CD, the area under the receiver operating characteristic curve (AUC) for PGE-MUM was 0.659, with a sensitivity of 46% and specificity of 80%, compared with an AUC of 0.957 for FC, which demonstrated 98% sensitivity and 80% specificity. For UC, PGE-MUM had an AUC of 0.693 (sensitivity = 37%, specificity = 97%), whereas FC achieved an AUC of 0.916 (sensitivity = 78%, specificity = 95%).
The combination of PGE-MUM and FC resulted in high AUC values (0.952 for CD and 0.926 for UC), comparable to FC alone, raising questions about the cost-effectiveness of using both biomarkers. Cluster analysis identified distinct inflammatory profiles, with three subgroups in CD and two in UC, offering potential insights for personalized treatment strategies.
This study had limitations, including potential inclusion bias from urine sample collection tied to FC testing and a small cohort size that restricted assessment of disease location and extent. Additionally, endoscopic confirmation was limited to clinical necessity, and factors influencing PGE-MUM levels, such as certain medications and smoking, were not recorded, though no participants had chronic lung fibrosis.
The researchers concluded that while PGE-MUM alone was less effective than FC, it may complement FC in refining inflammation profiling. This combination could reduce reliance on invasive procedures such as endoscopy. Further studies are needed to explore its role in predicting treatment responses and long-term outcomes in IBD.
Full disclosures can be found in the published study.
