A metabolomics-driven model for early remission prediction following vedolizumab treatment in patients with moderate-to-severe active ulcerative colitis
International Immunopharmacology, ISSN: 1567-5769, Vol: 128, Page: 111527
2024
- 3Citations
- 13Captures
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Article Description
To predict early remission following anti-integrin therapy (vedolizumab [VDZ]) in patients with moderate-to-severe active ulcerative colitis (UC) using non-invasive biomarkers. The clinical data of a cohort of 33 patients with moderate-to-severe active UC admitted to the Department of Gastroenterology at Suzhou Municipal Hospital between January 2021 and December 2022 were collected. Of these, 9 patients declined VDZ treatment, and 21 received VDZ at doses of 300 mg weeks 0, 2, and 6, each administered within a 30-minute infusion period. The treatment regimen aimed to induce remission of clinical symptoms; hence, the same dose was administered every 8 weeks. At weeks 0 and 14, serum C-reactive protein (CRP) and erythrocyte sedimentation rate were measured using a modified Mayo score. In addition to clinical assessment, stool samples at baseline and weeks 14 were collected and evaluated using 16SrRNA gene sequencing and gas chromatography-mass spectrometry (GC–MS). Clinical remission was determined based on the clinical symptoms and partial Mayo scores. In patients who received VDZ, the strains of bifidobacterium longum (P = 0.022) and bacteroides sartorii (P = 0.039) significantly increased after treatment than before treatment. GC–MS analysis showed that taurine (P = 0.047) and putrescine (P = 0.035) significantly decreased after treatment. Furthermore, while acetamide exhibited a notable increase (P = 0.001), arachidic acid (P < 0.001) and behenic acid (P = 0.005) demonstrated statistically significant elevations. The combined prediction model of acetamide, taurine, and putrescine demonstrated a high predictive value of early remission in patients with moderate-to-severe active UC following VDZ treatment (area under the curve = 0.911, P = 0.014).
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1567576924000456; http://dx.doi.org/10.1016/j.intimp.2024.111527; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85182380584&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/38215655; https://linkinghub.elsevier.com/retrieve/pii/S1567576924000456; https://dx.doi.org/10.1016/j.intimp.2024.111527
Elsevier BV
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