Correlation of serum-soluble triggering receptor expressed on myeloid cells-1 with clinical disease activity in inflammatory bowel disease

Jae Jun Park, Jae Hee Cheon, Bo Young Kim, Duk Hwan Kim, Eun Soo Kim, Tae Il Kim, Kyoung Ryul Lee, Won Ho Kim

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68 Citations (Scopus)

Abstract

Although triggering receptor expressed on myeloid cells-1 (TREM-1) has recently been shown to be upregulated in the intestines of patients with inflammatory bowel disease (IBD), it remains unclear whether serum-soluble TREM-1 (sTREM-1) level reflects disease activity in patients with IBD. This study aimed to evaluate the correlation of sTREM-1 level with disease activity in IBD. We prospectively enrolled consecutive patients with IBD and assessed their clinical disease activity using the guidelines of the American College of Gastroenterology. At the time that disease activity was assessed, sTREM-1 level (using an enzyme-linked immunosorbent assay method) and other laboratory findings including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were also measured. A total of 31 patients with ulcerative colitis (UC) and 22 with Crohn's disease (CD) were enrolled. The mean sTREM-1 level in patients with either UC (60.4 ± 41.8 pg/ml) or CD (66.5 ± 42.4 pg/ml) was significantly higher than in healthy controls (0.6 ± 1.4 pg/ml) (P = 0.003 and P = 0.002, respectively). In patients with UC, sTREM-1 level was more highly correlated with disease activity (r = 0.849) than was ESR (r = 0.619) or CRP level(r = 0.546). Moreover, sTREM-1 level correlated well with disease activity irrespective of disease extent. In patients with CD, sTREM-1 level was lower in those with remission compared with those without (46.8 ± 35.3 pg/ml versus 77.8 ± 43.1 pg/ml), but this trend did not reach statistical significance (P = 0.100). The results of our study suggest that sTREM-1 could be a potential marker for disease activity in IBD patients, especially those with UC.

Original languageEnglish
Pages (from-to)1525-1531
Number of pages7
JournalDigestive diseases and sciences
Volume54
Issue number7
DOIs
Publication statusPublished - 2009 Jul

Bibliographical note

Funding Information:
Acknowledgments This work was supported by the Yonsei University College of Medicine, Internal Medicine Research Grant 2006 and Korean Abbott Research Fund 2007.

All Science Journal Classification (ASJC) codes

  • Physiology
  • Gastroenterology

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