P159 The utility and benefit of procalcitonin to assess disease activity and severity in Crohn’s disease and intestinal Bechet disease
E. Hayashi, M. Saruta, S. Arihiro, M. Matsuoka, M. Mitsunaga, D. Ide, T. Iwasaki, M. Ogawa*, R. Sawada, Y. Nagata, T. Kato, H. Tajiri
The Jikei University School Of Medicine, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Tokyo, Japan
It has been supported that some bacterial infection or commensal enteric bacteria is related to the pathogenesis or the cause of acute exacerbation of inflammatory bowel disease (IBD). Procalcitonin (PCT) and C-reactive protein (CRP) are 2 acute phase proteins, and PCT is a more specific marker for sepsis and bacterial infections. PCT plays a major role in systemic inflammation and induces a dose-dependent increase in tumour necrosis factor (TNF) alpha secretion, and has been evaluated in chronic inflammatory and autoimmune disease such as Wegener’s granulomatosis as a marker of disease activity. Serum PCT level might also be helpful to predict the disease activity of IBD such as ulcerative colitis (UC), Crohn’s disease (CD), and intestinal Bechet’s disease (Int/BD).
This study aimed to assess the correlation of serum PCT level with clinical, biological, and endoscopic markers of disease activity in IBD, and to evaluate the additional diagnostic benefit of measuring serum PCT level to that of CRP for disease activity.
All eligible patients seen between September 2012 and November 2015 who had clinical evaluation with or without colonoscopy during IBD flare were included in this study. In total, 60 patients (18 CD patients, 37 UC patients, and 5 intestinal BD patients) were enrolled to this study. Apparent infectious cases unrelated to IBD were excluded. Further, 68 samples (27 CD samples, 32 UC samples, and 11 samples) were analysed. Serum PCT levels, CRP levels, and white blood cell (WBC) counts were obtained from all patients. Disease activity in CD was assessed by the CD activity index (CDAI), UC activity was assessed by the Mayo score, and disease activity in Int/BD was assessed by WBC counts and CRP levels, respectively.
In CD (27 samples), serum PCT was strongly correlated with CRP (r = 0.8, p < 0.0001), and PCT was significantly correlated with CDAI (r = 0.7, p < 0.0001). In Int/BD (11 samples), serum PCT was also significantly correlated with CRP (r = 0.8, p < 0.01) and WBC (r = 0.7, p < 0.05) respectively. Patients with severe active to fulminant CD (CDAI > 300) showed significantly higher PCT than that with non-severe active CD (CDAI < 300) (0.15 ng/mL, range 0.02–0.27 vs 0.04 ng/mL, range 0.02–0.08, p < 0.0001). In UC (32 samples); however, serum PCT was not correlated with CRP (r = 0.2) and with the Mayo score (r = -0.2).
In CD and Int/BD not UC, serum PCT level was correlated with disease activity markers and CRP. The serum PCT level was helpful to distinguish severe active to fulminant CD from mild to moderate active CD. Further, serum PCT levels may serve as a new serological marker of disease activity, as well as CRP, in CD and Int/BD not UC.