Disease activity assessment in IBD: clinical indices and biomarkers fail to predict endoscopic remission.
BACKGROUND
In the current management paradigm, mucosal healing is preferred over clinical remission as a therapeutic end point in inflammatory bowel disease (IBD) because of the benefits engendered with respect to durability of remission. Colonoscopy, however, is not suitable for regular disease monitoring, and routine clinical assessment is often inaccurate with respect to endoscopic disease activity. The current investigation set out to characterize the relationship that exists between endoscopically determined IBD activity and clinical and biochemical measures of disease severity and to determine clinically useful thresholds for use in clinical practice.


METHODS
Patients attending for colonoscopy with known or suspected IBD were recruited. Clinical disease activity was recorded as per the Harvey-Bradshaw Index for Crohn's disease or the simple clinical colitis activity index for ulcerative colitis. Endoscopic activity was recorded using the simple endoscopic score for Crohn's disease or the modified Baron score for ulcerative colitis. Receiver operating characteristic analysis determined the predictive value and optimal predictive thresholds for clinical and biomarker data.


RESULTS
The Harvey-Bradshaw Index was not able to distinguish active from inactive Crohn's disease. The sensitivity, specificity, and positive and negative predictive values of simple clinical colitis activity index to detect endoscopic active disease were 43%, 96%, 94%, and 51%, respectively. Any elevation of C-reactive protein or fecal calprotectin was predictive of active mucosal disease, however, no lower threshold could be identified that predicted disease in remission.


CONCLUSIONS
C-reactive protein and fecal calprotectin are useful for the identification of endoscopically active IBD, but normal results do not confirm endoscopic remission.
*Department of Gastroenterology, Christchurch Hospital, Christchurch, New Zealand; †Department of Medicine, University of Otago, Christchurch, New Zealand; ‡Department of Gastroenterology, North Shore Hospital, Auckland, New Zealand; §Department of Paediatrics, University of Otago, Christchurch, New Zealand; and ║Department of Paediatrics, Christchurch Hospital, Christchurch, New Zealand.
James D
JD
Falvey
Teagan
T
Hoskin
Berrie
B
Meijer
Anna
A
Ashcroft
Russell
R
Walmsley
Andrew S
AS
Day
Richard B
RB
Gearry
D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis*; D003093:Colitis, Ulcerative / Q000378:metabolism / Q000473:pathology; D003113:Colonoscopy; D003424:Crohn Disease / Q000378:metabolism / Q000473:pathology; D005243:Feces / Q000737:chemistry; D005260:Female; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000378:metabolism / Q000473:pathology*; D039841:Leukocyte L1 Antigen Complex / Q000032:analysis*; D008297:Male; D062072:Patient Acuity; D011237:Predictive Value of Tests; D012372:ROC Curve; D012075:Remission, Spontaneous; D012680:Sensitivity and Specificity; D055815:Young Adult
D015415:Biomarkers; D039841:Leukocyte L1 Antigen Complex; D002097:C-Reactive Protein