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P740 Toxin negative Clostridium difficile colonisation and outcome in acute severe ulcerative colitis: a retrospective single-centre study

K.S. Kok*1, S. Chan1, E. Tsiouli2, N. Elumogo2, M. Tremelling1

1Norfolk and Norwich University Hospital, Department of Gastroenterology, Norwich, United Kingdom, 2Norfolk and Norwich University Hospital, Department of Microbiology, Norwich, United Kingdom

Background

Toxin-producing Clostridium difficile (C.diff) significantly worsens outcomes in acute severe ulcerative colitis (ASUC).1 However, it is not known whether non-toxigenic C.diff colonisation (CDC) has a similar effect. To detect C.diff infection, our hospital adopts a 2-stage test algorithm comprising of an initial C.diff-specific glutamate dehydrogenase (GDH) assay followed by a C.diff toxin assay in positive cases.2 CDC is identified as GDH positivity with a negative toxin assay. From 2011 to 2013 only toxin results were reported, and hence GDH statuses were ‘blinded’ to the treating physicians. We are thus able to review in-patient outcomes during this time period to assess the effect of untreated CDC in ASUC.

Methods

We performed a retrospective notes and microbiology database review of all adult patients with ASUC from 2011 to 2013 at the Norfolk and Norwich University Hospital. ASUC was defined as new or existing patients with UC requiring in-patient management. Patients with Crohn’s or indeterminate colitis were excluded. Patients were excluded if they did not have stool cultures or were C.diff toxin positive. Duration of steroid therapy, need for rescue therapy (ciclosporin or infliximab), and emergency colectomy were used as primary outcomes. Cases were defined as ASUC patients with positive GDH but negative C.diff toxin assay. For statistical comparison, controls were ASUC patients with negative GDH stool tests during the same period. Odds ratios were calculated after adjusting for smoking.

Results

There were 130 ASUC admissions; 30 did not have a C.diff stool culture and were excluded, as was 1 patient who tested C.diff toxin positive. Further, 5 of the remaining 99 patients had CDC, with the remainder having no evidence of CDC. Duration of steroid use was not statistically different in the CDC group compared with controls. There was a non-significant increase in the proportion of patients requiring rescue therapy in the CDC group compared with C.Diff negative controls: 3/5 (60%) CDC patients and 31/94 (33.0%) controls, respectively (OR = 2.6, 95% CI 0.40–16.4, p = 0.32). There was a statistically significant increase in emergency colectomy rates in the CDC group (2/5) (40%) compared with the control group (6/94) (6.4%) (OR = 9.4, 95% CI 1.08–82.0, p < 0.05).

Conclusion

Our study suggests that even without toxin formation, CDC might increase risk of emergency colectomy in ASUC. Whether CDC decreases response to steroids or rescue therapy is debatable. Nonetheless, we recommend immediate testing and treatment of CDC in ASUC to reduce likelihood of subsequent colectomy.

References

[1] Issa M, Ananthakrishnan AN, Binion DG. Clostridium difficile and inflammatory bowel disease. Inflamm Bowel Dis 2008;14(10):1432–42.

[2] Shetty N, Wren MW, Coen PG. The role of glutamate dehydrogenase for the detection of Clostridium difficile in faecal samples: a meta-analysis. J Hosp Infect 2011;77(1):1–6.