CLINICAL SIGNIFICANCE OF CYTOMEGALOVIRUS (CMV) INFECTION IN INFLAMMATORY BOWEL DISEASE

Background and aim:The role of CMV in exacerbation of inflammatory bowel disease (IBD) remains a topic of ongoing debate. The aims of this study were to evaluate: the correlation between the presence of CMV in the colon, the clinical activity of the disease and the colonic extent of ulcerative colitis; the role of CMV infection in steroid-dipendent/refractory patients; the role of immunosuppressive therapies in CMV reactivation. Material and methods:We retrospectively evaluated 44 IBD patients (30 ulcerative colitis, UC; 13 Crohn’s disease, CD; 1 pouchitis) that, from 2009to 2011, were investigated about the presence of CMV on biopsy specimens of colon. In each patient we recorded: clinical activity; endoscopic extent; steroid-dipendent/refractory status and ongoing therapies. PCR amplification technique was used for detecting CMV-DNA in colonic tissue. Clinical severity of IBD was assessed according to Mayo Scoring Index for UC and Harvey-Bradshaw Index for CD. Results:The presence of CMV-DNA in colonic biopsies was detected in 14 out of 44 patients (13 UC; 1 CD), with an overall prevalence of 32%. 7 out of 14 CMV+ patients (50%) and 4 out of 30 CMV- patients (13%), showed clinically severe disease (P<0.05). 28 patients were resistant/dependent to steroids. CMV was detected in 12 out of these 28 patients (43%), and in 2 out of the 16 (13%) patients steroid-responsive (P<0.05). Considering the colonic extent of UC, among the 13 CMV+ patients: 2 had a rectosigmoiditis (16%), 5 had a left-sided colitis (38%) and 6 had a colitis extending beyond the left colonic flexure. Among the 17 CMV- patients: 5 had a rectosigmoiditis (28%), 4 had a left-sided colitis (25%) and 8 had a colitis extending beyond the left colonic flexure (47%). No significant statistical difference was found between these two groups. 16 out of 44 patients were under immunosuppressive treatment. Among these 16, 6 were CMV+ (38%) and 10 was CMV- (62%); among the other 28 patients, 8 was CMV+ (28%) and 20 was CMV- (72%). No significant statistical difference was found between these two groups. Conclusions:CMV appears to play a role in a subgroup of patients with severe or steroid-refractory IBD. It is not clear whether the virus causes steroid dependence/refractory or a prolonged steroid use reactivates a latent viral infection. No correlation was found between the extent of UC, the immunosuppressive therapy and the presence of CMV-DNA in colonic tissue.