Effect of intensive granulocyte and monocyte adsorptive apheresis in patients with ulcerative colitis positive for cytomegalovirus

Abstract

Background and aim: Cytomegalovirus (CMV) exacerbates ulcerative colitis (UC) refractory to immunosuppressive therapies. The conditions under which CMV reactivation occurs in patients with UC, however, is unclear. In addition, the diagnostic and treatment strategies for UC positive for CMV have not been established. Granulocyte and monocyte adsorptive apheresis (GMAA) is natural biological therapy for UC in which the granulocytes/macrophages producing inflammatory cytokines are removed. We investigated the rate of colonic CMV reactivation and the efficacy of GMAA in active UC patients positive for CMV without concomitant corticosteroid (CS) therapy. Methods: Fifty-one active UC patients without concomitant CS therapy were enrolled. Colonic CMV reactivation was examined by real-time polymerase chain reaction (PCR) using biopsy specimen and/or histological examination. All patients were treated with intensive GMAA (twice per week). Rates of clinical remission and mucosal healing were compared between UC patients positive and negative for CMV. Results: Of 51 patients, 15 (29.4%) were diagnosed as CMV positive. The clinical remission rates following intensive GMAA did not differ between UC patients positive and negative for CMV (73.3% vs 69.4%, p = 0.781). Proportion of patients achieving mucosal healing was also similar A v a i l a b l e o n l i n e a t w w w . s c i e n c e d i r e c t . c o m ScienceDirectJournal of Crohn's and Colitis (2013) 7, 803-811 Downloaded from https://academic.oup.com/ecco-jcc/article-abstract/7/10/803/378961 by guest on 07 June 2019 between these two groups. CMV-DNA became negative in all UC patients positive for CMV who achieved clinical remission 1 week after completion of intensive GMAA. Conclusions: Intestinal inflammation might trigger CMV reactivation in a subpopulation of active UC patients without CS treatment. GMAA could be a promising option for active UC positive for CMV.

Therapeutic effect of intensive granulocyte and monocyte adsorption apheresis combined with thiopurines for steroid- and biologics-naïve Japanese patients with early-diagnosed Crohn’s disease

“…Intensive GMAA treatment (twice per week, 10 sessions) was performed as previously described [11,12,16] for all patients with CD. Blood was accessed via the antecubital vein in one arm, and from the outflow blood was returned to patients via the antecubital vein in the other arm through 19 gauge needles.…”

Cytomegalovirus Colitis, Cytomegalovirus Hepatitis and Systemic Cytomegalovirus Infection: Common Features and Differences

“…Yoshino et al [52] demonstrated that 56.7% of UC patients refractory to immunosuppressive therapies were positive for CMV-DNA in colonic mucosa. Fukuchi et al [53] reported that 29.4% of active UC patients without receiving any immunosuppressive therapies were positive for CMV-DNA in their colonic mucosa. In addition, analysis in a newly established mouse model, which resembles human UC with concomitant CMV infection, strongly suggests that CMV infection can trigger intestinal inflammation [54].…”

“…This anti-inflammatory mechanism of GMAA comprises a promising treatment for UC patients with concomitant CMV infection because production of proinflammatory cytokines, particularly TNF-α, is strongly associated with colonic CMV reactivation. In fact, 2 Japanese studies reported that GMAA does not induce colonic CMV reactivation and leads to disappearance of colonic CMV replication in previously PCR CMV-DNA-positive UC patients [53, 75]. Thus, GMAA therapy offers optimal inflammatory control without the need for steroids.…”

Effects of cytomegalovirus infection on the prognosis of inflammatory bowel disease patients

“…It is estimated that CMV infection in IBD patients is within the range of 33–36% in patients with steroid-refractory UC and 21–34% in patients suffering from severe UC (11). Colonic CMV reactivation is considered to be an exacerbating factor in patients with UC and those refractory to immunosuppressive therapies due to the poor prognosis of UC patients with concomitant CMV infection (12). Previous studies have demonstrated that local intestinal inflammation and additional immunosuppressive therapies, such as corticosteroid administration, may induce colonic CMV reactivation in IBD patients (12,13).…”

“…Colonic CMV reactivation is considered to be an exacerbating factor in patients with UC and those refractory to immunosuppressive therapies due to the poor prognosis of UC patients with concomitant CMV infection (12). Previous studies have demonstrated that local intestinal inflammation and additional immunosuppressive therapies, such as corticosteroid administration, may induce colonic CMV reactivation in IBD patients (12,13). However, another study presented conflicting results on the association of CMV reactivation with the occurrence or severity of IBD exacerbation (1).…”