Postsurgical Recurrence of Ileal Crohn’s Disease: An Update on Risk Factors and Intervention Points to a Central Role for Impaired Host-Microflora Homeostasis

Cunningham, Michael F.; Docherty, Neil G.; Coffey, J. Calvin; Burke, John P.; O'Connell, P. Ronan
July 2010
World Journal of Surgery;Jul2010, Vol. 34 Issue 7, p1615
Academic Journal
A pressing need exists to identify factors that predispose to recurrence after terminal ileal resection for Crohn’s disease (CD) and to determine effective prophylactic strategies. This review presents an up-to-date summary of the literature in the field and points to a role for bacterial overproliferation in recurrence. The literature (Medline, Embase, and the Cochrane Library, 1971–2009) on ileal CD and postoperative recurrence was searched, and 528 relevant articles were identified and reviewed. Smoking is a key independent risk factor for recurrence. NOD2/CARD15 polymorphisms and penetrating phenotype are associated with aggressive disease and higher reoperation rates. Age at diagnosis, disease duration, gender, and family history are inconsistent predictors of recurrence. Prophylactic 5-aminosalicylic acid therapy and nitromidazole antibiotics are beneficial. Combination therapies with immunosuppressants are also effective. Anti-TNFα-based regimens show benefit but the evidence base is small. Corticosteroid, interleukin-10, and probiotic therapies are not effective. Wider, stapled anastomotic configurations are associated with reduced recurrence rates. Strictureplasty and laparoscopic approaches have similar long-term recurrence rates to open resection techniques. Length of resection and presence of microscopic disease at resection margins do not influence recurrence. A lack of consensus exists regarding whether the presence of granulomas or plexitis affects outcome. Current evidence points to defects in mucosal immunity and intestinal dysbiosis of either innate ( NOD2/CARD15) or induced (smoking) origin in postoperative CD recurrence. Prophylactic strategies should aim to limit dysbiosis (antibiotics, side-to-side anastomoses) or prevent downstream chronic inflammatory sequelae (anti-inflammatory, immunosuppressive, and immunomodulatory therapy).


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